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.

Cardiorespiratory effects of abdominal insufflation were evaluated in 8 dogs during isoflurane anesthesia. Each dog was studied 3 times, in 1 of the following orders of insufflation pressures: 10-20-30, 20-30-10, 30-20-10, 10-30-20, 20-10-30, and 30-10-20 mm of Hg. Anesthesia was induced by use of a mask, dogs were intubated, and anesthesia was maintained by isoflurane in 100% oxygen. After instrumentation, baseline values were recorded (time 0), and the abdomen was insufflated with nitrous oxide. Data were recorded at 5, 10, 15, 20, 25, and 30 minutes after insufflation. The abdomen was then desufflated, with recording of data continuing at 35 and 40 minutes. Mean arterial pressure increased at 5 minutes during 20 mm of Hg insufflation pressure, and from 20 to 30 minutes during 30 mm of Hg pressure. Tidal volume decreased from 5 to 30 minutes during 10 and 20 mm of Hg pressures, and from 5 to 40 minutes during 30 mm of Hg pressure. Minute ventilation decreased at 10 and 20 minutes during 20 mm of Hg pressure. End-tidal CO2 concentration increased from 5 to 30 minutes during 20 and 30 mm of Hg pressure. The PaCO2 decreased at 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Values for pH decreased from 10 to 30 minutes during 20 and 30 mm of Hg pressures. The PaO2 decreased from 20 to 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Percentage decrease in tidal volume was greater at 5 and 15 minutes with 30 mm of Hg pressure. Differences in percentage increase in end tidal CO2 concentration were observed among the 3 pressures from 5 to 30 minutes. Although significant, these changes do not preclude use of laparoscopy if insufflation pressure > 20 mm of Hg is avoided.

Anesthesia was induced and maintained in 6 Suffolk wethers by continuous IV infusion of guaifenesin (50 mg/ml), ketamine (1 mg/ml), and xylazine (0.1 mg/ml) in 5% dextrose in water (triple drip) to assess the anesthetic and cardiopulmonary effects. All sheep were positioned in right lateral recumbency. Dosages of triple drip used for induction and maintenance of anesthesia were 1.2 +/- 0.02 ml/kg and 2.6 ml/kg/h, respectively. Lack of gross purposeful movement of sheep to electrical stimulation indicated that analgesia and muscular relaxation induced by triple trip were adequate for surgical procedures. Heart rates and arterial blood pressure remained unchanged from baseline values during a 1-hour period of anesthesia. Arterial blood pressures were measured indirectly, using an inflation cuff placed over the metatarsal artery at the heart level. Significant decrease in arterial partial pressure of O2 (PaO2), coupled with an increase in arterial partial pressure of CO2 (PaCO2), from baseline values was observed throughout the course of the study. Decrease in PaO2 was observed concomitantly with significant (P < 0.05) increase in respiration rate. Changes in arterial blood gas tensions observed in this study were attributed to respiratory depressant effect induced by anesthetic drugs and right-to-left shunting, perfusion/ventilation mismatch, or both caused by right lateral recumbency. Administration of 100% O2 via the endotracheal tube reduced the magnitude of the decrease in PaO2. All sheep recovered smoothly and stood within 96.3 +/- 48.9 minutes after termination of triple drip administration.

The hemodynamic effects of 2 dosages of ephedrine were studied in 6 dogs anesthetized with isoflurane only (end-tidal concentration equivalent to 1.5 times minimum alveolar concentration). Following instrumentation, baseline (time 0) measurements included heart rate (HR), respiratory rate, mean arterial blood pressure (MAP), cardiac output, and blood gas tensions. Cardiac index (CI), stroke volume (SV), systemic vascular resistance (SVR), arterial oxygen content (CaO2), and oxygen delivery and consumption (DO2 and VO2, respectively) were calculated. Three dogs were given ephedrine IV at a dosage of 0.1 mg/ kg of body weight, and 3 dogs were given ephedrine IV at a dosage of 0.25 mg/kg. Measurements were recorded at 5, 10, 15, 30, and 60 minutes. Each dog then received the alternate dosage of ephedrine, and measurements were again recorded at the same intervals. Effects of ephedrine varied with dosage. Neither dosage was associated with significant changes in pH, PaO2, PaCO2, VO2, or respiratory rate. Ephedrine at a dosage of 0.1 mg/kg caused transient significant increases in MAP, CI, SV, CaO2, and DO2, significant decreases in HR and SVR, and a late, slight decrease in CaO2. Ephedrine at a dosage of 0.25 mg/kg caused a greater and more prolonged increase in MAP, as well as increases in CI, SV, and SVR, and a decrease in HR. The higher dosage of ephedrine also caused a pronounced increase in hemoglobin concentration and CaO2, resulting in a 20 to 35% increase in DO2 throughout the 60-minute experiment.

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1 (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [log(e) detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [log(e) detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). Plasma atrial natriuretic peptide concentration was significantly increased with increasing detomidine concentration (20.4 +/- 3.8 pg/ml at baseline to 33.5 +/- 9.1 at infusion 4). There were few significant changes in respiration rate and arterial blood gas and pH values. We conclude that maintenance of steady-state detomidine plasma concentrations resulted in cardiopulmonary changes that were quantitatively similar to those induced by detomidine bolus administration in horses.

The effect of furosemide-induced weight loss on the energetic responses of horses to running was examined in a 3-way crossover study. Eight 2- to 3-year-old Standardbred mares received, in random order, 10 ml of saline solution 4 hours before running on a treadmill (control trial, C); or, during 2 trials, 1 mg of furosemide/kg of body weight, IV, 4 hours before running. During one of the trials when the horses received furosemide, they carried weight equal to that lost over the 3.75 hours after furosemide administration while running (furosemide-loaded, FL), and during the other trial they did not carry weight equal to that lost after furosemide administration (furosemide-unloaded, FU). Horses performed an incremental exercise test on a treadmill during which rates of oxygen consumption (V(O2)) and carbon dioxide production (V(CO2)) were measured, respiratory exchange ratio was calculated, and blood samples were collected for determination of mixed venous plasma lactate concentration and arterial and mixed venous oxygen saturation. Furosemide treatment caused significantly (P < .001) greater weight loss than did saline administration; mean +/- SEM weight loss (exclusive of fecal loss) was 1.6, 8.8, and 10.2 kg (SEM = 2.0) for C, FL, and FU trials, respectively. The speed at which peak V(O2) was achieved was 9.31, 9.56, and 9.50 (SEM = 0.16) m/s, respectively, time to fatigue was 547, 544, and 553 (SEM = 26) seconds, respectively, and the highest speed attained was 10.3, 10.2, and 10.2 (SEM = 0.2) m/s, respectively. Mean peak rate of oxygen consumption was 130.7, 129.6, and 129.6 (SEM = 1.9) ml/min/kg, respectively. There was a significant (P = 0.070) group X speed interaction for V(CO2); during trial FU, horses had significantly (P < 0.05) lower rate of CO2 production at speed of 9 m/s and at the speed that caused peak V(O2), than during trial C. The respiratory exchange ratio during the FU trial was significantly (P < 0.05) less than that during the C trial at the speed that caused peak V(O2). Plasma lactate concentration at speed of 9 m/s for C, FL, and FU trials was 15.4, 16.5, and 13.3 (SEM = 0.8) mmol/L, respectively; values for the FL and C trials were not significantly different, whereas the mean value for the FU trial was significantly (P < 0.05) less than that for the C trial. Thus, administration of furosemide to horses altered the energetic response to exertion. Replacement of the furosemide-induced weight loss resulted in V(CO2), plasma lactate, and respiratory exchange values indistinguishable from those during the control trial.

We evaluated the effects of clenbuterol HCl (0.8 micrograms/kg, of body weight, IV), a beta 2, agonist, on ventilation-perfusion matching and hemodynamic variables in anesthetized (by IV route), laterally recumbent horses. The multiple inert gas elimination technique was used to assess pulmonary gas exchange. Clenbuterol HCl induced a decrease in arterial oxygen tension (from 57.0 +/- 1.8 to 49.3 +/- 1.2 mm of Hg; mean +/- SEM) as a result of increased shunt fraction (from 6.6 +/- 2.1 to 14.4 +/- 3.1%) and ventilation to regions with high ventilation-perfusion ratios. In contrast, no changes in these variables were found in horses given sterile water. In horses given clenbuterol HCl, O2 consumption increased from 2.23 +/- 0.18 to 2.70 +/- 0.14 ml . min-1 . kg-1, and respiratory exchange ratio decreased from 0.80 +/- 0.02 to 0.72 +/- 0.01. Respiratory exchange ratio and O2 consumption were not significantly modified in sterile water-treated (control) horses. Clenbuterol HCl administration was associated with increased cardiac index (from 57.4 +/- 4.0 to 84.2 +/- 6.3 ml . min-1 . kg- 1), decreased total peripheral vascular resistance (from 108.3 +/- 9.3 to 47.6 +/- 2.8 mm of Hg . s . kg . ml-1), and decreased pulmonary vascular resistance (from 31.3 +/- 3.8 to 13.6 +/- 0.7 mm of Hg . s . kg . ml-1). Our findings indicated that clenbuterol HCl may potentiate hypoxemia as a result of increased shunt fraction in horses anesthetized by the IV route, and caused changes in hemodynamic variables that were consistent with its ability to stimulate beta 2-adrenergic receptors.

Twelve horses (6 Standardbreds and 6 Thoroughbreds) received IM injections of furosemide (250 mg) or physiologic saline solution and performed standard exercise tests, to assess the effects of furosemide and breed on blood gas values, PCV, plasma lactate concentration, and heart rate during exercise. After furosemide administration, arterial and venous blood pH values were significantly (P < 0.05) increased. Partial pressures of O2 and CO2 in arterial blood and of CO2 in venous blood (Pa(O2), Pa(CO2), and Pv(CO2), respectively) were unaffected by furosemide treatment, whereas venous partial pressures of O2 (Pv(O2)) were significantly (P < 0.05) less during exercise after furosemide treatment, suggesting an increase in oxygen uptake by the exercising muscles or a change in cardiac output. A significant (P < 0.05) difference was found between Thoroughbred and Standardbred values for arterial and venous pH, Pa(O2), Pa(CO2), plasma lactate concentration, and heart rate, suggesting that Standardbreds exercised at a relatively higher work rate than did Thoroughbreds.

Twelve healthy dogs were used to determine the cardiorespiratory effects of IV administered ketamine (10 mg/kg of body weight) and midazolam (0.5 mg/ kg). Half the dogs received a ketamine-midazolam combination (K-M) as a bolus over 30 seconds and the other half received the K-M as an infusion over 15 minutes. Induction of anesthesia by use of K-M was good in all dogs. Ketamine-midazolam combination as a bolus or infusion induced minimal cardiorespiratory effects, except for significant (p < 0.05) increases in mean heart rate and rate-pressure product. The increase in heart rate was greater in dogs of the infusion group. Mild and transient respiratory depression was observed in dogs of both groups immediately after administration of K-M, but was greater in dogs of the bolus group than in dogs of the infusion group. Duration of action of K-M for chemical restraint was short. Salivation and defecation were observed in a few dogs. Extreme muscular tone developed in 1 dog after K-M bolus administration.