The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2, 35 to 45 mm of Hg), moderate hypercapnia (PaCO2, 60 to 70 mm of Hg), and severe hypercapnia (PaCO2, 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P < 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the beta-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.

Two digital oscillometric human blood pressure measuring devices were modified and evaluated as blood pressure monitors in 12 healthy anesthetized dogs. Direct arterial pressures were measured via cannulation of the dorsal pedal artery and were correlated with indirect measurements through an inflatable cuff placed over the dorsal pedal artery below the hock joint of the contralateral limb. Direct and indirect measurements were compared for systolic, diastolic, and calculated mean arterial pressures. Blood pressure ranges between 215/145 mm of Hg and 65/30 mm of Hg were obtained, using combinations of halothane, phenylephrine, calcium, and IV administered fluids. Machine A was found to be insufficient for clinical application, on the basis of correlation coefficients between direct and indirect pressures of 0.78, 0.65, and 0.74 for systolic, diastolic, and mean arterial pressures, respectively. Higher correlation coefficients between direct and indirect pressures (0.77, 0.87, and 0.87, respectively) were obtained with machine B. The results of the study reported here suggest machine B may be an effective blood pressure monitoring device in anesthetized dogs.

Cardiovascular responses to sublethal endotoxin infusion (Escherichia coli, 50 micrograms/ml in lactated Ringer solution at 100 ml/h until pulmonary arterial pressure increased by 10 mm of Hg) were measured 2 times in 5 standing horses. In a 2-period crossover experimental design, horses were either administered hypertonic (2,400 mosm/kg of body weight, IV) or isotonic (300 mosm/kg, IV) NaCl solution after endotoxin challenges. Each solution was administered at a dose of 5 ml/kg (infusion rate, 80 ml/min). Complete data sets (mean arterial, central venous, and pulmonary arterial pressures, pulmonary arterial blood temperature, cardiac output, total peripheral vascular resistance, heart rate, plasma osmolality, plasma concentration of Na, K, Cl, and total protein, blood lactate concentration, and PCV) were collected at 0 (baseline, before endotoxin infusion), 0.25, 1, 1.5, 2, 2.5, 3, 3.5, 4, and 4.5 hours after initiation of the endotoxin infusion. Blood constituents alone were measured at 0.5 hour and cardiovascular variables alone were evaluated at 0.75 hour. By 0.25 hour, endotoxin infusion was completed, a data set was collected, and saline infusion was initiated. By 0.75 hour, saline solutions had been completely administered. Mean (+/- SEM) cardiac output decreased (99.76 +/- 3.66 to 72.7 +/- 2.35 ml/min/kg) and total peripheral resistance (1.0 +/- 0.047 to 1.37 +/- 0.049 mm of Hg/ml/min/kg) and pulmonary arterial pressure (33.4 +/- 0.86 to 58.3 +/- 1.18 mm of Hg) increased for both trials by 0.25 hour after initiation of the endotoxin infusion and prior to fluid administration. For the remainder of the protocol, cardiac output was increased and total peripheral resistance was decreased during the hypertonic, compared with the isotonic, saline trial. Cardiac output was decreased and total peripheral resistance was increased during the isotonic saline trial, compared with baseline values. Both trials were associated with increased blood lactate concentration, but lactate values during the isotonic saline trial were greater and remained increased above baseline values for a longer period (4 hours) than during the hypertonic saline trial (2.5 hours). It was concluded for this model of endotoxemia, that IV administered hypertonic saline solution was associated with more-desirable cardiovascular and metabolic responses than was an equal volume of isotonic saline solution.

The cardiopulmonary effects of 4 positions (standing, right lateral, left lateral, and dorsal recumbency) were evaluated in conscious cattle in which no sedatives or anesthetic drugs were given. Each position was maintained for 30 minutes, during which time there were no significant changes in heart rate, respiratory rate, mean arterial blood pressure, arterial pH, PaCO2, arterial base excess, or venous blood gas values. Significant decreases in PaO2 developed when cattle were in lateral positions and dorsal recumbency. Cardiac index was unchanged in all positions, except in dorsal recumbency at 30 minutes, when it was significantly decreased.

The heart rate (HR) induced by maximal beta-adrenergic activation, which was elicited by infusion of isoproterenol, was studied in 8 healthy horses before (control) and after hyperthermia was induced by IV administration of 2,4-dinitrophenol (DNP). Isoproterenol was administered IV at 1.0 micrograms.kg-1.min-1 for 3 minutes and the HR was determined during the final 30 seconds of the infusion. As the rectal temperature increased (P < 0.001) from 38.2 +/- 0.1 C (mean +/- SEM; normothermic control) to 40.1 +/- 0.1 C at 60 minutes after DNP administration, the isoproterenol-induced HR also increased from 198 +/- 4 beats/min (control) to 214 +/- 4 beats/min (P < 0.001). It appeared that the values of HR achieved with maximal beta-adrenergic activation were augmented by the hypermetabolic, hyperthermic state induced by DNP.

Bovine pulmonary artery endothelial cells (BPAEC) were labeled with 3H-arachidonic acid. Exposure of the labeled BPAEC to Pasteurella haemolytica lipopolysaccharide (LPS) resulted in a time- and dose-dependent release of radioactivity. The release was inhibited by 5 mM indomethacin, but inhibition was not caused by less than or equal to 500 micromole indomethacin or hydrocortisone, which suggests that the release was caused primarily by a mechanism other than cyclooxygenase or phospholipase A2 metabolism of arachidonic acid. Pasteurella haemolytica LPS also caused increased adherence of bovine neutrophils to BPAEC through independent effects on both cell types. The increased adherence was inhibited by treatment of either cell type with cycloheximide or actinomycin D prior to LPS exposure, indicating that de novo protein synthesis was required in both cell types to promote the LPS-induced adherence. Lipopolysaccharide may be an important factor in neutrophil-mediated effects in pneumonic pasteurellosis by causing increased neutrophil adherence and, thus, the vascular sequestration of neutrophils. Together, these experiments provide additional evidence for the involvement of LPS in pneumonic pasteurellosis. Moreover, they provide evidence of LPS-induced endothelial activation, which could have broad ramifications in the inflammatory and immune responses of pneumonic pasteurellosis.

Electromyographic (EMG) evaluation of the external urethral sphincter (EUS) was conducted during cystometry in 11 adult male cats sedated with xylazine and ketamine. A percutaneously placed antepubic catheter was used for bladder infusion and recording intravesicular pressures during cystometrography (CMG). A fine-wire electrode was placed percutaneously into or near the EUS for recording EMG during CMG. The bladder was infused with sterile 0.9% NaCl solution at a rate of 2 to 3 ml/min until a detrusor reflex was initiated. Intravesicular pressures at the onset of infusion, immediately prior to micturition, at the onset of urine flow, and at the maximal voiding pressure were recorded. The time from infusion to micturition, from opening pressure to return to baseline, and from the beginning to the end of the CMG were also recorded. The total volume of 0.9% NaCl solution infused and the residual bladder volume after micturition were also measured. Recordings were replicated once during each trial in all cats, and trials were replicated once approximately 1 week later in 4 cats. Micturition patterns were characterized by slight to moderate EUS EMG activity during vesicular filling, with reduction in activity during emptying. Maximal EMG activity was recorded at the completion of the reflex and was associated with pulsatile expulsion of small amounts of urine. The simultaneous recording of CMG and EUS EMG with fine-wire electrodes was simple and reliable for assessing the neuromuscular integrity and synchrony of detrusor and EUS muscles. There were no significant differences in variables between recordings within trial 1, but there were differences (P less than or equal to 0.05) between trials for pressure at the onset of urine flow and maximal voiding pressure.

Six primiparous Holstein cows were fed a Se-deficient diet, beginning at least 90 days before their first calving, and 6 other primiparous cows were given the same diet plus a supplement of 2 mg of Se/cow/d as sodium selenite. All cows were fed their diets for the duration of the experimental period. One uninfected quarter of each cow was injected with 25 microgram of Escherichia coli endotoxin at postpartum week 5. Leukocytes were isolated by centrifugation from milk collected at postinjection hour 16. Isolated cells were 92 +/- 3% neutrophils and were incubated with Staphylococcus aureus or E coli in a 1:300 ratio. Phagocytosis and intracellular killing by neutrophils were assessed after 0, 30, 60, and 90 minutes by a fluorochrome assay, using acridine orange. Viability of neutrophils was assessed by use of trypan blue. Superoxide anion production and hydrogen peroxide production by neutrophils also were determined. Cows fed Se-deficient diets had significantly (P < 0.05) lower blood Se concentration and blood glutathione peroxidase activity than cows fed Se-supplemented diets. Selenium status had no effect on the phagocytic capacity of neutrophils. Neutrophils obtained from cows fed Se-supplemented diets killed a significantly (P < 0.05) higher percentage of ingested bacteria than did neutrophils from cows fed the Se-deficient diet. Viability was significantly (P < 0.05) reduced by incubation with S aureus in neutrophils from both groups of cows, with neutrophils from Se-deficient cows having lower viability. Superoxide anion production did not differ significantly between neutrophils from the 2 groups, but extracellular hydrogen peroxide concentration was significantly (P < 0.05) higher in neutrophils harvested from milk of cows fed the Se-deficient diet.

Myoelectric activity of the ileum, cecum, and right ventral colon (RVC) was studied in 4 mature ponies. Eight Ag-AgCl bipolar recording electrodes were sutured to the seromuscular layer of the ileum (2 electrodes), cecum (4 electrodes), and RVC (2 electrodes). Myoelectric activity was studied beginning 10 days after surgery. Eight, 60-minute recording sessions were performed in each pony during the interdigestive period, which was the period 3 to 7 hours after the morning feeding. On separate days, food was withheld for 24 hours, and 90-minute recordings were obtained during the nonfeeding period. Ponies were then fed a normal ration, and recordings were continued to obtain data for the digestive (feeding) period. All phases of the migrating myoelectric complex were seen at both ileal electrodes during the interdigestive period, including the periods of no spiking activity (phase 1), irregular spiking activity (phase 2), and regular spiking activity (phase 3). Phase 2 occupied 77% of the total recording time, and the mean duration of phases 1, 2, and 3 was 3.4 +/- 0.2, 12.8 +/- 1.2, and 6.7 +/- 0.7 min, respectively. Frequency of ileal slow waves was 11.8 +/- 0.1/min, and spike burst conduction velocity was 4.7 +/- 0.3 cm/s. A complete migrating myoelectric complex was seen in 11 of 32 tracings (34%) and had a mean duration of 24.2 +/- 2.6 min. The ileal migrating action potential complex, most often seen in phase 2, had a frequency of 4.8 +/- 0.5 spike bursts/h and a conduction velocity of 13.6 +/- 0.4 cm/s. The migrating action potential complex was detected directly before retrograde cecal myoelectric activity 73% of the time, indicating possible myoelectric coupling of the ileum and cecum. Motility patterns recognized in the cecum included: pattern I, spike bursts beginning at the apex and conducted to the cranial base; pattern II, spike bursts beginning at the caudal base and conducted to the apex; pattern III, spike bursts beginning at the cranial base and conducted to the apex; and pattern IV, termed the progressive pattern, beginning at the cecal apex, conducted through the cecal base and cecocolic orifice and into the RVC. The progressive pattern was detected at a frequency of 34.2 +/- 1.8 spike bursts/h and was often preceded by (71%), followed by (64%), or preceded and followed by (51%) pattern I or II. This recurring sequence of cecal myoelectric events was termed the cecal myoelectric complex. In the RVC, 2 patterns of myoelectric activity were seen: aborally directed propulsive spike bursts (3.6 +/- 0.6 spike bursts/h) and orally directed retropulsive spike bursts (7.2 +/- 1.2 spike bursts/h), confirming that propulsion and retropulsion exist in the RVC. Nonfeeding caused a significant decrease in the frequency of ileal migrating action potential complex (P = 0.008), cecal pattern III (P = 0.003), and the progressive motility pattern (P = 0.003). Nonfeeding caused a significant decrease (P less than or equal to 0.009) in the appearance of the cecal myoelectric complex. Feeding caused a significant increase (P = 0.003) in the mean frequency of the progressive pattern compared with the nonfeeding period, but this was significantly less than during the interdigestive period (P = 0.003).

Cardiovascular effects of butorphanol (0.2 mg/kg of body weight, IV) and responses associated with subsequent administration of naloxone (0.04 mg/kg, IV) were studied in halothane (1.2% end-tidal concentration)-anesthetized dogs. Transient, but statistically significant (P < 0.05), decreases in heart rate, mean and diastolic arterial blood pressures, and rate-pressure product were observed after butorphanol administration. Cardiac index, stroke volume, and systemic vascular resistance did not change significantly. Except for the decrease in heart rate, changes in the values of the cardiovascular variables measured after butorphanol administration did not appear to be clinically relevant. Sixty minutes after butorphanol administration, naloxone was given. Statistically significant (P < 0.05) increases in heart rate, arterial blood pressures, cardiac index, and rate-pressure product, along with dysrhythmias were observed. Stroke volume and systemic vascular resistance remained unchanged after administration of naloxone. Naloxone administration was associated with changes indicative of increased myocardial oxygen consumption.