Over a 54-hour period, blood was removed from 8 adult sheep (body weight, 38.1 +/- 0.5 kg mean +/- SEM) in 9 episodes, 5 on day 1, 3 on day 2, and 1 on day 3. Cumulative blood loss was 1,630 +/- 63, 2,380 +/- 71, and 2,693 +/- 69 ml on days 1, 2, and 3, respectively. Blood samples (20 ml) were collected from 5 control ewes (33.8 +/- 2.8 kg) at equivalent times. Over the first day, mean arterial blood pressure decreased in the hemorrhaged sheep from 101 +/- 2 mm of Hg to 76 +/- 5 mm of Hg, but returned to control values by the beginning of the second day and, thereafter, was not different from control values. Heart rate was increased after the first hemorrhage episode and remained high throughout the entire protocol. Over the entire period, there were statistically significant decreases in hematocrit, plasma osmolality, sodium, total calcium (P < 0.001), potassium, and chloride values (P < 0.05). There was no change in plasma phosphate, bicarbonate, creatinine, or magnesium concentrations and an increase in plasma urea nitrogen (P < 0.001) concentrations. Plasma arginine vasopressin concentration was increased significantly (P < 0.001) over the entire period. Plasma ACTH concentration was significantly (P < 0.05) increased over time, but only some values on day 1 were significantly outside the normal range of the control group data. Because of wide variation between sheep, the group data for aldosterone were not significantly different from control values. Blood volume was restored on day 1 with fluid of osmolality, Na, and Cl composition equivalent to that of plasma. The effects of arginine vasopressin were apparent by day 2, when the major decrease in osmolality and Na and Cl concentrations were observed The sheep has good capacity to withstand severe, prolonged hemorrhage, most likely because of a large reserve of RBC in the spleen; hematocrit remained at 31% of control values when an estimated 100% of initial circulating blood volume had been removed.

The effect of premedication with phenylbutazone on systemic hemodynamic and diuretic effects of furosemide was examined in 6 healthy, conscious, mares. Mares were instrumented for measurement of systemic hemodynamics, including cardiac output and pulmonary arterial, systemic arterial, and intracardiac pressures, and urine flow. Each of 3 treatments was administered in a randomized, blinded study; furosemide (1 mg/kg of body weight, IV) only, phenylbutazone (8.8 mg/kg PO, at 24 hours and 4.4 mg/kg IV, 30 minutes before furosemide) and furosemide, or 0.9% NaCl. Phenylbutazone administration significantly attenuated, but did not abolish, the diuretic effect of furosemide. Phenylbutazone completely inhibited the immediate effect of furosemide on cardiac output, stroke volume, total peripheral resistance, and right ventricular peak pressure. Premedication with phenylbutazone did not inhibit equally the diuretic and hemodynamic effects of furosemide, indicating that some of furosemide's hemodynamic effects are mediated by an extrarenal activity of furosemide.

During growth, central venous, right ventricular, pulmonary arterial, Pulmonary capillary wedge, and systemic arterial pressures, heart rate, and cardiac Output were repeatedly measured in 41 Friesian calves, considered as having conventional muscular conformation, and in 19 Belgian White and Blue double-muscled calves. A total of 123 and 70 recordings were collected in conventional and double-muscled calves, respectively. These circulatory indices were calculated: stroke volume, cardiac and stroke indices, pulmonary and systemic pulse pressures, pulmonary and systemic vascular resistance indices, and right and left ventricular work indices. Results indicated that systemic arterial and pulse pressures, as well as cardiac output, stroke volume, cardiac and stroke indices, and right and left ventricular work indices were significantly (P less than or equal to 0.05 to 0.001) lower but, in contrast, pulmonary and systemic vascular resistance indices were significantly (P less than or equal to 0.001) higher in double-muscled than in conventional calves. Right-sided vascular pressures and heart rate were similar in the 2 groups. These results indicated that global cardiac performance may be considerably poorer in double-muscled calves. Diminished cardiac performance of double-muscled calves appears to be related neither to relative bradycardia nor to reduced ventricular preload. The potential role of increased ventricular afterload or of reduced myocardial contractility in double-muscled cattle should be determined by direct measurements.

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (BL) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of BL. All horses were monitored for 6 hours after BL data were collected. Blood samples were collected from the colonic vein and main pulmonary artery (systemic venous (SV) for measurement of plasma endotoxin, 6-keto prostaglandin F1alpha (6-kPG), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (CV) serum samples. Data were analyzed, using two-was ANOVA, and post-hoc comparisons were made, using Dunnett's and Tukey's tests. Statistical significance was set at P < 0.05 Endotoxin was not detected in CV or SV plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at BL among groups for CV or SV 6-kPG, PGE2, or TXB2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group-2 horses. Colonic venous PGE2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 hors.

Right atrial, pulmonary artery, pulmonary capillary, pulmonary artery wedge, and systemic blood pressures of strenuously exercising horses increase markedly. As a consequence, myocardial metabolic O2 demand in exercising horses must be high. Experiments were, therefore, carried out on 9 healthy, exercise-conditioned horses (2.5 to 8 years old; 481 +/- 16 kg) to ascertain the regional distribution of myocardial blood supply in the atria and ventricles at rest and during exercise. Blood flow was measured, using 15-micrometer-diameter radionuclide-labeled microspheres that were injected into the left ventricle while reference blood samples were being withdrawn at a constant rate from the thoracic aorta. Myocardial blood flow was determined at rest and during 2 exercise bouts performed on a high-speed treadmill at 8 and 13 m/s (0% grade). The sequence of exercise bouts was randomized among horses, and a 60-minute rest period was permitted between exercise bouts. There was considerable heterogeneity in the distribution of myocardial perfusion in the atria and the ventricles at rest; the right atrial myocardium received significantly (P < 0.05) less perfusion than did the left atrium, and these values were significantly (P < 0.05) less than those for the respective ventricular myocardium. The right ventricular myocardial blood flow also was significantly less than that in the left ventricle. With exercise, myocardial blood flow in all regions increased progressively with increasing work intensity and marked coronary vasodilation was observed in all cardiac regions. During exercise at 8 or 13 m/s, right and left atrial myocardial blood flows (per unit weight basis) were not different from each other. Although at treadmill speed of 8 m/s, left ventricular myocardial blood flow exceeded that in the right ventricle, this was not the case at 13 m/s, when perfusion values (per unit weight basis) became similar.

In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (HWD), pulmonary hemodynamic measurements were obtained from 7 experimentally infected, anesthetized dogs before and after hydralazine administration (mean dose, 1.96 mg/kg of body weight). Five dogs were maintained on room air, while 2 were maintained on 100% oxygen during the hydralazine study. The hemodynamic effect of hydralazine in dogs with HWD was evaluated, using heart rate, cardiac index, mean pulmonary artery pressure, mean arterial pressure, total pulmonary resistance, total systemic resistance, total systemic resistance/total pulmonary resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure X heart rate] and [mean pulmonary artery pressure X heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased greater than or equal to 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was less than or equal to 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test. Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders.

The uterine hemodynamic response to maternal positioning in dorsal recumbency was evaluated in 7 conscious pregnant cows during the third trimester. Anesthetic or sedative drugs were not administered. Uterine artery flow was measured, using a previously implanted ultrasonic flow probe. Catheters implanted in the uterine artery and vein were used for measurement of blood pressure and for blood sample collections. Heart rate, systemic arterial pressure, uterine arterial blood flow, arterial and venous oxygen and carbon dioxide tensions, and pH were measured in cows in standing position. Cows were cast with ropes and positioned in dorsal recumbency, then measurements were repeated at 15 and 30 minutes. Compared with standing measurements, dorsal recumbency caused 50% increase in heart rate and 44% increase in arterial blood pressure. Uterine artery flow did not change significantly. Despite increased ventilation, arterial oxygenation was reduced during dorsal recumbency. There were minimal differences between measurements at 15 and 30 minutes of dorsal recumbency.

Six horses were subjected to 3 hours of low-flow ischemia and 3 hours of reperfusion of the large colon. After induction of anesthesia, the large colon was exteriorized through a ventral midline celiotomy. Colonic blood flow was measured continuously, using Doppler ultrasonic flow probes placed on the colonic arteries supplying the dorsal and ventral colons and was allowed to stabilize for 15 to 30 minutes after instrumentation. Low-flow ischemia was induced by reducing colonic arterial blood flow to 20% of baseline (BL) flow. Colonic mucosal, seromuscular, and full-thickness blood flow were determined on a tissue-weight basis by injecting colored microspheres proximally into the colonic artery supplying the ventral colon. Reference blood samples were obtained at a known flow rate from the colonic artery and vein at a site more distal to the site of injection. Left ventral colon biopsy specimens were harvested at BL, 3 hours of ischemia, and 15 minutes of reperfusion. Blood and tissue samples were digested and filtered to collect the microspheres, and dimethylformamide was added to release the colored dyes. Dye concentration in blood and tissue samples was measured by use of spectrophotometry, and tissue-blood flow was calculated. Data were analyzed, using two-way ANOVA for repeated measures; statistical significance was set at P < 0.05. Doppler blood flow decreased to approximately 20% of BL, whereas microsphere blood flow ranged between 13.7 and 15.5% of BL at 3 hours of ischemia. Doppler-determined blood flow increased immediately on restoration of blood flow, reached 183% of BL at 15 minutes of reperfusion, and remained at or above BL throughout 3 hours of reperfusion. This reactive hyperemia was also detected, using the colored microspheres; blood flow increased to 242 and 327% of BL at 15 minutes of reperfusion in the mucosal and seromuscular layers, respectively.

Prothrombotic changes occurring in the prodromal stages of carbohydrate-induced laminitis were investigated. Hemostatic alterations were evaluated by determining platelet counts, platelet survival, activated partial thromboplastin time, one-stage prothrombin time, and monocyte procoagulant activity. Thrombosis of vessels in the hoof wall was evaluated by contrast arteriography and histologic examination. Of 5 horses, 4 became lame between 28 and 52 hours after carbohydrate administration. Mean platelet count in laminitis-affected horses was lower throughout the prodromal stages of laminitis, compared with that in control horses, but differences were not statistically significant. However, survival of indium-111-labeled platelets was less than the value in control horses by 6 hours after carbohydrate administration. Arteriography of disarticulated feet revealed marked reduction in blood supply to hooves in laminitis-affected horses. Histologic examination of the laminar dermis disclosed microthrombi in venules of the laminar dermis in 2 of 4 affected horses. Statistically significant changes in prothrombin time were not observed, and changes in activated partial thromboplastin time were slight and occurred only at the onset of lameness. Statistically significant changes in monocyte procoagulant activity were not observed. Plasma endotoxin-like activity was not detected in laminitis-affected horses. These data indicate that platelet survival was decreased within the first 6 hours after induction of carbohydrate-induced laminitis, but systemic activation of the coagulation system was not detected.