Effects of propranolol on cardiopulmonary function in the pony during submaximal exercise

Cardiopulmonary responses of four ponies were monitored during standard exercise tests (SET), before and after beta-adrenergic receptor blockade with propranolol. The SET consisted of four 5 min increments of increasing speed from 1.0 to 2.8 m/sec on a treadmill at a 7 degrees incline. Data were collected at rest, throughout the SET and recovery. Administration of propranolol to ponies at rest had no effect on cardiopulmonary function. During the SET, increases in heart rate, mean pulmonary artery flow velocity (an index of cardiac output) and right ventricular dP/dt (an index of myocardial contractility) were progressively attenuated as running speed increased. Body temperature and mean pulmonary artery and right ventricular pressures were significantly elevated over normal. Propranolol treatment had no effect on the responses of mean arterial pressure, haematocrit, haemoglobin, blood lactate and arterial blood gases and pH to the SET. These results suggest that in the pony there is no sympathetic activity to the heart at rest and that during exercise there is pulmonary vasodilation mediated by beta-adrenergic receptors.     

Cardiovascular effects of 7.2% hypertonic saline solution in halothane anaesthetized ponies

The haemodynamic effects of intravenously (iv) administered hypertonic saline solution (7.2%, 4 ml/kg of body weight [bwt]) were investigated in normovolaemic ponies during halothane anaesthesia (dorsal recumbent position, intermittent pressure ventilation). Heart rate, arterial blood and pulmonary artery pressures, cardiac output, and arterial blood gases were measured throughout the experiment while related haemodynamic parameters (cardiac index, systemic and pulmonary vascular resistance, stroke volume, ventricular work) were calculated.
A transient decrease in arterial blood pressure occurred during the administration of the hypertonic solution. Significant increases in cardiac output and index, stroke work, and systolic arterial pressure were observed 5 min after the administration of the hypertonic infusion. A gradual normalization of the increased parameters occurred afterwards. Heart rate and arterial blood gases remained constant throughout the study. No clinical side-effects, except for an increase in urinary production in the recovery period, were seen during and after anaesthesia.     

Cardiovascular effects recorded in horses during anaesthesia after treatment with trichlorfon

Five horses were anaesthetised twice with thiopentone sodium, guaifenesin and halothane. The second anaesthesia was 16 days after the first and two days following oral administration of trichlorfon. Heart rate, carotid arterial, pulmonary arterial and right atrial pressures, cardiac output and blood temperature were measured every 15 minutes for 120 minutes. Heart rate, carotid arterial pressure and cardiac output were similar on both occasions. Pulmonary arterial and right atrial pressures were highest during anaesthesia after treatment with trichlorfon when compared with values obtained before treatment. Pulmonary vascular resistance was significantly decreased at four measurement times during anaesthesia after treatment with trichlorfon. All cardiovascular measurements were within ranges accepted as normal for halothane anaesthesia in horses. In a second experiment, four ponies were anaesthetised with xylazine and ketamine on two occasions one week apart. Two ponies received trichlorfon two days before the second anaesthesia. Heart rate, arterial pressure and respiratory rate recorded during anaesthesia were not different in ponies after organophosphate treatment. The time to standing after the second anaesthesia was significantly increased in all ponies.     

Cardiovascular and pulmonary effects of recumbency in two conscious ponies

Respiratory dead-space, tidal volume, respiratory rate, blood gases, cardiac output, heart rate and arterial and pulmonary arterial blood pressures were measured in two conscious, trained ponies in the standing position and in left lateral recumbency. The ponies were reluctant to remain lying down for more than about 20 mins but the reason for this did not become apparent. Tidal volume was reduced during recumbency but the respiratory rate increased, tending to maintain the minute volume at about that of the standing animal. Arterial carbon dioxide tension did not change significantly from standing values but the mean arterial oxygen tension values tended to decrease in both ponies during recumbency because of a slight increase in pulmonary venous admixture. Venous admixture in these two laterally recumbent conscious animals was considerably less than previously reported for anaesthetised subjects.     

Haemodynamic response to exercise in Standardbred trotters with red cell hypervolaemia

In order to evaluate the haemodynamic response to exercise in Standardbred trotters with red cell hypervolaemia (RCHV), 12 trotters with RCHV were compared with 9 normovolaemic (NV) trotters. Haemodynamic data were recorded during exercise at 4 different speeds on a treadmill. Oxygen uptake was determined with an open bias flow system. Pulmonary artery pressure (PAP), systemic artery pressure (SAP), heart rate, packed cell volume (PCV) and plasma lactate and haemoglobin ([Hb]) concentrations were measured. Arteriovenous O2 content difference, cardiac output, stroke volume, pulmonary vascular resistance (PVR) and total systemic resistance (TSR) were calculated. Oxygen uptake, arteriovenous O2 content difference, heart rate, cardiac output, stroke volume, TSR and lactate did not differ between groups. The RCHV horses had significantly higher both mean diastolic and systolic PAP compared to NV horses and this difference increased with higher workload. Further, a higher SAP, PVR, PCV and [Hb] were found in RCHV horses during the course of exercise. Eleven of the RCHV horses, but none of the NV, showed exercise-induced pulmonary haemorrhage on endoscopic examination. The increase in red cell volume, resulting in a high PCV and high total blood volume, is suggested to be an important contributor to both the increased blood pressures in pulmonary and systemic circulation during exercise and to the development of exercise-induced pulmonary haemorrhage in RCHV horses.     

Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats.

OBJECTIVE: To evaluate the cardiovascular effects of the alpha2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats. ANIMALS: 7 clinically normal cats. PROCEDURE: Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 microg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration. RESULTS: Heart rate, cardiac index, stroke index, rate-pressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: When administered alone to clinically normal cats, medetomidine (20 microg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central alpha2-adrenergic effect over peripheral vascular effects.     

Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock

A comparison of the haemodynamic benefits of small volume hypertonic saline (2,400 mOsm/litre) versus isotonic saline (300 mOsm/litre) was conducted in 12 adult horses using a haemorrhagic shock model. The horses were anaesthetised and intravascular catheters placed for the measurement of haemodynamic data. Mean systemic arterial pressure was then reduced to 50 to 60 mmHg by controlled haemorrhage and maintained at that level for 40 mins. Cardiac output, stroke volume, mean systemic arterial pressure, plasma volume and urine production decreased significantly following blood loss. Hypertonic or isotonic saline was administered randomly by intravenous infusion and haemodynamic data recorded for a 2 h period. Treatment with hypertonic saline produced rapid elevations in cardiac output, stroke volume, mean systemic and pulmonary arterial pressures, cardiac contractility and urine output, and was accompanied by expansion of the plasma volume. The changes in cardiac output and stroke volume were maintained for the duration of the recording period, whereas increases in mean systemic arterial pressure were not as remarkable. Infusion of isotonic saline caused only transient increases in cardiac output and mean systemic and pulmonary arterial pressure, and cardiac output; urine output and plasma volume did not change. This study indicates that hypertonic saline produces haemodynamic improvements in experimentally induced haemorrhagic shock in horses.     

Cardiopulmonary measurements in nonanesthetized, resting normal ponies.

Cardiopulmonary measurements were determined in 19 nonanesthetized, normal ponies. Mean values for arterial pressure, pulmonary arterial pressure, cardiac output, heart rate, packed cell volume, and hemoglobin are reported, as well as acid-base determinations of arterial blood and cerebrospinal fluid. Respiratory function test data include total ventilation, respiratory rate, alveolar ventilation, oxygen uptake, and carbon dioxide output. The data compare favorably with the available data from previous reports on ponies. Because of large day-to-day variations in total ventilation, alveolar ventilation should be measured if ponies are used in the study of pulmonary function.     

Cardiovascular adaptations to exercise and training

The cardiovascular system provides the link between pulmonary ventilation and oxygen usage at the cellular level. During exercise, efficient delivery of oxygen to working skeletal and cardiac muscles is vital for maintenance of ATP production by aerobic mechanisms. The equine cardiovascular response to increased demand for oxygen delivery during exercise contributes largely to the over 35-fold increases in oxygen uptake that occur during submaximal exercise. Cardiac output during exercise increases greatly owing to the relatively high heart rates that are achieved during exercise. Heart rate increases proportionately with workload until heart rates close to maximal are attained. It is remarkable that exercise heart rates six to seven times resting values are not associated with a fall in stroke volume, which is maintained by splenic contraction, increased venous return, and increased myocardial contractibility. Despite the great changes in cardiac output, increases in blood pressure during exercise are maintained within relatively smaller limits, as both pulmonary and systemic vascular resistance to blood flow is reduced. Redistribution of blood flow to the working muscles during exercise also contributes greatly to the efficient delivery of oxygen to sites of greatest need. Higher work rates and oxygen uptake at submaximal heart rates after training imply an adaptation due to training that enables more efficient oxygen delivery to working muscle. Such an adaptation could be in either blood flow or arteriovenous oxygen content difference. Cardiac output during submaximal exercise does not increase after training, but studies using high-speed treadmills and measurement of cardiac output at maximal heart rates may reveal improvements in maximal oxygen uptake due to increased stroke volumes, as occurs in humans. Improvements in hemoglobin concentrations in blood during exercise after training are recognized, but at maximal exercise, hypoxemia may reduce arterial oxygen content. More effective redistribution of cardiac output to muscles by increased capillarization and more efficient oxygen diffusion to cells may also be an important means of increasing oxygen uptake after training.     

Pulmonary vascular pressures of strenuously exercising Thoroughbreds during intravenous infusion of nitroglycerin

OBJECTIVE: To determine whether intravenous infusion of nitroglycerin would modify pulmonary arterial, capillary, or venous hypertension in strenuously exercising Thoroughbreds. ANIMALS: 5 healthy Thoroughbred horses. PROCEDURE: Right atrial, right ventricular, and pulmonary vascular pressures were measured. Each horse was used in a control treatment (not medicated) and a nitroglycerin infusion (20 microg/kg of body weight/min) at rest and during exercise on a treadmill. Sequence of treatments was randomized for each horse, and treatments were separated by a 7-day interval. Galloping at 14.2 m/s on a 5% uphill grade elicited maximal heart rate (mean +/- SEM, 212 +/- 2 beats/min) and could not be sustained for > 90 seconds. Nitroglycerin dosage was selected, because maximal pulmonary and systemic hemodynamic effects of i.v. nitroglycerin were elicited at 5 microg/kg/min and increasing the dosage to 20 microg/kg/min did not cause adverse effects. RESULTS: In the control treatment, exercise performed at maximal heart rate resulted in a significant increase in right atrial as well as pulmonary arterial, capillary, and wedge pressures. Nitroglycerin infusion in standing horses significantly decreased right atrial and pulmonary vascular pressures, whereas heart rate increased. Exercise in nitroglycerin-infused horses also resulted in a significant increase in right atrial as well as pulmonary arterial, capillary, and wedge pressures, and these values were not significantly different from data for the control treatment. All horses experienced exercise-induced pulmonary hemorrhage for both treatments. CONCLUSIONS AND CLINICAL RELEVANCE: I.v. administration of nitroglycerin does not modify exercise-induced pulmonary hypertension and is unlikely to affect the incidence or severity of exercise-induced pulmonary hemorrhage in Thoroughbreds.     

Pressures in the right side of the heart and esophagus (pleura) in ponies during exercise before and after furosemide administration

Pressures in the right side of the heart and esophagus (pleural) have not been determined in the exercising equine subjects. In the present study, 8 healthy ponies were examined to determine the changes in these variables caused by 2 degrees of exercise done on a treadmill (heart rate:183 +/- 5 beats/min [trot] and 220 +/- 6 beats/min [canter]). Measurements were also made during both degrees of exertion 10 minutes and 120 minutes after furosemide (1.0 mg/kg) administration. It was observed that both gaits resulted in significant increases in pulmonary artery, right ventricular, and right atrial pressures. The pulmonary artery systolic, mean, and diastolic pressures during strenuous exertion were 306%, 252%, and 242% of the respective resting values. At canter, when respiratory frequency (138 +/- 4 breaths/min) is synchronized with stride frequency, the delta esophageal pressure approached 30.4 +/- 2.86 cm of water. During exercise 10 minutes after furosemide administration, the increment in right atrial pressure was markedly attenuated. During strenuous exertion 120 minutes after furosemide administration, the right atrial and pulmonary arterial pressures increased, but to a significantly lower level than did the prefurosemide values. However, the mean pulmonary artery pressure was still 240% of the resting value. It is concluded that marked pulmonary hypertension is a consistent feature of moderate, as well as strenuous, exertion in the pony. Although furosemide administration attenuated the pulmonary hypertension somewhat, the significance remains unclear.     

Hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats

OBJECTIVE: To determine the hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats. ANIMALS: 12 healthy adult domestic shorthair cats. PROCEDURE: Cats were anesthetized by administration of isoflurane in oxygen. After instruments were inserted, end-tidal isoflurane concentration was set at 1.25 times the individual minimum alveolar concentration, and nitrous oxide was administered in a Latin-square design at 0, 30, 50, and 70%. Each concentration was administered for 25 minutes before measurements were obtained to allow for stabilization. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured before and during noxious stimulation for each nitrous oxide concentration. Arterial and mixed-venous bicarbonate concentrations and oxygen saturation, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, arterial and mixed-venous oxygen contents, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated. RESULTS: Arterial pressure, central venous pressure, pulmonary arterial pressure, rate-pressure product, systemic and pulmonary vascular resistance indices, arterial PCO2, and PCV increased during administration of 70% nitrous oxide. Arterial and mixed-venous pH, mixed-venous PO2, and alveolar-to-arterial oxygen difference decreased during administration of 70% nitrous oxide. Results before and during noxious stimulation were similar. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of 70% nitrous oxide to isoflurane-anesthetized cats resulted in improved arterial pressure, which was related to a vasoconstrictive effect.     

Cardiac output and other hemodynamic variables in anesthetized dogs undergoing laparotomy because of abdominal neoplasia

OBJECTIVE: To measure cardiac output and other hemodynamic variables in anesthetized dogs undergoing laparotomy because of abdominal neoplasia. DESIGN: Prospective case series. ANIMALS: 8 dogs with splenic or hepatic tumors. PROCEDURES: Dogs were anesthetized and underwent abdominal laparotomy. End-tidal isoflurane concentration, heart rate, arterial blood pressures, cardiac output, arterial pH, blood gas partial pressures, PCV, and plasma total protein concentration were measured at set intervals before, during, and after surgery. Cardiac index, stroke index, and systemic vascular resistance index were calculated. RESULTS: End-tidal isoflurane concentration was lowest before and after surgery. Heart rate did not change significantly throughout the anesthetic period. Arterial blood pressures and systemic vascular resistance index were highest shortly after surgery began; cardiac index and stroke volume index did not change significantly during surgery but increased significantly after surgery ended. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that in dogs undergoing laparotomy because of abdominal neoplasia, changes in arterial blood pressures were not necessarily indicative of qualitatively similar changes in cardiac index.     

Cardiovascular effects of romifidine in dogs

OBJECTIVE: To characterize the cardiovascular effects of romifidine at doses ranging from 5 to 100 microg/kg of body weight, IV. ANIMALS: 25 clinically normal male Beagles. PROCEDURE: Romifidine was administered IV at a dose of 5, 10, 25, 50, or 100 microg/kg (n = 5/group). Heart rate, arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, body temperature, cardiac output, and PCV were measured immediately prior to and at selected times after romifidine administration. Cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, and left and right ventricular stroke work indices were calculated. Degree of sedation was assessed by an observer who was blinded to the dose administered. RESULTS: Romifidine induced a decrease in heart rate, pulmonary arterial pressure, rate-pressure product, cardiac index, and right ventricular stroke work index and an increase in central venous pressure, pulmonary capillary wedge pressure, and systemic vascular resistance index. In dogs given romifidine at a dose of 25, 50, or 100 microg/kg, an initial increase followed by a prolonged decrease in arterial pressure was observed. Arterial pressure immediately decreased in dogs given romifidine at a dose of 5 or 10 microg/kg. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that IV administration of romifidine induces dose-dependent cardiovascular changes in dogs. However, the 2 lowest doses (5 and 10 microg/kg) induced less cardiovascular depression, and doses > or = 25 microg/kg induced similar cardiovascular changes, suggesting that there may be a ceiling on the cardiovascular effects of romifidine.     

Intravenous pentoxifylline does not affect the exercise-induced pulmonary arterial, capillary or venous hypertension in Thoroughbred horses

The present study was carried out to examine whether intravenously administered pentoxifylline-a phosphodiesterase inhibitor which increases red blood cell deformability and decreases blood viscosity-would attenuate the magnitude of exercise-induced pulmonary capillary hypertension in healthy, fit Thoroughbred horses and in turn, diminish the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. Hemodynamic data were collected at rest, and during exercise performed at 8 and 14 m/sec on 3.5% uphill grade in the control (no medications) and the pentoxifylline (8.5 mg/kg, i.v.) experiments. The sequence of treatments was randomized for every horse and 7 days were allowed between treatments. Galloping at 14 m/sec on 3.5% uphill grade elicited maximal heart rate. In both treatments, simultaneous measurements of phasic and mean right atrial and pulmonary arterial, capillary and wedge pressures were made using catheter-tip-manometers whose signals were carefully referenced at the point of the left shoulder. In the control study, exercise resulted in progressive significant increments in heart rate, right atrial and pulmonary arterial, capillary and venous pressures; thereby, confirming that exercising Thoroughbreds develop significant pulmonary hypertension. All horses experienced exercise-induced pulmonary hemorrhage (EIPH) in the control experiments. Pentoxifylline administration to standing horses caused anxiety, tachycardia, muscular fasciculations/tremors and mild sweating, but statistically significant changes in right atrial and pulmonary arterial, capillary and venous pressures were not detected. Exercise in the pentoxifylline treatment also resulted in progressive significant increments in heart rate and right atrial as well as pulmonary vascular pressures, but these data were not statistically significantly different from those in the control study and the incidence of EIPH remained unchanged. Thus, it was concluded that i.v. pentoxifylline is ineffective in attenuating the exercise-induced pulmonary arterial, capillary and venous hypertension in healthy, fit Thoroughbred horses.     

Cardiovascular, acid-base, electrolyte, and plasma volume changes in ponies developing alimentary laminitis.

Twelve Shetland ponies were fed a high-starch ration. Seven ponies which had a transitory metabolic acidosis developed laminitis 56 hours (+/- 3.5, SEM) after overfeeding. These ponies also developed persistent hypokalemia, hyperthermia, and increased heart rate 24 hours before the onset of lameness. Serum sodium, serum chloride, hematocrit, plasma volume, and blood volume were unchanged. At the onset of clinical signs of laminitis, cardiac output and blood pressure increased, but total peripheral resistance was unchanged. None of the measured or calculated values predicted the onset of laminitis. Hypertension appeared to be a response to, rather than a cause of, lameness. Three of the remaining ponies apparently died of shock 29.3 +/- 2.7 hours after overfeeding. All 3 had severe metabolic acidosis; decreased cardiac output, systemic arterial pressure, and plasma volume; and increased hematocrit, total peripheral resistance, and pulmonary vascular resistance. The 11th pony was unaffected and the 12th pony was euthanatized.     

Bronchial circulation during prolonged exercise in ponies.

Tracheal, bronchial, and renal flow were studied in 8 healthy ponies at rest and during exercise performed on a treadmill at a speed setting of 20.8 km/h and 7% grade (incline) for 30 minutes. Blood flow was determined with 15-microns-diameter radionuclide-labeled microspheres that were injected into the left ventricle when the ponies were at rest, and at 5, 15, and 26 minutes of exertion. Heart rate and mean aortic pressure increased from resting values (40 +/- 2 beats/min and 124 +/- 3 mm of Hg, respectively) to 152 +/- 8 beats/min and 133 +/- 4 mm of Hg at 5 minutes of exercise, to 169 +/- 6 beats/min and 143 +/- 5 mm of Hg at 15 minutes of exercise, and to 186 +/- 8 beats/min, and 150 +/- 5 mm of Hg at 26 minutes of exercise. Tracheal blood flow at rest and during exercise remained significantly (P less than 0.05) less than bronchial blood flow. Tracheal blood flow increased only slightly with exercise. Vasodilation caused bronchial blood flow to increase throughout exercise. Pulmonary arterial blood temperature of ponies also increased significantly (P less than 0.05) with exercise and a significant (P less than 0.005) correlation was found between bronchial blood flow and pulmonary arterial blood temperature during exertion. At 5 minutes of exercise, renal blood flow was unchanged from the resting value; however, renal vasoconstriction was observed at 15 and 26 minutes of exercise. We concluded that bronchial circulation of ponies increased with exercise in close association with a rise in pulmonary arterial blood temperature.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distribution of blood flow during moderate and strenuous exercise in ponies (Equus caballus)

Blood flow to the brain, heart, kidneys, diaphragm, and skeletal muscles was studied at rest and during graded treadmill exercise, using radionuclide-labeled microspheres (15 microns diameter), in 11 healthy adult ponies. Hemodynamic changes brought about by exercise included marked increases in cardiac output, mean aortic pressure, left ventricular end-diastolic pressure, and right ventricular systolic and end-diastolic pressures. Blood flow to the brain stem and cerebral hemispheres was unchanged during both moderate exercise (heart rate = 154 +/- 3 beats/min) and severe exercise (heart rate = 225 +/- 7 beats/min). Despite marked hypocapnia during severe exercise, cerebellar blood flow increased by 32% above control value (94 +/- 7 ml/min/100 g). Myocardial blood flow increased transmurally with both levels of exercise. The endo:epi (inner:outer) perfusion ratio for the left ventricle and the interventricular septum decreased during exercise. It was, however, not different from unity. During severe exercise, renal blood flow decreased to 19% of its control value. Blood flow to the diaphragm exceeded that to the skeletal muscles during both intensities of exercise. Blood flow to the exercising muscles of the brachium and thigh increased by 31- to 38-fold during moderate exercise and by 70- to 76-fold during severe exercise. It is concluded that the cardiovascular response to strenuous exercise in the pony included an increase in blood flow to the cerebellum, myocardium, diaphragm, and exercising skeletal muscles, while blood flow was diverted away from the kidneys. It would appear that the pony's cardiovascular response to severe exercise is similar to that of persons.     

Pulmonary vascular reactivity of the newborn pony foal

Adult ponies develop pulmonary hypertension at altitude (Bisgard, Orr and Will 1975), but the neonatal response to acute hypoxaemia is unknown. Seven foals aged five days were instrumented with a systemic and a Swan-Ganz pulmonary artery catheter while anesthetised and intubated. Cardiac index, pulmonary (PAP) and systemic (SAP) vascular pressures were measured as the foals breathed gas mixtures with FI02 of 8 to 94 per cent. Because foramen ovale or ductus arteriosus shunts might have altered thermodilution cardiac index measurements in the stressed foals, the ratio, PAP/SAP was calculated to define relative circulatory reactivity. Three foals, two of which were full siblings, had very marked elevation of PAP/SAP from 0.6 to 1.41 at low inspired oxygen tensions. Four different foals attained maximal PAP/SAP of only 0.2 to 0.92 at similarly low oxygen tensions (P less than 0.0001). Thus, pulmonary vascular reactivity to ventilatory hypoxaemia varied greatly in pony foals of the same age. The exaggerated reactivity in related foals suggested that, as in cattle, a genetic predisposition to develop reactive pulmonary hypertension under hypoxaemic stress may exist.     

Induced pasteurellosis and pulmonary vascular adrenoceptor function in bull calves

Effects of Pasteurella haemolytica inoculation on pulmonary vascular function were studied in 5 conscious standing Jersey bull calves. Instruments were implanted in each calf to measure pulmonary arterial, pulmonary arterial wedge, left atrial, and systemic arterial pressures and cardiac output. Each calf was challenge exposed with 5 sequential 3-minute infusions of isoproterenol (a beta agonist) or phenylephrine (an alpha agonist) for maximal doses of 1.8 micrograms of isoproterenol or 2.3 micrograms of phenylephrine/kg of body weight/min. The calf was allowed 1 hour to recover, was anesthesized, and administered a 20-ml intratracheal infusion of live P haemolytica (10(6) colony-forming units/ml) followed by a 20-ml saline flush. The pulmonary hemodynamic response to isoproterenol and phenylephrine was examined again in each calf 4 days later. Calves developed a pneumonic pasteurellosis involving 26 to 43% of the lungs. There was a significantly (P less than 0.05) reduced resistance in the pulmonary arterial compartment after inoculation. Isoproterenol infusion decreased resistance in the pulmonary arterial, pulmonary venous, and systemic vascular compartments. The decrease in the pulmonary venous compartment in response to isoproterenol was significantly (P = 0.01) smaller after P haemolytica inoculation. After administration of 1.8 micrograms of isoproterenol/kg/min, resistance in the pulmonary venous compartment was 0.90 +/- 0.22 (mean +/- SD) before and 1.25 +/- 0.39 after Pasteurella inoculation. Phenylephrine resulted in an increase in pulmonary arterial, pulmonary venous, and systemic vascular compartments. There was a mild (P = 0.08) decrease in the pulmonary arterial compartment response to phenylephrine. Seemingly, Pasteurella inoculation blunted beta-receptor function in the pulmonary vascular bed, mainly in the veins, contributing to edema.