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1.
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. 相似文献
2.
The frusemide dose-response for attenuation of exercise-induced pulmonary capillary hypertension was studied in 7 healthy, exercise-conditioned Thoroughbred horses using previously described haemodynamic procedures. Four different doses of frusemide were tested: 250 mg regardless of bodyweight (amounting to 0.56 +/- 0.03 mg/kg bwt), 1.0 mg/kg bwt, 1.5 mg/kg bwt and 2.0 mg/kg bwt. Frusemide was administered i.v., 4 h before exercise. Haemodynamic data were obtained at rest and during treadmill exercise performed at 14.2 m/s on a 3.5% uphill grade; this workload elicited maximal heart rate of horses. Airway endoscopy was performed post exercise to detect exercise-induced pulmonary haemorrhage (EIPH). In standing horses, frusemide administration resulted in a significant (P<0.05) decrease in mean pulmonary arterial, pulmonary capillary and pulmonary artery wedge pressures, but significant differences among the various frusemide doses were not observed. In the control experiments, exercise caused significant increments in the right atrial as well as pulmonary arterial, wedge, and capillary pressures, and all horses experienced EIPH. Following frusemide administration, the exercise-induced rise in right atrial and pulmonary vascular pressures was significantly attenuated, but significant differences between the frusemide doses of 250 mg, 1.0 mg/kg, and 1.5 mg/kg were not discerned and all horses remained positive for EIPH. Although a further significant (P<0.05) attenuation of the exercise-induced rise in pulmonary capillary blood pressure occurred when frusemide dose increased from 250 mg to 2.0 mg/kg bwt, all horses still experienced EIPH. It is concluded that a linear response to increasing frusemide dosage in terms of attenuation of the pulmonary capillary hypertension does not exist in strenuously exercising Thoroughbred horses. 相似文献
3.
S C Olsen C P Coyne B S Lowe N Pelletier E M Raub H H Erickson 《American journal of veterinary research》1992,53(5):742-747
Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only RAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling. 相似文献
4.
R. J. ROSE R. J. CARTER JAN E. ILKIW 《Journal of veterinary pharmacology and therapeutics》1980,3(2):111-119
Six dogs with previously implanted arterial, central venous, pulmonary arterial and left atrial catheters received halothane anaesthesia, and halothane anaesthesia plus administration of a balanced electrolyte solution given over one hour, in a cross-over experiment. Parameters measured included temperature, heart rate (HR), respiratory rate (f), arterial and mixed venous blood-gases and acid-base parameters, mean arterial pressure ( AP ), mean pulmonary artery pressure ( PAP ), mean left atrial pressure ( LAP ), mean central venous pressure ( CVP ), packed cell volume (PCV), total plasma protein (TPP), plasma sodium, potassium and chloride concentrations, and urinary sodium and potassium concentrations.
During halothane anaesthesia there were significant decreases in AP , PCV, TPP, f, and significant increases in arterial and mixed venous oxygen, and glucose concentrations, when compared with conscious control values. When intravenous fluid was administered during anaesthesia, there were significant decreases in temperature, AP , PCV and TPP, with significant increases in PAP , CVP and f, when compared with values during anaesthesia alone. After one hour recovery period from anaesthesia, dogs receiving intravenous fluids had significantly decreased PaO2 values and significantly increased pH when compared with anaesthesia alone. There was an average urinary excretion of 7 mmol of sodium and 5 mmol of potassium during anaesthesia, and 36 mmol of sodium and 8 mmol potassium during fluid administration. 相似文献
During halothane anaesthesia there were significant decreases in AP , PCV, TPP, f, and significant increases in arterial and mixed venous oxygen, and glucose concentrations, when compared with conscious control values. When intravenous fluid was administered during anaesthesia, there were significant decreases in temperature, AP , PCV and TPP, with significant increases in PAP , CVP and f, when compared with values during anaesthesia alone. After one hour recovery period from anaesthesia, dogs receiving intravenous fluids had significantly decreased PaO
5.
S C Olsen C P Coyne B S Lowe N Pelletier E M Raub H H Erickson 《American journal of veterinary research》1992,53(9):1562-1567
Furosemide, which commonly is used as a prophylactic treatment for exercise-induced pulmonary hemorrhage in horses, may mediate hemodynamic changes during exercise by altering prostaglandin metabolism. To determine if furosemide's hemodynamic effects during exercise in horses could be reversed, cyclooxygenase inhibitors were administered with furosemide. Four treatments were administered 4 hours prior to treadmill exercise at 9 and 13 m/s. They included a control treatment (10 ml of 0.9% NaCl solution, IV), furosemide (1 mg/kg of body weight, IV) administered alone, and furosemide in combination with phenylbutazone (4 mg/kg, IV, q 12 h for 2 days) or with flunixin meglumine (1.1 mg/kg, IV, on the day of experiment). Five horses were randomly assigned to complete all treatments. Physiologic variables at rest prior to exercise were not influenced by treatments. Furosemide, administered alone, reduced mean right atrial pressure and mean pulmonary artery pressure during exercise. The combinations of furosemide and flunixin meglumine or furosemide and phenylbutazone, at both levels of exercise intensity, returned mean right atrial pressure and mean pulmonary artery pressure to the value of the control treatment. During rest and exercise, plasma lactate concentration, PCV, heart rate, mean carotid artery pressure, oxygen consumption, carbon dioxide elimination, and cardiac output were not altered by any of the treatments. At 5 minutes after exercise, the administration of furosemide, alone or with phenylbutazone, reduced mean right atrial pressure. Other measured variables were not significantly influenced by treatments during recovery from exercise. These results suggested that cyclooxygenase inhibition partially reverses the decrease in mean right atrial pressure or pulmonary artery pressure induced by furosemide during exercise.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
6.
Hubbell JA Hinchcliff KW Grosenbaugh DA Beard WL Beard LA 《Equine veterinary journal》2002,34(6):580-586
Frusemide reduces pulmonary vascular pressures in resting horses and attenuates exercise-induced increases in these pressures in exercising horses. The mechanism underlying these effects of frusemide is unclear. We tested the hypothesis that the haemodynamic effects of frusemide are dependent on diuresis by examining the effect of frusemide in anaesthetised horses in which diuresis was prevented by ligation of ureters. Twenty four horses were assigned randomly to one of 4 treatments: 1) frusemide (1 mg/kg bwt i.v.) and intact ureters; 2) frusemide and ligated ureters; 3) saline placebo and ligated ureters; and 4) frusemide and phenylbutazone (4.4 mg/kg bwt i.v. 12 h and 15 min before frusemide) and ligated ureters. Frusemide administration to anaesthetised horses with intact ureters increased plasma total protein concentration and reduced mean right atrial, pulmonary artery and aortic pressures. There was no significant effect of frusemide administration on haemodynamic variables or plasma total protein concentration in horses with ligated ureters. The combination of frusemide and phenylbutazone increased mean right atrial, pulmonary artery and aortic pressures in horses with ligated ureters. This study demonstrates that, in anaesthetised horses, the haemodynamic effect of frusemide is dependent upon diuresis. We interpret these results as providing further evidence that the haemodynamic effect of frusemide in horses is attributable to a reduction in plasma and blood volume. 相似文献
7.
The present study was carried out to examine whether pentoxifylline administration to horses premedicated with frusemide would attenuate the exercise-induced pulmonary arterial, capillary and venous hypertension to a greater extent than frusemide alone, thereby affecting the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Using established techniques, we determined right heart and pulmonary vascular pressures in 6 healthy, sound Thoroughbred horses at rest and during exercise performed at maximal heart rate at a workload of 14 m/s on 3.5% uphill grade in the control (no medications), frusemide (250 mg i.v., 4 h pre-exercise)-control, and the frusemide (250 mg i.v., 4 h pre-exercise) + pentoxifylline (8.5 mg/kg bwt i.v., 15 min preexercise) treatments. Sequence of the 3 treatments was randomised for every horse and 7 days were allowed between them. In the control study, galloping at 14 m/s on 3.5% uphill grade elicited significant right atrial as well as pulmonary arterial, capillary and venous hypertension and all horses experienced EIPH as detected by the presence of fresh blood in the trachea on endoscopic examination. Frusemide administration was not attended by changes in heart rate at rest or during exercise. Although in the frusemide-control experiments, a significant reduction in mean pulmonary arterial, capillary and wedge pressures was observed both at rest and during galloping at 14 m/s on 3.5% uphill grade, all horses still experienced EIPH. Pentoxifylline administration to standing horses premedicated with frusemide caused nervousness, muscular fasciculations, sweating and tachycardia. Although these symptoms had largely abated within 15 min, there were no significant changes in the right atrial or pulmonary vascular pressures. Exercise in the frusemide + pentoxifylline experiments also caused significant right atrial as well as pulmonary arterial, capillary and venous hypertension, but these data were not found to be significantly different from the frusemide-control experiments. All horses in the frusemide + pentoxifylline experiments also experienced EIPH. In conclusion, our data indicate that pentoxifylline (8.5 mg/kg bwt i.v., 15 min pre-exercise) is ineffective in modifying the pulmonary haemodynamic effects of frusemide in exercising horses. It should be noted, however, that we did not examine whether erythrocyte plasticity was altered by the administration of pentoxifylline. Since the intravascular force exerted onto the blood-gas barrier of exercising horses premedicated with frusemide remained unaffected by pentoxifylline administration, it is concluded that concomitant pentoxifylline administration is unlikely to offer additional benefit to horses experiencing EIPH. 相似文献
8.
Hackett RP Ducharme NG Ainsworth DM Erickson BK Erb HN Soderholm LV Thorson LM 《American journal of veterinary research》1999,60(4):485-494
OBJECTIVE: To determine whether dorsal displacement of the soft palate (DDSP) results in pulmonary artery hypertension and leads to increases in transmural pulmonary artery pressure (TPAP); to determine whether pulmonary hypertension can be prevented by prior administration of furosemide; and to determine whether tracheostomy reduces pulmonary hypertension. ANIMALS: 7 healthy horses. PROCEDURE: Horses were subjected to 3 conditions (control conditions, conditions after induction of DDSP, and conditions after tracheostomy). Horses were evaluated during exercise after being given saline (0.9% NaCl) solution or furosemide. RESULTS: Controlling for drug, horse, and speed of treadmill, DDSP-induced increase in intrathoracic pressure was associated with a significant increase in minimum (36 mm Hg), mean (82 mm Hg), and maximum (141 mm Hg) pulmonary artery pressure, compared with values for control horses (30, 75, and 132 mm Hg, respectively). Increases in pulmonary artery pressure did not induce concomitant increases in TPAP. Tracheostomy led to a significant reduction of minimum (53 mm Hg), and mean (79 mm Hg) TPAP pressure, compared with values for control horses (56 and 83 mm Hg, respectively). When adjusted for horse, speed of treadmill, and type of obstruction, all aspects of the pulmonary artery and TPAP curves were significantly decreased after administration of furosemide, compared with those for horses given saline (0.9% NaCl) solution. CONCLUSIONS: DDSP was associated with increases in pulmonary artery pressure but not with increases in TPAP. CLINICAL RELEVANCE: Expiratory obstructions such as DDSP are likely to result in pulmonary hypertension during strenuous exercise, but may not have a role in the pathogenesis of exercise-induced pulmonary hemorrhage. 相似文献
9.
The present study was carried out to ascertain whether beta2-adrenergic receptor stimulation with clenbuterol would attenuate the pulmonary arterial, capillary and venous hypertension in horses performing high-intensity exercise and, in turn, modify the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Experiments were carried out on 6 healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications) and the clenbuterol (0.8 pg/kg bwt, i.v.) treatments. The sequence of these treatments was randomised for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, right heart/pulmonary vascular pressures were determined at rest, sub-maximal exercise and during galloping at 14.2 m/s on a 3.5% uphill grade--a workload that elicited maximal heart rate and induced EIPH in all horses. In the control experiments, incremental exercise resulted in progressive significant increments in right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures and all horses experienced EIPH. Clenbuterol administration to standing horses caused tachycardia, but significant changes in mean right atrial or pulmonary vascular pressures were not observed. During exercise performed after clenbuterol administration, heart rate as well as right atrial and pulmonary arterial, capillary and wedge pressures also increased progressively with increasing work intensity. However, these values were not found to be statistically significantly different from corresponding data in the control study and the incidence of EIPH remained unaffected. Since clenbuterol administration also does not affect the transpulmonary pressure during exercise, it is unlikely that the transmural force exerted onto the blood-gas barrier of exercising horses is altered following i.v. clenbuterol administration at the recommended dosage. 相似文献
10.
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. 相似文献
11.
Funkquist P Sandhagen B Persson SG Hedenstierna G Essén-Gustavsson B Nyman G 《Equine veterinary journal》2001,33(4):417-424
Five Standardbred trotters with red cell hypervolaemia (RCHV) were compared before and after removal of approximately 22% (36 ml/kg bwt) of the total blood volume in order to evaluate the haemodynamic responses, haemorheological alterations and oxygen transport during exercise to fatigue. Data were recorded during submaximal exercise at 4 different speeds on a treadmill and then during continued running at the highest speed step until fatigue. Oxygen uptake (VO2), pulmonary artery pressure (PAP), systemic artery pressure (SAP), heart rate (HR), haematocrit and haemoglobin concentrations (Hb) were measured. Arteriovenous O2 content difference (C(a-v)O2), pulmonary vascular resistance (PVR) and total systemic resistance (TSR) were calculated. Whole blood and plasma viscosity and erythrocyte aggregation tendency were determined with a rotational viscometer. Endoscopy was performed after exercise. ANOVA was used for statistical analysis. Phlebotomy resulted in a decrease in haematocrit and Hb during the course of exercise. Blood and plasma viscosity were lower and erythrocyte aggregation tendency was higher after phlebotomy. Throughout exercise, including submaximal work and continued running to fatigue, PAP, SAP, PVR, TSR and C(a-v)O2 were lower after phlebotomy. HR was higher after phlebotomy during submaximal exercise. Oxygen delivery and VO2 were lower after phlebotomy in the period from submaximal exercise to fatigue. Run time to fatigue was shorter after phlebotomy. Four horses showed exercise-induced pulmonary haemorrhage (EIPH) before phlebotomy and the degree of bleeding was diminished but not abolished after phlebotomy. The reductions in PVR, TSR, PAP and SAP after phlebotomy were probably a result of reduced blood viscosity. In conclusion, although a 22% reduction in blood volume improved the haemodynamic and haemorheological parameters and the degree of EIPH, it was found that RCHV trotters have to rely on high oxygen delivery to the working muscles for maintenance of maximal performance. 相似文献
12.
The heart rate and the pulmonary artery wedge pressure (PWP) was measured in 10 healthy warmblood horses and in six warmblood horses with atrial fibrillation (AF) at rest and during standardised treadmill exercise. During treadmill exercise, the increase in heart rate was significantly higher in the horses with AF than in the healthy horses. Horses with AF showed a significantly higher increase in PWP at treadmill velocities of 5m/s and faster, than did the healthy horses. The differences in PWP between both groups increased with treadmill strain. The present study demonstrates that there is an influence on the haemodynamics in horses with AF during treadmill exercise, which could explain exercise intolerance in some horses with lone AF. 相似文献
13.
In 12 healthy warmblood horses and 10 horses with mitral valve insufficiencies (MVI) of various degrees heart rate and pulmonary artery wedge pressure (PWP) was measured at rest and during standardised exercise on a high speed treadmill. There was a significant increase in PWP with each change in speed of the treadmill (p < 0.01). The PWP of horses with mild mitral valve regurgitation under working conditions was not significantly different compared to the healthy horses. The horses with moderate mitral valve regurgitation showed a significant higher pulmonary artery wedge pressure at rest and during exercise compared to the healthy horses (p < 0.01) at rest and during treadmill velocity. The tendencies were seen that mild mitral valve regurgitation results only in mild hemodynamic changes during exercise, while moderate MVI have an important influence on haemodynamics. 相似文献
14.
In 12 healthy warmblood horses (six trained and six untrained) the pulmonary wedge pressure and heart frequency was measured at rest and during a standardised exercise test on a treadmill. The mean pulmonary wedge pressure at rest was 14.53 +/- 2.36 mmHg. There was no significant difference in pulmonary wedge pressure either at rest or during exercise between trained and untrained horses. During walking (1.8 m/s) the mean pulmonary wedge pressure was 19.62 +/- 4.03 mmHg, during trotting (4 und 5 m/s) it was between 22.38 +/- 3.92 mmHg and 25.28 +/- 3.7 mmHg. During canter (6 m/s) and gallop (8 m/s) the mean pulmonary wedge pressure increased to a level of 25.54 +/- 4.3 mmHg and 31.86 +/- 4.29 mmHg. There was a significant increase in pulmonary wedge pressure with each incremental step of the standardised treadmill test. Concerning mean heart frequency a highly significant increase could be observed at the beginning and at the end (treadmill speed of 7 and 8 m/s) of the standardised exercise test. At higher intensity of the exercise test (7 m/s and 8 m/s) untrained horses showed a significantly increased heart rate compared to trained horses. Neither at rest nor during the different exercise levels a significant correlation factor greater 0.5 between heart frequency and pulmonary wedge pressure could be observed. The increase of heart frequency and pulmonary wedge pressure during exercise showed no correlation. Between left atrial size and pulmonary wedge pressure a statistical weak correlation could be observed up to a treadmill velocity of 6 and 7 m/s. 相似文献
15.
In 18 horses, the pulmonary artery wedge pressure and the heart rate were measured during pharmacological stress load. 12 horses were healthy (4 trained, 8 untrained) and 6 horses had a heart disease (3 trained, 3 untrained). Pharmacological stress induction was carried out with the sympathomimetic drug dobutamine at a dosage rate of 7.5 microg/kg/min over 10 minutes of infusion. At the fourth minute, the parasympatholytic drug atropine was administered (5 microg/kg bw), and the heart rate and the pulmonary artery wedge pressure were continuously measured over 26 minutes. During sole dobutamine infusion, a significant decrease in heart rate and a significant increase in pulmonary artery wedge pressure were observed. After the application of atropine in the fourth minute, a significant increase in heart rate (from 35.7 +/- 6 up to 106 +/- 38/ min) and in pulmonary artery wedge pressure (from 15.7 +/- 3 up to 24 +/- 8.6 mmHg) were visible in the group of healthy horses. The horses with heart diseases had a significantly higher increase in both parameters (heart rate and pulmonary artery wedge pressure) with a significantly positive correlation (r = 0.7). The heart rate increased in the horses with heart diseases from 35.2 +/- 2,8 beats/min up to 132 +/- 45.7 beats/min and the pulmonary artery wedge pressure increased from 17.3 +/- 3,2 mmHg up to 32.7 +/- 13 mmHg. The cardiac status (healthy or heart disease) as well as the training level of the horses (untrained or trained) had a significant influence on the heart rate and the pulmonary artery wedge pressure. The untrained horses (healthy and heart disease) showed significantly higher values over a longer period of time than did the trained horses with the same cardiac status. Additionally the influence of pharmacological stress induction on echocardiographic parameters was investigated. The left atrial size (p = 0.015) and left ventricular diameter were significanly different in the systole (p = 0.008) and in the diastole (p = 0.001) between healthy horses and horses with heart diseases. All horses showed a positive correlation between the pulmonary artery wedge pressure and the left atrial size (r = 0.8), as well as between the left ventricular systolic (r = 0.6) and the diastolic diameter (r = 0.6). The correlation between the pulmonary artery wedge pressure and the left atrial size was nearly the same in the healthy horses (r = 0.74) and in the horses with heart diseases (r = 0.76). Regarding the training level, all untrained horses had a significantly higher correlation between the pulmonary artery wedge pressure and the left atrial size (r = 0.87) in comparison to the trained horses (r = 0.74). Particularly in the untrained horses with heart diseases, this correlation was remarcable (r = 0.99). 相似文献
16.
Based on previous in vitro studies, we hypothesised that endothelin (ET) would induce vasoconstriction in the pulmonary circululation of the horse and that this action would be mediated via ET(A) receptors. Pulmonary and systemic haemodynamic responses to endothelin-1 (ET-1), a potent vasoactive endogenous peptide, were investigated in 6 conscious, nonsedated horses at rest. Bolus i.v. injections of exogenous ET-1 (0.1, 0.2 and 0.4 microg/kg bwt) caused significant increases in pulmonary (PAP) and carotid (CAP) artery pressures, with peak increases of 79% and 51% for mean PAP and CAP, respectively. The effect of ET-1 on PAP and CAP was rapid and transient for PAP (-10 min) but prolonged for CAP (up to 60 min). ET-1 significantly decreased cardiac output by up to 35% and significantly increased systemic vascular resistance (SVR) by up to 104%. Pulmonary vascular resistance (PVR) showed a trend (P>0.05) to increase with 0.2 and 0.4 microg/kg bwt ET-1. Infusion of a selective ET(A) receptor antagonist (TBC11251) completely inhibited the responses to a subsequent bolus of 0.2 microg/kg bwt ET-1. We conclude that exogenous ET-1 exerts a potent vasoconstrictive action on the pulmonary and systemic circulations of the horse. These effects appear to be mediated largely through ET(A) receptors in both circulations. Endothelin may play a role in hypertensive conditions in the horse. 相似文献
17.
E P Steffey A B Kelly D S Hodgson J L Grandy M J Woliner N Willits 《American journal of veterinary research》1990,51(1):11-16
Cardiovascular and respiratory functions were serially characterized in 7 healthy, spontaneously breathing, adult horses (from which food had been withheld) during 5 hours of constant 1.06% alveolar halothane (end-expired halothane concentration of 1.06%; equivalent to 1.2 times the minimal alveolar anesthetic concentration for horses). To enable comparison of temporal results in relation to 2 body postures, horses were studied in lateral recumbency (LR) and dorsal recumbency (DR) on separate occasions. Temporal changes in results of measures of circulation previously reported from this laboratory for horses in LR were confirmed (ie, a time-related increase in systemic arterial blood pressure, cardiac output, stroke volume, and PCV). During DR, systemic arterial blood pressure was initially significantly (P less than 0.05) greater and pulmonary artery pressure less than results at comparable periods during LR. Differences ceased to exist with duration of anesthesia. Except for a greater heart rate at hour 5 of DR, no other significant differences in circulation were found between LR and DR. In general, except for PaO2, measures of ventilation did not change with time in either LR or DR. The PaO2 was significantly greater during LR, compared with DR, but the average did not change significantly with time in either body posture. 相似文献
18.
Manohar M Goetz TE Rothenbaum P Humphrey S 《Journal of veterinary pharmacology and therapeutics》2000,23(5):317-322
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. 相似文献
19.
Do Thoroughbred and Standardbred horses have similar increases in pulmonary vascular pressures during exertion?
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R. P. Hackett N. G. Ducharme R. D. Gleed L. Mitchell L. V. Soderholm B. K. Erickson H. N. Erb 《Canadian journal of veterinary research》2003,67(4):291-296
To test the hypothesis that the pulmonary vascular pressures of Thoroughbred and Standardbred horses behave similarly during exertion. Measurements were made on 5 Thoroughbred and 5 Standardbred horses on a treadmill at rest and during 3-minute exercise intervals at speeds predicted to produce 75%, 90%, and 100% maximal heart rate. Left forelimb acceleration, heart rate, esophageal pressure, and pulmonary artery pressure were measured continuously. Pulmonary capillary and wedge pressures were measured during intermittent occlusion of the pulmonary artery. Breathing rate and gait frequency were the fundamental frequencies of the esophageal pressure and limb acceleration signals respectively. The ratio of speed:gait frequency gave stride length. The effects of exertion and breed were evaluated using two-way analysis of variance. Exertion produced significant increases in pulmonary artery (P = 0.001), capillary (P= 0.002), and wedge (P= 0.005) pressures. No significant effect of breed was detected on pulmonary artery pressure, but at exertion pulmonary capillary and wedge pressures were 15% (P= 0.03) and 23% (P= 0.04) greater in Thoroughbreds, respectively. Treadmill speed was ~12% greater (P= 0.04), stride length was ~25% greater (P= 0.0003), gait frequency was ~10% less (P= 0.006), breathing rate was ~10% less (P= 0.001), and heart rate was ~6% less (P= 0.06) for Thoroughbreds. There was no effect of breed on inspiratory or expiratory esophageal pressure although mean esophageal pressure was ~2 mmHg greater (P= 0.03) in exercising Standardbreds. In conclusion, pulmonary capillary and wedge pressures are greater in Thoroughbreds than in Standardbreds at similar fractions of maximal heart rate. This is compatible with the higher incidence of exercise-induced pulmonary hemorrhage observed in Thoroughbreds. 相似文献
20.
This study was designed to determine whether calcium antagonists, diltiazem and nifedipine, can depress low temperature‐induced pulmonary hypertension (PH) in broilers (also known as ascites) and to characterize their efficacy on hemodynamics and pulmonary artery function. Chicks were randomly allocated into six experimental groups and orally administered with vehicle, 5.0 mg/kg body weight (BW)/12 h nifedipine or 15.0 mg/kg BW/12 h diltiazem from 16 to 43 days of age under low temperature. The mean pulmonary arterial pressure (mPAP), the ascites heart index (AHI), the erythrocyte packed cell volume (PCV) and the relative percentage of medial pulmonary artery thickness were examined on days 29, 36 and 43. The data showed that administration of diltiazem protected broilers from low temperature‐induced pulmonary hypertension and vascular remodeling. Although nifedipine prevented mPAP from increasing during the early stage, it did not suppress the development of PH during the late stage and did not keep heart rate (HR), PCV, AHI and the thickness of pulmonary small artery smooth muscle layer at the normal levels. Taken together, our results showed that diltiazem can effectively prevent low temperature‐induced pulmonary hypertension in broilers with fewer side‐effects and may be a potential compound for the prevention of this disease in poultry industry. 相似文献