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Biomedical subjects

M Manohar

Publications and source records attributed to M Manohar.

At least 19 recordsLinked to original sources
PubMed2006

Hyperhydration prior to a simulated second day of the 3-day moderate intensity equestrian competition does not cause arterial hypoxemia in Thoroughbred horses.

Dehydration and the associated impairment of cardiovascular and thermoregulatory function comprise major veterinary problems in horses performing prolonged exercise, particularly under hot and humid conditions. For these reasons, there is considerable interest in using pre-exercise hyperhydration to help maintain blood volume in the face of the excessive fluid loss associated with sweat production during prolonged exertion. However, recently it was reported that pre-exercise hyperhydration causes arterial hypoxemia in horses performing moderate intensity exercise simulating the second day of an equestrian 3-day event competition (E3DEC) which may adversely affect performance (Sosa Leon et al. in Equine Vet J Suppl 34:425-429, 2002). These findings are contrary to data from horses performing short-term maximal exertion, wherein hyperhydration did not affect arterial O2 tension/saturation. Thus, our objective in the present study was to examine the impact of pre-exercise hyperhydration on arterial oxygenation of Thoroughbred horses performing an exercise test simulating the second day of an E3DEC. Control and hyperhydration studies were carried out on seven healthy Thoroughbred horses in random order, 7 days apart. In the control study, horses received no medications. In the hyperhydration experiments, nasogastric administration of NaCl (0.425 g/kg) 5 h pre-exercise induced a plasma volume expansion of 10.9% at the initiation of exercise. This methodology for inducing hypervolemia was different from that of Sosa Leon et al. (2002). Blood-gas tensions/pH as well as plasma protein, hemoglobin and blood lactate concentrations were measured pre-exercise and during the exercise test. Our data revealed that pre-exercise hyperhydration neither adversely affected arterial O2 tension nor hemoglobin-O2 saturation at any time during the exercise test simulating the second day of an E3DEC. Further, it was observed that arterial blood CO2 tension, pH, and blood lactate concentrations also were not affected by pre-exercise hyperhydration. However, hemodilution in hyperhydrated horses caused an attenuation of the expansion in the arterial to mixed-venous blood O2 content gradient during phases B and D of the exercise protocol, which was likely offset by an increase in cardiac output. It is concluded that pre-exercise hyperhydration of horses induced in the manner described above is not detrimental to arterial oxygenation of horses performing an exercise test simulating the second day of an E3DEC.

Animals↗
PubMed2006

Isolation and characterization of a novel banana rhizosphere bacterium as fungal antagonist and microbial adjuvant in micropropagation of banana.

AIM: Isolation and characterization of a bacterial isolate (strain FP10) from banana rhizosphere with innate potential as fungal antagonist and microbial adjuvant in micropropagation of banana. METHODS AND RESULTS: Bacterium FP10 was isolated from the banana rhizosphere and identified as Pseudomonas aeruginosa based on phenotypic, biochemical traits and sequence homology of partial 622-bp fragment of 16S ribosomal DNA (rDNA) amplicon, with the ribosomal database sequences. Strain FP10 displayed antibiosis towards fungi causing wilt and root necrosis diseases of banana. Production of plant growth hormone, indole-3-acetic acid (IAA), siderophores and phosphate-solubilizing enzyme in FP10 was determined. Strain FP10 tested negative for hydrogen cyanide, cellulase and pectinase, the deleterious traits for plant growth. Screening of antibiotic genes was carried out by polymerase chain reaction using gene-specific primers. Amplification of a 745-bp DNA fragment confirmed the presence of phlD, which is a key gene involved in the biosynthesis of 2,4-diacetylphloroglucinol (DAPG) in FP10. The antibiotic produced by FP10 was confirmed as DAPG using thin layer chromatography, high performance liquid chromatography and Fourier transform infrared and tested for fungal antibiosis towards banana pathogens. Procedures for encapsulation of banana shoot tips with FP10 are described. CONCLUSIONS: Strain FP10 exhibited broad-spectrum antibiosis towards banana fungi causing wilt and root necrosis. DAPG by FP10 induced bulb formation and lysis of fungal mycelia. Encapsulation of banana shoot tips with FP10 induced higher frequency of germination (plantlet development) than nontreated controls on Murashige and Skoog basal medium. Treatment of banana plants with FP10 enhanced plant height and reduced the vascular discolouration as a result of Fusarium oxysporum f. sp. cubense FOC. SIGNIFICANCE AND IMPACT OF THE STUDY: Because of the innate potential of fungal antibiosis by DAPG antibiotic and production of siderophore, plant-growth-promoting IAA and phosphatase, the strain FP10 can be used as biofertilizer as well as a biocontrol agent.

Agriculture↗
PubMed2001

Inhibition of nitric oxide synthase with L-NAME does not increase lactate production at rest or during short-term high-intensity exercise in Thoroughbred horses.

The present study was carried out to determine whether inhibition of nitric oxide (NO) synthase promotes anaerobic metabolism in exercising horses, resulting in a significantly increased blood lactate concentration. N(omega)-nitro-L-arginine methyl ester (L-NAME) is a potent inhibitor of NO synthase that has been tested in horses and other species. Two sets of experiments, namely placebo (saline control) and L-NAME (20 mg/kg, i.v.) studies, were carried out on seven healthy, sound, exercise-trained, Thoroughbred horses in random order, 6 to 7 days apart. In both experiments, an incremental exercise protocol was used and data were obtained at rest, during submaximal exercise performed at 8 m/s on a 4.5% uphill grade, and during galloping at 14 m/s on a 4.5% uphill grade--a workload that not only elicited maximal heart rate and induced exercise-induced pulmonary haemorrhage, but also could not be sustained for more than 90 s. Measurements were also made in the recovery period. Mixed-venous blood samples, obtained at matched intervals in the two sets of experiments, were analysed in triplicate for determining the lactate concentration. Following administration of L-NAME, significant bradycardia occurred at rest (27 +/- 1 vs 37 +/- 2 beats/min in the placebo trials; p<0.0001) as well as during submaximal exercise (183 +/- 4 vs 200 +/- 4 beats/min in the placebo trials; p<0.001), but the heart rate increased during galloping at 14 m/s on a 4.5% uphill grade to reach values observed in the placebo trials (215 +/- 2 beats/min) and significant differences were not found. At rest, the mixed-venous blood lactate concentration was similar in the two experiments. With exercise, the mixed-venous blood lactate concentration increased progressively as work intensity increased in both trials, but significant differences were not found between the placebo and the L-NAME experiments during submaximal exercise, near-maximal exercise or recovery. These experiments demonstrated that inhibition of NO synthase in Thoroughbred horses does not promote enhanced anaerobic metabolism at rest or during short-term incremental exercise leading to galloping at maximal heart rate.

Animals↗
PubMed2001

Gut colonization of mice with actA-negative mutant of Listeria monocytogenes can stimulate a humoral mucosal immune response.

We used Listeria monocytogenes, a gram-positive, facultative intracellular bacterium, to study the gut mucosal immune responses following oral infection. We employed a germfree (GF) mouse model to try to accentuate the development of a humoral mucosal immune response in the gut, and we used oral colonization with one of the mutants, actA-negative (DeltaactA) L. monocytogenes, to restrict infection largely to the gut. The DeltaactA mutant was able to colonize the intestinal mucosa of formerly GF mice for long periods of time without causing disease while eliciting secretory immunoglobulin A (IgA) responses, as evidenced by gut tissue fragment culture assays. Flow cytometric analyses and immunohistochemical methods showed the development of only minimal germinal center reactions (GCR) in Peyer's patches and more robust GCR in mesenteric lymph nodes. Pronounced increases in total (natural) IgA production occurred in gut tissues by day 7 and were maintained for up to 90 days. Levels of specific IgA were modest in gut tissues on day 14, increased until day 76, and stabilized at day 90. We also observed a significant rise in serum IgA and IgG1 levels following oral infection by listeriae. Upon colonization, the organisms mainly infected the intestines and intestinal lumen, and we only sporadically observed few colony-forming bacteria in the liver and spleen. We observed a marked rise in IgA-secreting cells, including listeria-specific IgA antibody-secreting cells, in the lamina propria of the small intestine by enzyme-linked immunospot assays. To ascertain whether some of the IgA was specific for listeriae, we performed Western blot analysis to test the reactivity of IgA from fragment cultures to antigens in sonicates of L. monocytogenes. We detected IgA binding to antigenic proteins with molecular masses of 96, 60, 40, and 14 kDa in the Listeria sonicates.

Animals↗
PubMed2001

Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses.

Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial PCO2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial PO2 values were significantly (P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar PO2, as arterial PCO2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.

Animals↗
PubMed2001

Nasal strips do not affect pulmonary gas exchange, anaerobic metabolism, or EIPH in exercising Thoroughbreds.

The present study was carried out to examine whether nasal strip application would improve the exercise-induced arterial hypoxemia and hypercapnia, diminish anaerobic metabolism, and modify the incidence of exercise-induced pulmonary hemorrhage (EIPH) in horses. Two sets of experiments, control and nasal strip experiments, were carried out on seven healthy, sound, exercise-trained Thoroughbred horses in random order, 7 days apart. Simultaneous measurements of core temperature, arterial and mixed venous blood gases/pH, and blood lactate and ammonia concentrations were made at rest, during submaximal and near-maximal exercise, and during recovery. In both treatments, whereas submaximal exercise caused hyperventilation, near-maximal exercise induced significant arterial hypoxemia, desaturation of Hb, hypercapnia, and acidosis. However, O2 content increased significantly with exercise in both treatments, while the mixed venous blood O2 content decreased as O2 extraction increased. In both treatments, plasma ammonia and blood lactate concentrations increased significantly with exercise. Statistically significant differences between the control and the nasal strip experiments could not be discerned, however. Also, all horses experienced EIPH in both treatments. Thus our data indicated that application of an external nasal dilator strip neither improved the exercise-induced arterial hypoxemia and hypercapnia nor diminished anaerobic metabolism or the incidence of EIPH in Thoroughbred horses performing strenuous exercise.

Ammonia↗
PubMed2001

Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses.

Because sensitivity of equine pulmonary vasculature to endogenous as well as exogenous nitric oxide (NO) has been demonstrated, we examined whether endogenous NO production plays a role in exercise-induced arterial hypoxemia. We hypothesized that inhibition of NO synthase may alter the distribution of ventilation-perfusion mismatching, which may affect the exercise-induced arterial hypoxemia. Arterial blood-gas variables were examined in seven healthy, sound Thoroughbred horses at rest and during incremental exercise protocol leading to galloping at maximal heart rate without (control; placebo = saline) and with N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (20 mg/kg iv). The experiments were carried out in random order, 7 days apart. At rest, L-NAME administration caused systemic hypertension, pulmonary hypertension, and bradycardia. During 120 s of galloping at maximal heart rate, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, hyperthermia, and acidosis occurred in the control as well as in NO synthase inhibition experiments. However, statistically significant differences between the treatments were not found. In both treatments, exercise caused a significant rise in hemoglobin concentration, but the increment was significantly attenuated in the NO synthase inhibition experiments, and, therefore, arterial O(2) content (Ca(O(2))) increased to significantly lower values. These data suggest that, whereas L-NAME administration does not affect pulmonary gas exchange in exercising horses, it may affect splenic contraction, which via an attenuation of the rise in hemoglobin concentration and Ca(O(2)) may limit performance at higher workloads.

Animals↗
PubMed2001

Intravenous pentoxifylline does not enhance the pulmonary haemodynamic efficacy of frusemide in strenuously exercising thoroughbred horses.

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.

Animals↗
PubMed2000

Pulmonary vascular pressures of thoroughbred horses exercised 1, 2, 3 and 4 h after furosemide administration.

Furosemide premedication of horses 4 h prior to exercise significantly attenuates exercise-induced pulmonary capillary hypertension which may help diminish the severity of exercise-induced pulmonary haemorrhage. As pulmonary hemodynamic effects of furosemide may be mediated via a reduction in plasma volume (which is most pronounced 15-30 min postfurosemide administration, with plasma volume recovering thereafter), we hypothesized that administration of furosemide at intervals shorter than 4 h before exertion may be more effective in attenuating the exercise-induced rise in pulmonary capillary blood pressure. Thus, our objective was to determine whether furosemide-induced attenuation of exercise-induced pulmonary arterial, capillary and venous hypertension would be enhanced when the drug is administered at intervals shorter than 4 h before exercise. Using established techniques, right atrial, and pulmonary arterial, capillary and wedge (venous) pressures were ascertained in seven healthy, sound, exercise-trained Thoroughbred horses in a randomized split-plot experimental design. Measurements were made at rest and during exercise performed at maximal heart rate (217 +/- 3 beats/min) in the control (no medications) experiments and following furosemide administration (250 mg intravenously (i.v.)) at 1, 2, 3 and 4 h before exercise. Sequence of treatments was randomized and 7 days were allowed between experiments on each horse. Although furosemide administration in the four treatment groups caused only insignificant changes in the pulmonary arterial, capillary and wedge pressures of standing horses, furosemide-induced reduction in mean right atrial pressure achieved statistical significance in the 2 h postfurosemide experiments. In the control studies, exercise was attended by statistically significant increments in mean right atrial, as well as pulmonary arterial, capillary and wedge pressures. Although exercise in each of the four furosemide experiments was also attended by significant increments in right atrial as well as pulmonary vascular pressures, in the 1, 2 and 3 h postfurosemide experiments, mean right atrial pressure increased to a significantly lower value than in the control study. Exercise-induced changes in pulmonary vascular pressures in the 1 h postfurosemide experiments were not different from the pressures in the control study. There was a significant attenuation of exercise-induced pulmonary capillary and venous hypertension in the 2, 3 and 4 h postfurosemide experiments, but significant differences among these treatments were not found. Thus, these data did not support the contention that administration of furosemide at intervals shorter than 4 h before exercise is more effective in attenuating exercise-induced pulmonary capillary or venous hypertension in Thoroughbred horses.

Animals↗
PubMed2000

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.

Animals↗
PubMed2000

Clenbuterol administration does not enhance the efficacy of furosemide in attenuating the exercise-induced pulmonary capillary hypertension in Thoroughbred horses.

The stimulation of pulmonary beta2-adrenergic receptors causes a decrease in vascular resistance. Thus, the present study was carried out to examine whether concomitant administration of clenbuterol-a beta2-adrenergic receptor agonist, to horses premedicated with furosemide would attenuate the exercise-induced pulmonary capillary hypertension to a greater extent than furosemide alone, and in turn, affect the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications), furosemide (250 mg i.v., 4 h pre-exercise)-control, and furosemide (250 mg i.v., 4 h pre-exercise)+clenbuterol (0.8 microg/kg i.v., 11 min pre-exercise) experiments. The sequence of these treatments was randomized 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, 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. In the control study, incremental exercise resulted in progressive significant (P<0.05) increments in heart rate, right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures, and all horses experienced EIPH. Furosemide administration caused a significant (P<0.05) reduction in mean right atrial as well as pulmonary capillary and venous pressures of standing horses. Although exercise in the furosemide-control experiments also caused right atrial and pulmonary vascular pressures to increase significantly (P<0.05), the increment in mean pulmonary capillary and wedge pressures was significantly (P<0.05) attenuated in comparison with the control study, but all horses experienced EIPH. Clenbuterol administration to standing horses premedicated with furosemide caused tachycardia, but significant changes in right atrial or pulmonary vascular pressures were not discerned at rest. During exercise in the furosemide+clenbuterol experiments, heart rate, mean right atrial as well as pulmonary arterial, capillary and wedge pressures increased significantly (P<0.05), but these data were not different from the furosemide-control experiments, and all horses experienced EIPH as well. Thus, it was concluded that clenbuterol administration is ineffective in modifying the pulmonary hemodynamic effects of furosemide in standing or exercising horses. Because the intravascular force exerted onto the blood-gas barrier of horses premedicated with furosemide remained unaffected by clenbuterol administration, it is believed that concomitant clenbuterol administration is unlikely to offer additional benefit to healthy horses experiencing EIPH.

Adrenergic beta-Agonists↗
PubMed2000

Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horses.

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.

Adrenergic beta-Agonists↗
PubMed1999

Pulmonary vascular resistance of horses decreases with moderate exercise and remains unchanged as workload is increased to maximal exercise.

This study was carried out to examine changes in pulmonary vascular resistance (PVR) induced by moderate and strenuous exercise; the objective being to understand why pulmonary artery blood pressure of exercising horses increases progressively as work intensity increases. Pulmonary arterial and wedge pressures (referenced at the point of the left shoulder) were determined simultaneously with cardiac output in 2 groups of healthy, sound, exercise-trained horses. Horses in Group 1 (n = 8) were studied at rest and during exercise performed at 8 and 13 m/s; the latter workload eliciting maximal heart rate (mean +/- s.e. 212 +/- 3 beats/min). Horses in Group 2 (n = 7 Thoroughbreds) were studied at rest and during galloping at 14.5 m/s on 5% uphill grade, a workload which elicited maximal heart rate (217 +/- 3 beats/min) and could not be sustained for > 90 s. Pulmonary vascular resistance was calculated by dividing pulmonary perfusion pressure gradient (i.e. mean pulmonary arterial pressure minus mean pulmonary wedge pressure) with cardiac output. Pulmonary arterial and wedge pressures, pulmonary perfusion pressure gradient and cardiac output increased significantly (P < 0.05) with exercise in both groups. There were no differences in PVR between the 2 groups of horses at rest. In Group 1 horses PVR decreased significantly (P < 0.05) with exercise at 8 m/s, but further pulmonary vasodilation did not occur as workload increased to 13 m/s. During exercise at 14.5 m/s on 5% grade, PVR of Group 2 horses also decreased significantly and was not different from values for 8 or 13 m/s in Group 1 horses. It is concluded that PVR reaches its nadir during moderate exercise, presumably due to upper limit of recruitment and distension having been reached. Therefore, in accordance with Ohm's law (P alpha Q x PVR), in going to higher workloads pulmonary blood flow (Q) remained the sole determinant of the rise in pulmonary arterial blood pressure (P). Our data also indicate that pulmonary artery wedge pressure is another variable that is important in determining the absolute value of pulmonary arterial blood pressure.

Animals↗
PubMed1999

Repeated administration of frusemide does not offer an advantage over single dosing in attenuating exercise-induced pulmonary hypertension in thoroughbred horses.

The objective of the present study was to ascertain whether administration of a second dose of frusemide would attenuate exercise-induced pulmonary hypertension more than a single dose. Right atrial, right ventricular and pulmonary vascular pressures were determined in 7 healthy, sound, exercise-trained Thoroughbred horses at rest and during exercise (14.2 m/s + a 3.5% uphill grade) performed at maximal heart rate (217 +/- 3 beats/min [mean +/- s.e.]). Horses were studied during the following 3 treatments in random order 7 days apart: control (no medication), frusemide single dose (250 mg i.v. 4 h pre-exercise), and frusemide double dose (250 mg i.v., 4 h pre-exercise + 250 mg i.v. 2 h pre-exercise). In the control study, exercise resulted in significant (P < 0.05) right atrial as well as pulmonary arterial, capillary and venous hypertension. In the frusemide single dose experiments, a significant (P < 0.05) attenuation of the exercise-induced rise in right atrial and pulmonary vascular pressures was observed. However, compared with frusemide single dose experiments, significant changes in the exercise-induced right atrial and pulmonary arterial, capillary and venous hypertension were not observed in the frusemide double dose experiments. Therefore, it is concluded that administration of an additional dose of frusemide is unlikely to affect the severity of EIPH in racing Thoroughbred horses more than a single dose.

Animals↗
PubMed1999

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.

Animals↗
PubMed1998

Pulmonary vascular pressures of strenuously exercising Thoroughbred horses after administration of phenylbutazone and frusemide.

The present study was carried out to examine the effects of phenylbutazone treatment on the pulmonary haemodynamic effects of frusemide in strenuously exercising horses. Using catheter mounted manometers, whose in vivo signals were referenced at the point of the shoulder, heart rate, right atrial, right ventricular and pulmonary vascular pressures were measured in 3 different sets of experiments. Seven Thoroughbreds were subjected to 1) control (no medications), 2) frusemide control and 3) phenylbutazone + frusemide. The experiments were carried out in random order and were separated by 7 days. Measurements were made at rest and during incremental exercise performed on a treadmill set at 3.5% uphill grade. In the frusemide control experiment, horses received frusemide 250 mg i.v., 4 h pre-exercise. In the phenylbutazone + frusemide experiment, horses received 4 i.v. injections of phenylbutazone (4.4 mg/kg bwt) at 12 h intervals. Twenty-four hours after the last phenylbutazone injection, horses received frusemide 250 mg i.v. and exercise was performed 4 h later. This latter regimen mimics prevailing veterinary practice at Illinois racetracks. The highest work intensity (14.2 m/s, 3.5% uphill grade) elicited maximal heart rate of horses. Significant right atrial, as well as pulmonary arterial, capillary and venous hypertension occurred with exertion in all 3 experiments. However, in the frusemide-control and the phenylbutazone + frusemide studies, the exercise induced rise in mean right atrial and pulmonary vascular pressures was significantly (P<0.05) attenuated in comparison with that in the control experiments. Statistically significant differences were not found between the frusemide control study and the phenylbutazone + frusemide study either at rest or during any level of exertion. Therefore, it was concluded that the phenylbutazone treatment in our study did not mitigate the pulmonary haemodynamic effects of frusemide in strenuously exercising Thoroughbred horses.

Animals↗
PubMed1998

L-NAME does not affect exercise-induced pulmonary hypertension in thoroughbred horses.

The present study was carried out to examine the effects of nitric oxide synthase inhibition with Nomega-nitro-L-arginine methyl ester (L-NAME) on the right atrial as well as on the pulmonary arterial, capillary, and venous blood pressures of horses during rest and exercise performed at maximal heart rate (HRmax). Experiments were carried out on seven healthy, sound, exercise-trained Thoroughbred horses. Using catheter-tip manometers, with signals referenced at the point of the shoulder, we determined phasic and mean right atrial and pulmonary vascular pressures in two sets of experiments [control (no medications) and L-NAME (20 mg/kg iv given 10 min before exercise studies)]. The studies were carried out in random order 7 days apart. Measurements were made at rest and during treadmill exercise performed on a 5% uphill grade at 6, 8, and 14.2 m/s. Exercise on a 5% uphill grade at 14.2 m/s elicited HRmax and could not be sustained for >90 s. In quietly standing horses, L-NAME administration caused a significant rise in right atrial, as well as pulmonary arterial, capillary, and venous pressures. This indicates that nitric oxide synthase inhibition modifies the basal pulmonary vasomotor tone. In both treatments, exercise caused progressive significant increments in right atrial and pulmonary vascular pressures, but the values recorded in the L-NAME study were not different from those in the control study. The extent of exercise-induced tachycardia was significantly decreased in the L-NAME study at 6 and 8 m/s but not at 14.2 m/s. Thus, L-NAME administration may not modify the equine pulmonary vascular tone during exercise at HRmax. However, as indicated by a significant reduction in heart rate, L-NAME seems to modify the sympathoneurohumoral response to submaximal exercise.

Animals↗