Indirect immunofluorescent antibody (IFA), latex agglutination (IA), and enzyme immunoassay (EIA) methods were compared for evaluation of the serum antibody responses of dogs experimentally and naturally exposed to spotted fever-group rickettsiae. Selected sera (obtained on days 1, 42, 53, 124, 145, 236, 255, 264, and 292) were examined from three 8-month-old female Beagles inoculated with Rickettsia rickettsii on days 34 and 250 of the study. A second group of dogs comprised three 8-month-old female Beagles inoculated with R montana on days 34 and 102. Subsequently, these dogs were inoculated with R rickettsii on day 250. Serum samples were obtained from the second group of dogs on days 1, 96, 103, 132, 180, 215, 292, and 494. A third group consisted of 21 naturally exposed dogs, from which sequentially obtained serum samples were available, and which had clinical signs compatible with Rocky Mountain spotted fever. Clinical signs of disease in dogs of the third group resolved after treatment with tetracycline (22 mg/kg of body weight, Po, q 8 h) was instituted. At least 2 sequentially obtained serum samples from each dog were tested. In general, the first sample was obtained just prior to treatment and the convalescent serum samples were obtained at weekly or greater intervals thereafter. For correlation and reactivity data, an IFA test for IgG/IgM (using heavy and light chains-specific conjugate) was used as the reference standard for comparison of results with those of the other tests,.

Indirect immunofluorescent antibody (IFA), latex agglutination (IA), and enzyme immunoassay (EIA) methods were compared for evaluation of the serum antibody responses of dogs experimentally and naturally exposed to spotted fever-group rickettsiae. Selected sera (obtained on days 1, 42, 53, 124, 145, 236, 255, 264, and 292) were examined from three 8-month-old female Beagles inoculated with Rickettsia rickettsii on days 34 and 250 of the study. A second group of dogs comprised three 8-month-old female Beagles inoculated with R montana on days 34 and 102. Subsequently, these dogs were inoculated with R rickettsii on day 250. Serum samples were obtained from the second group of dogs on days 1, 96, 103, 132, 180, 215, 292, and 494. A third group consisted of 21 naturally exposed dogs, from which sequentially obtained serum samples were available, and which had clinical signs compatible with Rocky Mountain spotted fever. Clinical signs of disease in dogs of the third group resolved after treatment with tetracycline (22 mg/kg of body weight, Po, q 8 h) was instituted. At least 2 sequentially obtained serum samples from each dog were tested. In general, the first sample was obtained just prior to treatment and the convalescent serum samples were obtained at weekly or greater intervals thereafter. For correlation and reactivity data, an IFA test for IgG/IgM (using heavy and light chains-specific conjugate) was used as the reference standard for comparison of results with those of the other tests,

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses. High transmural pressures may cause stress failure of pulmonary capillaries, resulting in exercise-induced pulmonary hemorrhage.

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses. High transmural pressures may cause stress failure of pulmonary capillaries, resulting in exercise-induced pulmonary hemorrhage.

Microscopic examination of the nasal mucosa of clinically normal specific-pathogen-free pigs and of toxicogenic type-D Pasteurella multocida toxin challenge-exposed specific-pathogen-free pigs indicated that the surface epithelium in pigs of both groups was microscopically normal; erosions or appreciable inflammatory changes were not evident. In pigs of both groups and in aU 3 regions of the nasal cavity, the endothelial lining of all blood vessels appeared normal without detectable changes to the walls at postinoculation day 10. Vascular injury in the cartilage or the bone was not discernible in control or challenge-exposed pigs. There were marked differences in the osseous structures of the conchae when the 2 groups were compared. In control pigs, active bone formation and remodeling were observed, and the septal cartilage was normal. In toxin challenge-exposed pigs, there likewise was normal bone formation and remodeling in the vestibular region, and the septal cartilage was normal. In marked contrast, conspicuous changes were observed in the osseous core of the conchae of the respiratory and, sometimes, the olfactory regions. These changes consisted of bone necrosis and resorption by large numbers of osteoclasts with variable replacement by dense mesenchymal stroma, which resulted in conchal atrophy. In the absence of any discernible damage or injury (angiopathy) to the nasal vessels, it appears that the action of the dermonecrotoxin of P multocida serotype D is on the most active osteoblasts and the associated organic matrix of the bone, with subsequent disruption of normal bone formation and remodeling of the nasal conchae.

Microscopic examination of the nasal mucosa of clinically normal specific-pathogen-free pigs and of toxicogenic type-D Pasteurella multocida toxin challenge-exposed specific-pathogen-free pigs indicated that the surface epithelium in pigs of both groups was microscopically normal; erosions or appreciable inflammatory changes were not evident. In pigs of both groups and in aU 3 regions of the nasal cavity, the endothelial lining of all blood vessels appeared normal without detectable changes to the walls at postinoculation day 10. Vascular injury in the cartilage or the bone was not discernible in control or challenge-exposed pigs. There were marked differences in the osseous structures of the conchae when the 2 groups were compared. In control pigs, active bone formation and remodeling were observed, and the septal cartilage was normal. In toxin challenge-exposed pigs, there likewise was normal bone formation and remodeling in the vestibular region, and the septal cartilage was normal. In marked contrast, conspicuous changes were observed in the osseous core of the conchae of the respiratory and, sometimes, the olfactory regions. These changes consisted of bone necrosis and resorption by large numbers of osteoclasts with variable replacement by dense mesenchymal stroma, which resulted in conchal atrophy. In the absence of any discernible damage or injury (angiopathy) to the nasal vessels, it appears that the action of the dermonecrotoxin of P multocida serotype D is on the most active osteoblasts and the associated organic matrix of the bone, with subsequent disruption of normal bone formation and remodeling of the nasal conchae.

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 X 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus. Age at puberty was similar between gilts exposed to low or moderate concentration of ammonia (208 vs 205 days; SEM, 1.3 days), even though weight at puberty was less (P < 0.03) for gilts exposed to low concentration of ammonia than for gilts exposed to moderate concentration of ammonia (109.7 vs 118.2 kg; SEM, 4.5 kg).

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 X 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus. Age at puberty was similar between gilts exposed to low or moderate concentration of ammonia (208 vs 205 days; SEM, 1.3 days), even though weight at puberty was less (P < 0.03) for gilts exposed to low concentration of ammonia than for gilts exposed to moderate concentration of ammonia (109.7 vs 118.2 kg; SEM, 4.5 kg). At day 30 of gestation, number of live fetuses (10.6 vs 11.7), fetal length (2.53 vs 2.57 cm), and fetus-to-corpus luteum ratio (0.85 vs 0.78) were similar between gilts at low and moderate ammonia environments. These data indicate that exposure of gilts to mean aerial ammonia concentration of 35 ppm in environmentally regulated rooms depressed MDG for 2 weeks, but failed to alter onset of puberty or litter size at day 30 of gestation.

Studies were undertaken to determine the efficacy of milbemycin oxime against the enteric adult stages of Trichinella spiralis and of albendazole against the muscle stage larvae in experimentally infected dogs and cats. Specific-pathogen-free Beagle pups (n = 6) and domestic shorthair kittens (n = 6) were inoculated with 7,500 first-stage larvae of Trichinella spiralis. Physical examination (including collection of blood and fecal samples) was performed weekly. During the first week after inoculation, all animals had mild gastrointestinal tract disturbances, but stages of T. spiralis were not observed in the feces. Beginning on postinoculation day (PID) 10, 3 pups and 3 kittens were treated with milbemycin oxime (1.25 mg/kg of body weight, PO, q 12 h) for 10 days. Muscle biopsy specimens were taken from dogs and cats on PID 26 and 29, respectively. Mean numbers of larvae per gram of muscle were 30.3 in the control and 37.7 in the treated dogs. Mean numbers of larvae per gram of muscle in the control and treated cats were 318.7 and 89.3, respectively. Two dogs and 2 cats were removed from the study at that time. The remaining animals, 2 each of the control and milbemycin oxime-treated animals, were given albendazole (50 mg/kg, PO, q 12 h) for 7 days starting at PID 31 and 34 in dogs and cats, respectively. Muscle biopsy specimens were again taken at PID 46 and 49, for dogs and cats, respectively; mean numbers of larvae recovered from muscle were 0.6 for dogs and 13.5 for cats.

Studies were undertaken to determine the efficacy of milbemycin oxime against the enteric adult stages of Trichinella spiralis and of albendazole against the muscle stage larvae in experimentally infected dogs and cats. Specific-pathogen-free Beagle pups (n = 6) and domestic shorthair kittens (n = 6) were inoculated with 7,500 first-stage larvae of Trichinella spiralis. Physical examination (including collection of blood and fecal samples) was performed weekly. During the first week after inoculation, all animals had mild gastrointestinal tract disturbances, but stages of T. spiralis were not observed in the feces. Beginning on postinoculation day (PID) 10, 3 pups and 3 kittens were treated with milbemycin oxime (1.25 mg/kg of body weight, PO, q 12 h) for 10 days. Muscle biopsy specimens were taken from dogs and cats on PID 26 and 29, respectively. Mean numbers of larvae per gram of muscle were 30.3 in the control and 37.7 in the treated dogs. Mean numbers of larvae per gram of muscle in the control and treated cats were 318.7 and 89.3, respectively. Two dogs and 2 cats were removed from the study at that time. The remaining animals, 2 each of the control and milbemycin oxime-treated animals, were given albendazole (50 mg/kg, PO, q 12 h) for 7 days starting at PID 31 and 34 in dogs and cats, respectively. Muscle biopsy specimens were again taken at PID 46 and 49, for dogs and cats, respectively; mean numbers of larvae recovered from muscle were 0.6 for dogs and 13.5 for cats.

A serologic survey was conducted to determine the prevalence and seroconversion rates for ovine adenovirus (OAV) serotypes 1-4 and bovine adenovirus (BAV) serotypes 2, 3, and 7 in sheep in Iowa and in surrounding states. For 2 consecutive years, paired serum samples were obtained from 1- to 2-month-old lambs as they entered a ram test station and, again, 2 months later. Sera were tested for adenovirus antibodies by use of a microtitration serum virus-neutralization test. At the time of entry, high prevalence of antibody (titer greater than or equal to 2) was detected to all tested adenoviruses except BAV-3. All adenoviruses were active in the ram test station both years, as indicated by greater than or equal to fourfold increase in adenovirus antibody titer (seroconversion) in some of the lambs. The prevalence and seroconversion rate for OAV-1 was 94.0 and 7.2%, respectively; for OAV-2, 98.6 and 15.1%; for OAV-3, 86.5 and 11.0%; for OAV-4, 98.4 and 13.2%; for BAV-2, 97.6 and 22.4%; for BAV-3, 11.4 and 3.8%; and for BAV-7, 81.6 and 4.5%. The results indicate that adenovirus infections were widespread in the sheep population and that the prevalence of active infection based on seroconversion rates was approximately 45%.

A serologic survey was conducted to determine the prevalence and seroconversion rates for ovine adenovirus (OAV) serotypes 1-4 and bovine adenovirus (BAV) serotypes 2, 3, and 7 in sheep in Iowa and in surrounding states. For 2 consecutive years, paired serum samples were obtained from 1- to 2-month-old lambs as they entered a ram test station and, again, 2 months later. Sera were tested for adenovirus antibodies by use of a microtitration serum virus-neutralization test. At the time of entry, high prevalence of antibody (titer greater than or equal to 2) was detected to all tested adenoviruses except BAV-3. All adenoviruses were active in the ram test station both years, as indicated by greater than or equal to fourfold increase in adenovirus antibody titer (seroconversion) in some of the lambs. The prevalence and seroconversion rate for OAV-1 was 94.0 and 7.2%, respectively; for OAV-2, 98.6 and 15.1%; for OAV-3, 86.5 and 11.0%; for OAV-4, 98.4 and 13.2%; for BAV-2, 97.6 and 22.4%; for BAV-3, 11.4 and 3.8%; and for BAV-7, 81.6 and 4.5%. The results indicate that adenovirus infections were widespread in the sheep population and that the prevalence of active infection based on seroconversion rates was approximately 45%.

Anesthesia was induced in 8 healthy llamas by administration of guaifenesin and ketamine, and was maintained with halothane in oxygen. On 2 separate experimental days, atracurium was given to induce 95 to 99% reduction of evoked hind limb digital extensor tension (twitch). For the first part of the study, atracurium was given iv as repeat boluses, with muscle twitch strength being allowed to return without intervention to 75% of baseline after each bolus before the subsequent bolus was given. A total of 5 bolus doses of atracurium was given. For the first bolus, 0.15 mg/kg of body weight iv, and for subsequent boluses, 0.08 mg/kg, induced desired relaxation. Onset of relaxation was slightly more rapid for repeat, compared with initial, bolus. Duration of relaxation and recovery time were similar to initial and repeat doses. Maximal twitch reduction was observed in 4 +/- 0.2 minutes (mean +/- SEM). Duration from maximal twitch reduction to 10% recovery was 6.3 +/- 0.4 minutes. Twitch recovery from 10 to 50% of baseline took 11.6 +/- 0.6 minutes. Twitch recovery from 10 to 75% recovery took 19.5 +/- 1.1 minutes. Recovery from 10% twitch to 50% fade took 12.8 +/- 0.5 minutes. Fade at 50% recovery of twitch was 39 +/- 0.02%. Significant (P < 0.05) animal-to-animal variation was observed in twitch recovery times. For the second part of the study, atracurium was initially given IV as a 0.15-mg/kg bolus, followed by infusion for 1 to 2 hours. Infusion rate required some early adjustment to maintain desired relaxation, but the rate that prevailed was 1.07 +/- 0.07 ml/kg/h (0.4 mg of atracurium/ml of saline solution). Recovery of muscle twitch was similar to that previously mentioned for repeat bolus administration, At the end of the study, edrophonium (0.5 mg/kg) with atropine (0.01 mg/kg, IV) was effective in antagonizing residual neuromuscular blockade by atracurium. All llamas recovered without injury from anesthesia, although 1 llama had a rough recovery. It was concluded that atracurium can provide neuromuscular blockade by either repeat bolus administration or continuous infusion in llamas.

Anesthesia was induced in 8 healthy llamas by administration of guaifenesin and ketamine, and was maintained with halothane in oxygen. On 2 separate experimental days, atracurium was given to induce 95 to 99% reduction of evoked hind limb digital extensor tension (twitch). For the first part of the study, atracurium was given iv as repeat boluses, with muscle twitch strength being allowed to return without intervention to 75% of baseline after each bolus before the subsequent bolus was given. A total of 5 bolus doses of atracurium was given. For the first bolus, 0.15 mg/kg of body weight iv, and for subsequent boluses, 0.08 mg/kg, induced desired relaxation. Onset of relaxation was slightly more rapid for repeat, compared with initial, bolus. Duration of relaxation and recovery time were similar to initial and repeat doses. Maximal twitch reduction was observed in 4 +/- 0.2 minutes (mean +/- SEM). Duration from maximal twitch reduction to 10% recovery was 6.3 +/- 0.4 minutes. Twitch recovery from 10 to 50% of baseline took 11.6 +/- 0.6 minutes. Twitch recovery from 10 to 75% recovery took 19.5 +/- 1.1 minutes. Recovery from 10% twitch to 50% fade took 12.8 +/- 0.5 minutes. Fade at 50% recovery of twitch was 39 +/- 0.02%. Significant (P < 0.05) animal-to-animal variation was observed in twitch recovery times. For the second part of the study, atracurium was initially given IV as a 0.15-mg/kg bolus, followed by infusion for 1 to 2 hours. Infusion rate required some early adjustment to maintain desired relaxation, but the rate that prevailed was 1.07 +/- 0.07 ml/kg/h (0.4 mg of atracurium/ml of saline solution). Recovery of muscle twitch was similar to that previously mentioned for repeat bolus administration, At the end of the study, edrophonium (0.5 mg/kg) with atropine (0.01 mg/kg, IV) was effective in antagonizing residual neuromuscular blockade by atracurium. All llamas recovered without injury from anesthesia, although 1 llama had a rough recovery. It was concluded that atracurium can provide neuromuscular blockade by either repeat bolus administration or continuous infusion in llamas.

Transcutaneous oxygen (PO2.TC) monitoring is commonly used in human medicine for evaluating skin viability. The application of transcutaneous monitoring for evaluating skin viability in dogs was investigated. The changes in PO2-TC values were measured from 16 avascular skin flaps created along the lateral hemithoraces of 4 dogs. Transcutaneous oxygen values were serially recorded from the vascular base and avascular apex of each flap for 12 hours after surgery. A single transcutaneous measurement was obtained from each flap base and apex 24 hours after surgery. Serial arterial blood gas analyses were obtained to compare central oxygen values with PO2-TC values. Full-thickness skin biopsy specimens were harvested from the base and apex of each flap 24 hours after surgery. The flaps were observed for 4 days and then excised for histologic examination. A subjective grading scale was used to assess histologic changes. Throughout the 12-hour period and at 24 hours, a statistically significant difference was found between the PO2-TC values for apices and bases of the flaps. The mean PO2-TC for all bases was 90.9 mm of Hg +/- 3.3 SEM, and the mean PO2-TC for all apices was 21.2 mm of Hg +/- 1.8 SEM. The mean regional perfusion index (apex PO2.TC/base PO2-TC) was 0.23 +/- 0.02. The subjective numbers assigned to the biopsy specimens were statistically evaluated by using a paired Student's t test and a Wilcoxon signed-rank test. A significant difference was found between the numbers for the collective bases and apices with both tests. A statistically significant difference was found between the numbers for the apex biopsy specimens taken 24 hours after creation of the skin flap and those taken when the flap was excised, whereas no difference was found between the numbers for the base biopsy specimens. On the basis of our findings, PO2-TC monitoring is a useful technique for assessing skin viability in dogs.

Transcutaneous oxygen (PO2.TC) monitoring is commonly used in human medicine for evaluating skin viability. The application of transcutaneous monitoring for evaluating skin viability in dogs was investigated. The changes in PO2-TC values were measured from 16 avascular skin flaps created along the lateral hemithoraces of 4 dogs. Transcutaneous oxygen values were serially recorded from the vascular base and avascular apex of each flap for 12 hours after surgery. A single transcutaneous measurement was obtained from each flap base and apex 24 hours after surgery. Serial arterial blood gas analyses were obtained to compare central oxygen values with PO2-TC values. Full-thickness skin biopsy specimens were harvested from the base and apex of each flap 24 hours after surgery. The flaps were observed for 4 days and then excised for histologic examination. A subjective grading scale was used to assess histologic changes. Throughout the 12-hour period and at 24 hours, a statistically significant difference was found between the PO2-TC values for apices and bases of the flaps. The mean PO2-TC for all bases was 90.9 mm of Hg +/- 3.3 SEM, and the mean PO2-TC for all apices was 21.2 mm of Hg +/- 1.8 SEM. The mean regional perfusion index (apex PO2.TC/base PO2-TC) was 0.23 +/- 0.02. The subjective numbers assigned to the biopsy specimens were statistically evaluated by using a paired Student's t test and a Wilcoxon signed-rank test. A significant difference was found between the numbers for the collective bases and apices with both tests. A statistically significant difference was found between the numbers for the apex biopsy specimens taken 24 hours after creation of the skin flap and those taken when the flap was excised, whereas no difference was found between the numbers for the base biopsy specimens. On the basis of our findings, PO2-TC monitoring is a useful technique for assessing skin viability in dogs.

Cardiovascular and at accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, PCV, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2, and PaCO2, did not significantly change during the 12 hours of study, PVO2 increased significantly P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time significantly [P < 0.05] starting at 9 hours), despite supplemental IV administered NaHCO3. Plasma concentrations of eicosanoids: 6-ketoprostaglandin F1 alpha (PGF1 alpha, a stable metabolite of PGI2), PGF2 alpha, PGE, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.

Cardiovascular and at accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, PCV, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2, and PaCO2, did not significantly change during the 12 hours of study, PVO2 increased significantly P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time significantly [P < 0.05] starting at 9 hours), despite supplemental IV administered NaHCO3. Plasma concentrations of eicosanoids: 6-ketoprostaglandin F1 alpha (PGF1 alpha, a stable metabolite of PGI2), PGF2 alpha, PGE, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.

Middle carpal cartilage explants from 4 horses with mild osteoarthritis involving that joint were maintained in tissue culture to test the effects of a polysulfated glycosaminoglycan (PSGAG) on proteoglycan synthesis and degradation. Cultures were exposed to 0.025 or 25 mg of PSGAG/ml for 48 hours, after which the medium was replaced with medium containing similar doses of PSGAG and 35S. Subsequently, the sulfated proteoglycan content of the medium and extracts of the explants was measured. Gel filtration chromatography was used to estimate the size and to purify the principal, large proteoglycan monomer, which was further characterized by digestion, using glycosidic enzymes. In a second experiment, explants were incubated with 35S for 48 hours, and were subsequently exposed to the same concentrations of the PSGAG for an additional 48 hours. The amount of remaining labeled proteoglycan was determined for culture medium and cartilage extracts. Gel filtration chromatography was used to assess the hydrodynamic size of the large proteoglycan monomer. Aliquots of proteoglycans from the second experiment were incubated in high-molecular weight hyaluronate and chromatographed to assess reaggregation. Polysulfated glycosaminoglycan caused a significant (P < 0.04) decrease in sulfated proteoglycan synthesis by cartilage explants. Radioactive proteoglycan content in explants labeled prior to exposure to PSGAG were similar. Large proteoglycan monomer size was similar in both experiments (median partition coefficient [K(AV)] = 0.40), and was not influenced by PSGAG treatment. Prelabeled explants exposed to hyaluronate and chromatographed under associative conditions had similar proportions of the radiolabel eluting as proteoglycan aggregate. Enzymatic digestion of newly synthesized large monomer revealed a mild dose-dependent increase in the proportion of keratan sulfate substitution on core protein. It was concluded that PSGAG in vitro, at the dosages evaluated, caused a decre.

Middle carpal cartilage explants from 4 horses with mild osteoarthritis involving that joint were maintained in tissue culture to test the effects of a polysulfated glycosaminoglycan (PSGAG) on proteoglycan synthesis and degradation. Cultures were exposed to 0.025 or 25 mg of PSGAG/ml for 48 hours, after which the medium was replaced with medium containing similar doses of PSGAG and 35S. Subsequently, the sulfated proteoglycan content of the medium and extracts of the explants was measured. Gel filtration chromatography was used to estimate the size and to purify the principal, large proteoglycan monomer, which was further characterized by digestion, using glycosidic enzymes. In a second experiment, explants were incubated with 35S for 48 hours, and were subsequently exposed to the same concentrations of the PSGAG for an additional 48 hours. The amount of remaining labeled proteoglycan was determined for culture medium and cartilage extracts. Gel filtration chromatography was used to assess the hydrodynamic size of the large proteoglycan monomer. Aliquots of proteoglycans from the second experiment were incubated in high-molecular weight hyaluronate and chromatographed to assess reaggregation. Polysulfated glycosaminoglycan caused a significant (P < 0.04) decrease in sulfated proteoglycan synthesis by cartilage explants. Radioactive proteoglycan content in explants labeled prior to exposure to PSGAG were similar. Large proteoglycan monomer size was similar in both experiments (median partition coefficient [K(AV)] = 0.40), and was not influenced by PSGAG treatment. Prelabeled explants exposed to hyaluronate and chromatographed under associative conditions had similar proportions of the radiolabel eluting as proteoglycan aggregate. Enzymatic digestion of newly synthesized large monomer revealed a mild dose-dependent increase in the proportion of keratan sulfate substitution on core protein. It was concluded that PSGAG in vitro, at the dosages evaluated, caused a decrease in proteoglycan synthesis, had little effect on labeled proteoglycan degradation, did not influence the size of large monomer, and caused a modest increase in the concentration of keratan sulfate in proteoglycans synthesized by osteoarthritic equine chondrocytes.