Dynamic baroreflex sensitivity for increasing arterial pressure (DBSI) was used to quantitatively assess the effects of anesthesia on the heart rate/arterial pressure relationship during rapid (less than or equal to 2 minutes) pressure changes in the horse. Anesthesia was induced with IV administration of xylazine and ketamine and maintained with halothane at a constant end-tidal concentration of 1.1 to 1.2% (1.25 to 1.3 minimal alveolar concentration). Systolic arterial pressure (SAP) was increased a minimum of 30 mm of Hg in response to an IV bolus injection of phenylephrine HCl. Linear regression was used to determine the slope of the R-R interval/SAP relationship. During dynamic increases in SAP, a significant correlation between R-R interval and SAP was observed in 8 of 8 halothane-anesthetized horses. Correlation coefficients between R-R interval and sap were > 0.80 in 5 of 8 horses. Mean (+/- SD) DBSI was 4.8 +/- 3.4 ms/mm of Hg in anesthetized horses. A significant correlation between R-R interval and SAP was observed in only 3 of 6 awake horses during dynamic increases in SAP. Lack of correlation between R-R interval and SAP in 3 of 6 awake horses indicated that rapidly increasing SAP with an IV phenylephrine bolus is a poor method to evaluate baroreceptor-mediated heart rate changes in awake horses. Reflex slowing of heart rate in response to a rising arterial pressure appeared to have been overridden by the effects of excitement. Mean (+/- SD) DBSI (3 horses) was 7.3 +/- 3.3 ms/mm of Hg in awake horses.

The effect of methoxamine on retrograde flow of spermatozoa into the urinary bladder of domestic cats during electroejaculation and the incidence of retrograde flow during the collection of semen with an artificial vagina, or during mating was examined. In experiment 1, urine collected by cystocentesis prior to electroejaculation was azoospermic or contained few, nonmotile spermatozoa, whereas urine collected after electroejaculation contained more (P = 0.002) spermatozoa, and motile spermatozoa were evident in urine obtained from 6 of 8 cats. Administration of methoxamine hydrochloride (200 microgram/kg of body weight, IV) did not affect spermatozoal output or percentage of retrograde flow. Percentage of retrograde flow for control cats ranged from 61.18 to 92.95% (mean +/- SD, 80.00 +/- 14.28%) and for methoxamine-treated cats, ranged from 15.25 to 92.49% (mean +/- SD, 58.10 +/- 32.28%), but the difference was not significant. In experiment 2, an artificial vagina was used to collect semen from 5 of the 8 cats used in experiment 1. Urine collected by cystocentesis after ejaculation contained spermatozoa, and motile spermatozoa were evident in the urine from 4 of 5 cats. The mean (+/- SD) percentage of retrograde flow for these 5 cats was 46.82 +/- 31.67% (range, 14.56 to 90.32%). In experiment 3, each of the 5 cats that were used in experiments 1 and 2 were mated. Spermatozoa were recovered from the vagina of each mated female, and motile spermatozoa were also present in postejaculation urine obtained by cystocentesis from each of the 5 male cats. Mean total number of spermatozoa in the postmating urine was 29.42 +/- 33.58 X 10(6) (range, 0.22 X 10(6) to 76.05 X 10(6) spermatozoa). Anesthesia of cats with ketamine facilitated the obtention of urine by cystocentesis, but did not cause spermatozoal displacement into the urinary bladder. Results of this study confirm the fact that, in cats, appreciable numbers of spermatozoa are lost because of retrograde flow into the urinary bladder during electroejaculation. Recovery of spermatozoa from the urinary bladder after collection of semen with an artificial vagina or following natural mating, indicates that retrograde flow of spermatozoa is not an artifact derived from electrical stimulation but is a component of the ejaculatory process in cats.

A double-blind study was conducted to compare gastric ulcer healing time in nontreated dogs with that in dogs treated with either cimetidine or omeprazole. Single ulcers were created in the gastric antrum by use of a suction biopsy capsule. Each dog was given 25 mg of aspirin/kg of body weight orally for 20 days after ulcer induction. Five control dogs were given aspirin only (no anti-ulcer medication) during the 20-day study. Six dogs were given cimetidine at dosage of 10 mg/kg orally every 8 hours, and 6 dogs were given omeprazole orally at dosage of 2 micromole/kg (0.7 mg/kg) once daily. All dogs were examined endoscopically on days 5, 10, 15, and 20 and were given a score for the size of the mechanically created ulcer and a score for the degree of aspirin-induced gastritis. All dogs were euthanatized on day 21, and gastric lesions were examined histologically. Significant differences were not evident in ulcer healing scores or degree of aspirin-induced gastritis among treated and nontreated dogs on days 5, 10, 15, and 20. However, aspirin-induced gastritis was less severe in dogs of the omeprazole group than in dogs of the cimetidine or control group on each day observations were made. The effect of omeprazole given once daily was comparable with that of cimetidine given every 8 hours in lessening aspirin-induced gastritis.

The Escherichia coli heat-stable enterotoxin (STb) is the most prevalent toxin associated with diarrheagenic E coli isolates of porcine origin. Unequivocal biological activity of this toxin has been observed only in swine intestine. In this study, when endogenous protease activity was blocked with soybean trypsin inhibitor, intestinal secretion was stimulated by STb in jejunal loops of rats, mice, calves, and rabbits. Compared with pigs, rats, mice, and calves, rabbits were relatively insensitive to STb. These data demonstrate that the activity of STb is not a species-specific toxic activity; there is species variation in sensitivity to STb, and some common laboratory animals may have potential to be used to measure biological activity Of STb.

During the years 1984 through 1987, 2,574 isolates of obligately anaerobic bacteria were isolated from samples submitted for analysis. The most common anaerobic isolates were members of the genus Bacteroides, representing 44.6% of the isolates. Of these, the most commonly isolated identifiable microorganisms were bile-resistant and nonpigmented, belonging to the B fragilis group of Bacteroides. Importantly, obvious predilections for any one species or group of Bacteroides were not apparent for animal or site (condition), except that the proportion of isolates belonging to the nonpigmented, bile-resistant group obtained from the respiratory tract was significantly (P < 0.005) higher than that not belonging to this group. On the other hand, the proportion of isolates of the nonpigmented, bile-resistant group obtained from abscesses was significantly lower than that not belonging to this group.

The Cooper isolate of bovine herpesvirus-1, which causes abortion in cattle, was used to construct a thymidine kinase-negative (TK-) deletion mutant virus. Twelve heifers were inoculated IV at 25 to 29 weeks of pregnancy with either TK- or thymidine kinase-positive (TK+) Cooper virus. All heifers developed fevers of 1 to 2 C during the first week after inoculation. Temperatures of TK+ inoculates were slightly higher and remained above normal a few days longer than in TK- inoculates. Viremia was detected in 5 of 6 TK+ inoculates and in all 6 TK- inoculates. More virus isolations were made from nasal and vaginal swab specimens of TK+ inoculates than from swab specimens of TK- inoculates. All heifers developed virus neutralizing antibody within 14 days after inoculation and antibody titers were similar between the 2 groups. None of the TK- inoculated heifers aborted and their calves did not have neutralizing antibody at birth. Abortion occurred in 5 of 6 heifers given TK+ virus. All aborted fetuses were infected with bovine herpesvirus-1, as demonstrated by virus isolation or detection of viral antigen in fetal tissues. These results indicate that inactivation of the TK gene reduces abortifacient activity of bovine herpesvirus-1.

The respiratory, renal, hematologic, and serum biochemical effects of hypertonic saline solution (HSS) treatment were examined in 12 endotoxic, pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli endotoxin (055:B5) was infused IV at a rate of 0.1 microgram/kg of body weight over 30 minutes. Endotoxin induced severe respiratory effects, with marked hypoxemia and increases in arterial-alveolar O2 gradient (P[A-a]O2), physiologic shunt fraction (Qs/Qt), and physiologic dead space to tidal volume ratio (Vd/Vt). Oxygen consumption was decreased, despite an increase in the systemic O2 extraction ratio. Peak effects were observed at the end of endotoxin infusion. The renal response to endotoxemia was characterized by a decrease in free-water reabsorption and osmotic clearance, as well as a decrease in sodium and phosphorus excretion. Endotoxemia induced leukopenia, thrombocytopenia, hyperphosphatemia, hypoglycemia, acidemia, and increased serum alkaline phosphatase concentrations. Calves were treated with HSS (2,400 mosm/L of NaCl, 4 ml/kg, n = 4) or an equivalent sodium load of isotonic saline solution (ISS; 300 mosm/L of NaCl, 32 ml/kg, n = 4) 90 minutes after the end of endotoxin administration. Both solutions were infused over a 4- to 6-minute period. A control group (n = 4) was not treated. Infusion of HSS or ISS failed to induce a significant change in PaO2, P(A-a)O2, (Qs/Qt), (Vd/Vt), or oxygen consumption. Both solutions increased systemic oxygen delivery to above preendotoxin values. Hypertonic saline infusion induced significant (P < 0.05) increases in serum Na and Cl concentrations and osmolality, whereas ISS induced a significant increase in serum Cl concentration and a significant decrease in serum phosphorus concentration. Both HSS and ISS reversed the endotoxin-induced changes in renal function, with increases in free water reabsorption and osmotic clearance, as well as increases in sodium and phosphorus excretion. Sodium retention was greater following HSS administration. On the basis of these findings, hypertonic saline solutions can be rapidly and safely administered to endotoxic calves.

Ticlopidine hydrochloride was evaluated for its effectiveness in inhibiting platelet aggregation and serotonin release in 5 laboratory Beagles before and after heartworm implantation with 7 adult Dirofilaria immitis, and after embolization with 7 dead heartworms to mimic what happens after heartworm adulticide treatment. Five other laboratory Beagles, similarly implanted and embolized with heartworms, were used as nonmedicated controls. During the heartworm-negative stage, the dosage of ticlopidine that inhibited adenosine diphosphate (ADP)-induced platelet aggregation in 5 dogs by at least 50% after 5 days of treatment was 62 mg/kg of body weight once a day. In the same dogs implanted with 7 adult heartworms 21 days previously, mean (+/- SD) ticlopidine dosage required to obtain similar results was 71 (+/- 13) mg/kg given once daily. During the 21 days after dead heartworms were implanted in heartworm-infected dogs, mean ticlopidine dosage was 108 (+/- 35) mg/kg (range, 62 to 150 mg/kg). Ticlopidine treatment was associated with increased platelet numbers in all 5 dogs during the heartworm-negative stage and in 4 of 5 dogs during the heartworm implantation and heartworm embolization stages. Mean platelet volume tended to decrease as platelet numbers increased. At necropsy, gross and histologic pulmonary lesions were less severe in ticlopidine-treated dogs than in nonmedicated control dogs.

The hemodynamic effects of hypertonic saline solution (HSS) resuscitation on endotoxic shock were examined in pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused IV at dosage of 0.1 microgram/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+ dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with HSS (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (ISS: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused IV over a 4- to 6-minute period. Administration of HSS induced immediate and significant (P < 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to HSS administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by HSS was minimal 60 minutes after resuscitation. Administration of ISS induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with HSS, ISS induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow. The rapid administration of large-volume ISS appears superior to small-volume HSS for initial resuscitation of acutely endotoxemic, anesthetized calves. At this time, we do not advocate rapid infusion of ISS to septicemic calves because exacerbation of pulmonary hypertension may potentially depress respiratory function, and rapid increase in preload may hemodynamically compromise calves with depressed cardiac contractility.

A series of experiments was performed in vitro and in vivo to determine the influence of FK-565, a heptanoyl tripeptide, on lymphocyte and macrophage function in swine. Compared with values for control cultures, mitogen-stimulated lymphocyte blastogenesis and interleukin-2 production were unaffected in cells preincubated with 0.1, 1.0, and 10.0 microgram of FK-565/ml. Natural killer cell activity was increased by preincubation with 1.0 microgram of FK-565/ml; however, this increase was not statistically significant. In vitro treatment of porcine alveolar macrophages with FK-565 did not enhance cytolytic activity or bactericidal activity. In in vivo experiments, FK-565 given orally to pigs at concentrations of 6 or 60 microgram-kg-l.-d-1 for 5 days did not affect lymphocyte blastogenesis, interleukin-2 production, or alveolar macrophage bactericidal activity. A trend toward increased natural killer cell activity was evident in pigs treated with FK-565. In contrast, pigs treated with 6 microgram-kg-1.-d-1 had significantly (P less than 0.01) decreased alveolar macrophage cytolytic activity. These data indicate that at the dosages tested, FK-565 is not a suitable immunomodulator for enhancement of nonspecific immunity in swine.