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Biomedical subjects

M Manohar

Publications and source records attributed to M Manohar.

At least 37 records · Page 2Linked to original sources

Regional distribution of blood flow in the brain of horses at rest and during exercise.

OBJECTIVE: To examine regional distribution of blood flow in the brain of horses at rest and during exercise. ANIMALS: 9 clinically normal horses. PROCEDURE: Regional brain blood flow was measured using radionuclide-labeled 15-microns-diameter microspheres injected into the left ventricle, while reference blood samples were obtained from the aorta. RESULTS: At rest, cerebral cortex and caudate nuclei received significantly higher blood flow, compared with cerebral white matter. A similar perfusion heterogeneity existed in the cerebellum. In the brain stem, a gradual tapering of blood flow from thalamus-hypothalamus towards medulla was observed in standing horses. Progressive significant increases in heart rate and in aortic and right atrial pressures occurred during exercise at 8 and 13 m/s, and horses developed significant arterial hypoxemia and hypercapnia. Cerebral and cerebellar gray- to white-matter perfusion heterogeneity was maintained during exercise, indicating differential metabolic O2 needs. Despite arterial hypoxemia, hypercapnia, and hypertension, exercise did not result in significant changes in blood flow to the cerebral cortex and caudate nuclei whereas, in cerebral white matter, a significant decrease in blood flow was observed. In all cerebral tissues, vascular resistance increased during exercise, indicating autoregulation of cerebral blood flow. In the cerebellar cortex, blood flow increased significantly with strenuous exercise as vasodilation occurred. Vascular resistance in cerebellar white matter increased during exercise at 13 m/s. Blood flow in the medulla, pons, midbrain, and thalamus-hypothalamus was not significantly altered during exercise from that at rest. CONCLUSION: Despite arterial hypoxemia, hypercapnia, and hypertension, autoregulation of cerebral and cerebellar blood flow is maintained in horses during exercise.

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Pulmonary vascular pressures of strenuously exercising Thoroughbreds after administration of varying doses of frusemide.

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.

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Expression of the superantigen Mycoplasma arthritidis mitogen in Escherichia coli and characterization of the recombinant protein.

Mycoplasma arthritidis mitogen (MAM), is a soluble protein with classical superantigenic properties and is produced by an organism that causes an acute and chronic proliferative arthritis. Unfortunately, the process of obtaining purified MAM from M. arthritidis culture supernatants is extremely time-consuming and costly, and very little material is recovered. Thus, our laboratory has expressed MAM in Escherichia coli by using a protein fusion expression system. The construction and expression of recombinant MAM (rMAM), as well as a comparison of the biological properties of rMAM to those of native MAM, are discussed. Briefly, conversion of the three UGA codons to UGG codons was required to obtain full-length expression and mitogenic activity of rMAM. Antisera to native MAM recognized both rMAM and the fusion protein. The T-cell receptor Vbeta and major histocompatibility complex class II receptor usages by rMAM and the fusion protein were identical to that of native MAM. In addition, the ability to induce suppression and form the superantigen bridge could also be demonstrated with rMAM. Importantly, dose-response experiments indicated that homogeneous native MAM and rMAM were of equal potency. Thus, MAM has been successfully expressed in E. coli, thereby creating a viable alternative to native MAM.

Antigens↗

The sequence of the Mycoplasma arthritidis superantigen, MAM: identification of functional domains and comparison with microbial superantigens and plant lectin mitogens.

Mycoplasma arthritidis, an agent of chronic proliferative arthritis of rodents, secretes a potent soluble superantigen, MAM, that is active for both murine and human T and B lymphocytes. We now report the complete nucleotide and amino acid sequence of MAM and show it to be distinct from other proteins and not closely related phylogenetically to other superantigens. Two functional domains on MAM are identified based on the ability of peptides encompassing these regions to inhibit lymphocyte proliferation by the intact MAM molecule. One of these domains shares short sequences or epitopes with other microbial superantigens. The second domain contains the consensus legume lectin motif-beta, which is important for T cell activation by concanavalin (Con) A. MAM and Con A peptides containing this motif are functionally cross reactive, suggesting a novel secondary pathway for T cell activation by MAM.

Amino Acid Sequence↗

Pulmonary vascular pressures of exercising thoroughbred horses with and without endoscopic evidence of EIPH.

Exercise-induced pulmonary hemorrhage (EIPH) is a common occurrence in racehorses. The objective of this study was to compare pulmonary vascular pressures of healthy Thoroughbred horses with and without postexertion endoscopically detectable fresh blood in the trachea. The nasopharynx, larynx, and trachea (down to the carina) of horses were examined weekly with an endoscope 55-60 min postexertion, and the diagnosis of EIPH was confirmed by the presence of fresh blood in the trachea. Measurements of heart rate and right atrial, pulmonary arterial, and pulmonary arterial wedge pressures were made during quiet rest and during treadmill exercise performed at 14.5 m/s on a 5% uphill grade. This workload elicited maximal heart rate of the horses. Mean pulmonary capillary pressure was estimated to be halfway between the mean pulmonary arterial pressure and the mean pulmonary arterial wedge pressure. These data from 7 healthy sound exercise-trained horses that were positive on 12 consecutive occasions (at 1-wk intervals) for the postexercise presence of fresh blood in the trachea were compared with those in 8 healthy horses that were consistently negative for the evidence of fresh blood in the trachea on postexercise endoscopic examination over 12-16 wk. The heart rate and the right heart and/or pulmonary vascular pressures in the two groups of horses were similar at rest. Exercise was attended by a large significant (P < 0.05) increase in these pressures and heart rate in both groups. However, statistically significant differences between endoscopically EIPH-positive and endoscopically EIPH-negative horses for heart rate and right atrial and pulmonary vascular pressures were not found during exercise. Thus these data revealed that the magnitude of exercise-induced right atrial as well as pulmonary arterial, capillary, and venous hypertension in endoscopically EIPH-positive horses that are otherwise healthy is quite similar to that in endoscopically EIPH-negative horses during comparable exertion.

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Pulmonary vascular pressures of strenuously exercising thoroughbreds after administration of phenylbutazone.

OBJECTIVE: To determine the effects of phenylbutazone administration on heart rate and right atrial and pulmonary vascular pressures in Thoroughbreds during rest and during exercise performed at maximal heart rate. ANIMALS: 7 healthy, exercise-conditioned Thoroughbreds. PROCEDURE: Horses were studied on 3 occasions: without medication [control], after i.v. administration of phenylbutazone (4.4 mg/kg of body weight) at 12-hour intervals for 2 days and a final dose given 1 hour before exercise, and after i.v. administration of phenylbutazone for 2 days in the same manner, but with the final dose given 24 hours before exercise. Horses were studied at rest and during exercise performed at maximal heart rate on a treadmill. Right atrial and pulmonary vascular pressures were measured with catheter-tip manometers referenced at the point of the shoulder. RESULTS: We did not detect significant differences in heart rate or right atrial and pulmonary vascular pressures among values recorded when horses were not given medication and values recorded when phenylbutazone was administered by either regimen. Exercise-induced pulmonary hemorrhage occurred in 6 of the 7 horses regardless of whether phenylbutazone was administered or the dosage regimen used. CONCLUSIONS: In these Thoroughbreds, phenylbutazone treatment did not modify heart rate or right atrial and pulmonary vascular pressures at rest or during exercise capable of eliciting exercise-induced pulmonary hemorrhage. Thus, because phenylbutazone is a potent inhibitor of cyclooxygenase, prostaglandins probably do not play a role in mediating exercise-induced pulmonary hypertension in horses. CLINICAL RELEVANCE: Phenylbutazone administration did not modify the pulmonary capillary hypertension in the strenuously exercising Thoroughbreds, and therefore, is unlikely to alter the prevalence or severity of exercise-induced pulmonary hemorrhage in Thoroughbred race-horses.

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Effects of glyceryl trinitrate (nitroglycerin) on pulmonary vascular pressures in standing thoroughbred horses.

Strenuously exercising Thoroughbreds exhibit a dramatic increase in pulmonary capillary blood pressure, which contributes to stress failure of pulmonary capillaries resulting in exercise induced pulmonary haemorrhage (EIPH). One strategy to prevent EIPH is, therefore, to lower the pulmonary capillary blood pressure of exercising horses. Recent work in several species suggests that nitric oxide plays a significant role in maintaining low vascular resistance in the pulmonary circulation; however, the effects of nitrovasodilators (which work via the same mechanism as nitric oxide) on equine pulmonary circulation have not been examined. The present study examined the effects of glyceryl trinitrate (nitroglycerin) on right atrial and pulmonary vascular pressures in 7 healthy sound Thoroughbred horses. Freshly prepared nitroglycerin solution was infused for 240 s into the right atrium of quietly standing Thoroughbreds at dose rates of 350, 700, 1400 and 2100 g/min in a randomised manner. All infusions were performed in duplicate. Heart rate, right atrial, pulmonary artery, pulmonary capillary and pulmonary artery wedge pressures were determined preinfusion, at 30 s intervals during nitroglycerin infusions and at 60 s post infusion. Measurements were made using catheter mounted manometers whose in vivo signals had been matched with fluid-filled systems referenced at the level of the point of the shoulder. It was observed that nitroglycerin infusions caused a dose related increase in heart rate while dose related reductions occurred in the mean right atrial, pulmonary artery, pulmonary artery wedge and pulmonary capillary pressures. At 2100 micrograms/min, nitroglycerin induced reduction in pulmonary artery wedge pressure was significantly greater than that in the pulmonary artery pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

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Thyroid, renal, and splanchnic circulation in horses at rest and during short-term exercise.

Using radionuclide-labeled 15-microm-diameter microspheres injected into the left ventricle, we examined blood flow to the thyroid gland, adrenal glands, kidneys, and various gastrointestinal tract tissues in 9 healthy horses while they were standing quietly (rest) and during exercise at 2 work intensities (8 and 1 m/s). Hemodynamic measurements were made during steady-state conditions, as judged by the stability of heart rate as well as aortic, pulmonary, and right atrial pressures. The similarity of blood flow values for the left and the right kidneys during each of the 3 conditions indicated adequate mixing of microspheres with blood. In standing horses, of all tissues examined, the thyroid gland had the highest blood flow (1,655.2 +/- 338.5 ml/min/100 g)--being about threefold that in the kidneys. Adrenal blood flow, by contrast, was only 25% of that in the kidneys (589.5 +/- 50.4 ml/min/100 g). Among the gastrointestinal tract tissues, glandular stomach and pancreas had the highest blood flows (214.3 +/- 21.6 and 197.6 +/- 23.4 ml/min/100 g, respectively). Small intestinal perfusion was not different from that in the ventral colon and cecum, but their values exceeded those for the dorsal and small colons. Exercise at 8 and 13 m/s caused significant increase in adrenal blood flow as vascular resistance decreased significantly. In the kidneys, blood flow was only insignificantly affected during exercise at 8 m/s, but at 13 m/s there was a profound reduction in renal blood flow as intense renal vasoconstriction occurred. Vasoconstriction also caused thyroid and pancreatic blood flow to decrease significantly at both levels of exertion. Significant vasoconstriction occurring in all gastrointestinal tract tissues at 8 and 13 m/s caused blood flow to be diverted away from these vascular beds. Thus, our data indicated that renal, adrenal, and splanchnic organ/tissue blood flow responses of strenuously exercising horses closely resemble those described for exercising ponies.

Adrenal Glands↗

Pulmonary vascular pressures of thoroughbreds increase rapidly and to a higher level with rapid onset of high-intensity exercise than slow onset.

Previous studies of pulmonary vascular pressures have utilised gradual incremental step exercise protocols, but in competitive racing at the track, horses perform rapid acceleration high-intensity exercise. The rate of rise in pulmonary vascular pressures under conditions of quick onset high-intensity exercise is unknown. Catheter mounted manometers, whose in vivo signals were matched with pressure signals obtained via transducers connected to fluid-filled lumens from same cardiovascular sites, were used to compare right heart and pulmonary vascular pressures in 8 healthy Thoroughbreds performing 2 separate exercise protocols on a high speed treadmill (gradually incremental vs. rapid acceleration exercise protocol where the belt speed was raised from 8 m/s to 15 m/s in 8 s). Heart rate, right atrial and pulmonary vascular pressures at rest were similar for the 2 protocols. Rapid acceleration of horses from 8 to 15 m/s was attended by an equally rapid escalation in the right heart and pulmonary vascular pressures such that these pressures reached their zenith as belt speed approached 15 m/s. Although exercise at 15 m/s resulted in similar heart rate in the 2 protocols, the mean +/- s.e. values of mean right atrial pressure, mean pulmonary artery pressure, mean pulmonary artery wedge pressure and mean pulmonary capillary pressure (91.5 +/- 3.9 mmHg) in the rapid acceleration exercise were significantly (P < 0.05) higher than respective values at 15 m/s in the gradual incremental step exercise protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

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Frusemide attenuates the exercise-induced rise in pulmonary capillary blood pressure in horses.

Catheter mounted micro-tip-manometers (the signals from which were matched with fluid-filled pressure signals from same cardiovascular sites and zeroed at the point of the shoulder), were used to study pulmonary haemodynamics in 8 healthy sound horses at rest and during exercise performed at 8, 10, 12 and 14 m/s on a treadmill. Measurements were made without frusemide (control) and 4 h after iv administration of 250 mg frusemide. Post-frusemide data were also obtained on a separate day, and these observations were not significantly different from those made on the same day as controls. Pre-frusemide values of heart rate, mean right atrial pressure, mean pulmonary artery pressure, mean pulmonary artery wedge pressure and mean pulmonary capillary pressure at 14 m/s were 214 +/- 5 beats/min, 54 +/- 4, 92 +/- 4, 65 +/- 6 and 79 +/- 5 mmHg, respectively. Exercise at 14 m/s after frusemide resulted in a similar heart rate (216 +/- 4 beats/min), but the mean right atrial, pulmonary arterial, pulmonary artery wedge and pulmonary capillary pressures were all significantly lower, i.e. 34 +/- 5, 79 +/- 4, 45 +/- 4, and 62 +/- 3 mmHg, respectively. Attenuation, by frusemide, of the exercise-induced rise in pulmonary capillary pressure would lower the magnitude of the transmural force exerted on the pulmonary capillaries. If, therefore, exercise-induced pulmonary haemorrhage (EIPH) is caused by stress failure of pulmonary capillaries, frusemide pretreatment has the potential for reducing/limiting the extent of EIPH.

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Pulmonary vascular pressures of strenuously exercising thoroughbreds after administration of flunixin meglumine and furosemide.

High-intensity exercise results in a dramatic increase in mean pulmonary capillary blood pressure of horses, and administration of furosemide 4 hours before exertion significantly attenuates this exercise-induced increment. To test whether this effect of furosemide is mediated via release of prostaglandins, right atrial and pulmonary vascular pressures were measured in 8 healthy, sound, exercise-trained Thoroughbreds at rest and during incremental-step exercise on a treadmill. Horses were studied on 3 separate occasions: after i.v. administration of saline (0.9% NaCl) solution, after administration of furosemide (250 mg, i.v., 4 hours before exercise) alone, and after administration of flunixin meglumine (1.1 mg/kg, i.v., q 8 h for 3 days) and furosemide (250 mg, i.v., 4 hours before exercise; last dose of flunixin meglumine was administered 90 seconds after furosemide injection). Experiments on each horse were separated by at least 7 days and were performed in random order. At rest and at the highest workload (14.5 m/s on a 5% uphill incline), mean pulmonary capillary blood pressure recorded after administration of furosemide alone was not significantly different from that recorded after administration of flunixin meglumine and furosemide. However, these values were significantly (P < 0.05) less than corresponding values of mean pulmonary capillary blood pressure recorded after administration of saline solution. Thus, it was concluded that furosemide-induced attenuation of the increment in pulmonary capillary blood pressure during strenuous exercise is probably not mediated via prostaglandin production.

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Atrial and ventricular myocardial blood flows in horses at rest and during exercise.

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-micron-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.(ABSTRACT TRUNCATED AT 250 WORDS)

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Furosemide attenuates the exercise-induced increase in pulmonary artery wedge pressure in horses.

Right atrial (RA), right ventricular (RV), pulmonary artery (PA), and pulmonary artery wedge (PAW) pressures were examined, using catheter-mounted micromanometers, in 8 healthy horses at rest and during galloping on a treadmill at belt speeds of 8, 10, and 13 m/s. The in vivo signals from the micromanometers were matched with those from conventional fluid-filled catheter transducers leveled at the scapulohumeral joint. Thirty minutes after completing control exercise measurements, furosemide was administered IV at a dosage of 1 mg/kg of body weight, and resting, as well as exercise, measurements were repeated 4 hours later. Studies also were performed on a separate day, when only postfurosemide resting and exercise data were collected. Prefurosemide and postfurosemide heart rate values for rest (37 +/- 2 beats/min, mean +/- SEM), as well as for exercise (213 +/- 5 beats/min at 13 m/s), were similar. Prefurosemide mean RA, PA, and PAW pressures were increased significantly (P < 0.05) from resting values of 8 +/- 2, 31 +/- 2, and 18 +/- 2 mm of Hg, respectively, to 44 +/- 4, 89 +/- 5, and 56 +/- 4 mm of Hg with exercise at 13 m/s. Furosemide administration resulted in marked diuresis, and resting mean RA, PA, and PAW pressures decreased significantly (P < 0.05) to 1 +/- 1, 27 +/- 2, and 11 +/- 2 mm of Hg, respectively, 4 hours after furosemide administration.(ABSTRACT TRUNCATED AT 250 WORDS)

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Pulmonary artery wedge pressure increases with high-intensity exercise in horses.

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses.(ABSTRACT TRUNCATED AT 250 WORDS)

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Nonesterified fatty acids and lipid peroxidation.

Oxygen free radicals damage cells through peroxidation of membrane lipids. Gastrointestinal mucosal membranes were found to be resistant to in vitro lipid peroxidation as judged by malonaldehyde and conjugated diene production and arachidonic acid depletion. The factor responsible for this in this membrane was isolated and chemically characterised as the nonesterified fatty acids (NEFA), specifically monounsaturated fatty acid, oleic acid. Authentic fatty acids when tested in vitro using liver microsomes showed similar inhibition. The possible mechanism by which NEFA inhibit peroxidation is through iron chelation and iron-fatty acid complex is incapable of inducing peroxidation. Free radicals generated independent of iron was found to induce peroxidation of mucosal membranes. Gastrointestinal mucosal membranes were found to contain unusually large amount of NEFA. Circulating albumin is known to contain NEFA which was found to inhibit iron induced peroxidation whereas fatty acid free albumin did not have any effect. Addition of individual fatty acids to this albumin restored its inhibitory capacity among which monounsaturated fatty acids were more effective. These studies have shown that iron induced lipid peroxidation damage is prevented by the presence of nonesterified fatty acids.

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Regional brain blood flow during prolonged submaximal exercise in ponies.

Experiments were carried out on 8 healthy ponies to examine the effects of prolonged submaximal exercise on regional distribution of brain blood flow. Brain blood flow was ascertained by use of 15-microns-diameter radionuclide-labeled microspheres injected into the left ventricle. The reference blood was withdrawn from the thoracic aorta at a constant rate of 21.0 ml/min. Hemodynamic data were obtained with the ponies at rest (control), and at 5, 15, and 26 minutes of exercise performed at a speed setting of 13 mph on a treadmill with a fixed incline of 7%. Exercise lasted for 30 minutes and was carried out at an ambient temperature of 20 C. Heart rate, mean arterial pressure, and core temperature increased significantly with exercise. With the ponies at rest, a marked heterogeneity of perfusion was observed within the brain; the cerebral, as well as cerebellar gray matter, had greater blood flow than in the respective white matter, and a gradually decreasing gradient of blood flow existed from thalamus-hypothalamus to medulla. This pattern of perfusion heterogeneity was preserved during exercise. Regional brain blood flow at 5 and 15 minutes of exercise remained similar to resting values. However, at 26 minutes of exercise, vasoconstriction resulted in a significant reduction in blood flow to all cerebral and brain-stem regions. In the cerebellum, the gray matter blood flow and vascular resistance remained near control values even at 26 minutes of exercise. Vasoconstriction in various regions of the cerebrum and brainstem at 26 minutes of exertion may have occurred in response to exercise-induced hypocapnia, arterial hypertension, and/or sympathetic neural activation.

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Respiratory muscle perfusion in ponies during prolonged submaximal exercise in thermoneutral environment.

Distribution of blood flow among various respiratory muscles was examined in 8 healthy ponies during submaximal exercise lasting 30 minutes, using radionuclide labeled 15-microns diameter microspheres injected into the left ventricle. From the resting values (40 +/- 2 beats/min; 37.3 +/- 0.2 C), heart rate and pulmonary arterial blood temperature increased significantly at 5 (152 +/- 8 beats/min; 38.6 +/- 0.2 C), 15 (169 +/- 6 beats/min; 39.8 +/- 0.2 C), and 26 (186 +/- 8 beats/min; 40.8 +/- 0.2 C) minutes of exertion, and the ponies sweated profusely. Mean aortic pressure also increased progressively as exercise duration increased. Blood flow increased significantly with exercise in all respiratory muscles. Among inspiratory muscles, perfusion was greatest in the diaphragm and ventral serratus, compared with external intercostal, dorsal serratus, and scalenus muscles. Among expiratory muscles, blood flow in the internal abdominal oblique muscle was greatest, followed by that in internal intercostal and transverse thoracic muscles, in which the flow values remained similar. The remaining 3 abdominal muscles had similar blood flow, but these values were less than that in the internal intercostal, transverse thoracic, and internal abdominal oblique muscles. Blood flow values for all inspiratory and expiratory muscles remained similar for the 5 and 15 minutes of exertion. However, at 26 minutes, blood flow had increased further in the diaphragm, external intercostal, internal intercostal, transverse thoracic, and the external abdominal oblique muscle as vascular resistance decreased. On the basis of our findings, all respiratory muscles were activated during submaximal exercise and their perfusion had marked heterogeneity.(ABSTRACT TRUNCATED AT 250 WORDS)

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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)

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