H1-receptor antagonist, tripelennamine, does not affect arterial hypoxemia in exercising Thoroughbreds

2002 ◽  
Vol 92 (4) ◽  
pp. 1515-1523 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Sarah Humphrey ◽  
Tracy Depuy
Keyword(s):  
Histamine Release ◽  
Receptor Antagonist ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Mixed Venous Blood ◽  
Maximal Heart Rate ◽  
Pulmonary Injury ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Exercise Induced

It has been suggested that pulmonary injury and inflammation-induced histamine release from airway mast cells may contribute to exercise-induced arterial hypoxemia (EIAH). Because stress failure of pulmonary capillaries and EIAH are routinely observed in exercising horses, we examined whether preexercise administration of an H1-receptor antagonist may mitigate EIAH. Two sets of experiments, placebo (saline) and antihistaminic (tripelennamine HCl at 1.10 mg/kg iv, 15 min preexercise) studies, were carried out on seven healthy, exercise-trained Thoroughbred horses in random order 7 days apart. Arterial and mixed venous blood-gas and pH measurements were made at rest before and after saline or drug administration and during incremental exercise leading to maximal exertion at 14 m/s on 3.5% uphill grade for 120 s. Galloping at this workload elicited maximal heart rate and induced exercise-induced pulmonary hemorrhage in all horses in both treatments, thereby indicating that capillary stress failure-related pulmonary injury had occurred. In both treatments, EIAH, desaturation of hemoglobin, hypercapnia, and acidosis of a similar magnitude developed during maximal exertion, and statistically significant differences between the placebo and antihistaminic studies could not be demonstrated. The failure of the H1-receptor antagonist to modify EIAH significantly suggests that pulmonary injury-induced histamine release may not play a major role in bringing about EIAH in Thoroughbred horses.

NaHCO3 does not affect arterial O2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds

2004 ◽  
Vol 96 (4) ◽  
pp. 1349-1356 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Physiological Saline ◽  
Mixed Venous Blood ◽  
Maximal Heart Rate ◽  
Arterial Hypoxemia ◽  
Arterial Blood ◽  
Exercise Induced ◽  
Mixed Venous

The objective of the present study was to examine the effects of preexercise NaHCO3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO3 (250 mg/kg iv), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO3 administration caused alkalosis and hemodilution in standing horses, but arterial O2 tension and hemoglobin-O2 saturation were unaffected. Thus NaHCO3 administration caused a reduction in arterial O2 content at rest, although the arterial-to-mixed venous blood O2 content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO3-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O2 content of exercising horses was less in the NaHCO3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient was observed. It was concluded that preexercise NaHCO3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.

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

2001 ◽  
Vol 90 (6) ◽  
pp. 2378-2385 ◽  
Author(s):  
Thomas E. Goetz ◽  
Murli Manohar ◽  
Aslam S. Hassan ◽  
Gordon J. Baker
Keyword(s):  
Blood Lactate ◽  
Anaerobic Metabolism ◽  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Mixed Venous Blood ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Exercise Induced ◽  
Mixed Venous

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.

Intrapulmonary arteriovenous shunts of >15 μm in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses

2005 ◽  
Vol 99 (1) ◽  
pp. 224-229 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Blood Oxygenation ◽  
Mixed Venous Blood ◽  
Arteriovenous Shunting ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Arteriovenous Shunts ◽  
Exercise Induced ◽  
Mixed Venous

The present study examined whether Thoroughbred horses performing strenuous exercise exhibit intrapulmonary arteriovenous shunting that may contribute to the observed arterial hypoxemia. Experiments were carried out on seven healthy, exercise-trained Thoroughbreds at rest, maximal exercise (galloping at 14 m/s on a 3.5% uphill grade for 120 s), and submaximal exertion (8 m/s on a 3.5% uphill grade for 150 s). Along with blood gas/hemodynamic parameters, intrapulmonary arteriovenous shunting was studied by injecting 15-μm-diameter microspheres, labeled with different stable isotopes, into the right atrium while simultaneous blood samples were being withdrawn at a constant rate from the pulmonary artery and the aorta. Arterial hypoxemia was observed only during maximal exercise. Also, despite significant pulmonary arterial hypertension during submaximal and maximal exertion, 15-μm microspheres did not traverse the pulmonary microcirculation to appear in the aortic blood. Thus our findings did not support a role for intrapulmonary arteriovenous shunts of >15 μm in diameter in the exercise-induced arterial hypoxemia in racehorses. Interestingly, our observation that, in going from 30 to 120 s of maximal exertion, arterial O2 tension had remained unchanged despite significant reductions in mixed venous blood O2 tension, hemoglobin-O2 saturation, and O2 content also discounts the importance of intrapulmonary arteriovenous shunts in causing arterial hypoxemia. This is because, assuming that a constant fraction of total pulmonary blood flow bypasses the gas-exchange areas of the equine lungs via intrapulmonary arteriovenous shunts during 30–120 s of maximal exertion, the observed significant reductions in mixed venous blood oxygenation should cause a significant reduction in arterial O2 tension, which was not the case in our horses. Thus it is suggested that intrapulmonary arteriovenous shunting probably does not contribute to the exercise-induced arterial hypoxemia in racehorses.

Anti-inflammatory agent, dexamethasone, does not affect exercise-induced arterial hypoxemia in Thoroughbreds

2002 ◽  
Vol 93 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan ◽  
Tracy Depuy ◽  
Sarah Humphrey
Keyword(s):  
Pulmonary Hemorrhage ◽  
Exercise Duration ◽  
Pulmonary Injury ◽  
Arterial Hypoxemia ◽  
Inflammatory Agent ◽  
Pulmonary Capillaries ◽  
Anti Inflammatory ◽  
Gas Measurements ◽  
Exercise Induced ◽  
Chemical Mediators

In view of the suggestion that pulmonary injury-induced release of histamine and/or other chemical mediators from airway inflammatory and mast cells contribute to the exercise-induced arterial hypoxemia (EIAH) in human athletes, we examined the effects of pretreatment with a potent anti-inflammatory agent, dexamethasone, on EIAH and desaturation of hemoglobin in horses. Seven healthy, sound, exercise-trained Thoroughbreds were studied in the control (no medications) experiments, followed in 7 days by intravenous dexamethasone (0.11 mg·kg−1·day−1for 3 consecutive days) studies. Blood-gas measurements were made at rest and during incremental exercise leading to maximal exertion at 14 m/s on a 3.5% uphill grade. Galloping at this workload induced pulmonary hemorrhage in all horses in both treatments, thereby indicating that stress failure of pulmonary capillaries had occurred. In both treatments, significant EIAH, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but significant differences between the control and dexamethasone treatments were not discerned. The failure of pretreatment with dexamethasone to significantly affect EIAH suggests that pulmonary injury-evoked airway inflammatory response may not play a major role in EIAH in racehorses. However, our observations in both treatments that EIAH developed quickly (being evident at 30 s of exertion) and that its severity remained unaffected by increasing exercise duration (to 120 s) suggest that EIAH has a functional basis, probably related to significant shortening of the transit time for blood in the pulmonary capillaries as cardiac output increases dramatically.

l-NAME does not affect exercise-induced pulmonary hypertension in Thoroughbred horses

1998 ◽  
Vol 84 (6) ◽  
pp. 1902-1908 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Nitric Oxide Synthase ◽  
Venous Blood ◽  
Right Atrial ◽  
Maximal Heart Rate ◽  
Thoroughbred Horses ◽  
Pulmonary Arterial ◽  
Exercise Induced ◽  
Oxide Synthase

The present study was carried out to examine the effects of nitric oxide synthase inhibition with N ω-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 thel-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.

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

2001 ◽  
Vol 90 (6) ◽  
pp. 2371-2377 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
High Intensity ◽  
Structural Changes ◽  
Pulmonary Hemorrhage ◽  
Exercise Bout ◽  
Blood Gas ◽  
Gas Barrier ◽  
Arterial Hypoxemia ◽  
Pulmonary Capillaries ◽  
Thoroughbred Horses ◽  
Exercise Induced

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 Pco 2, 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 Po 2 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 Po 2, as arterial Pco 2 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.

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

2001 ◽  
Vol 91 (3) ◽  
pp. 1105-1112 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Hemoglobin Concentration ◽  
No Synthase ◽  
Systemic Hypertension ◽  
Maximal Heart Rate ◽  
Arterial Hypoxemia ◽  
Arterial Blood ◽  
Thoroughbred Horses ◽  
Exercise Induced

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 ω-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 O2 content (CaO2 ) increased to significantly lower values. These data suggest that, whereasl-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 CaO2 may limit performance at higher workloads.

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

1996 ◽  
Vol 81 (4) ◽  
pp. 1589-1593 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz
Keyword(s):  
Heart Rate ◽  
Pulmonary Hemorrhage ◽  
Venous Hypertension ◽  
Right Atrial ◽  
Maximal Heart Rate ◽  
Fresh Blood ◽  
Thoroughbred Horses ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Exercise Induced

Manohar, Murli, and Thomas E. Goetz. Pulmonary vascular pressures of exercising Thoroughbred horses with and without endoscopic evidence of EIPH. J. Appl. Physiol.81(4): 1589–1593, 1996.—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.

Fluid-regulating and sympathoadrenal hormonal responses to peak exercise following cardiac transplantation

1994 ◽  
Vol 76 (1) ◽  
pp. 230-235 ◽  
Author(s):  
H. Perrault ◽  
B. Melin ◽  
C. Jimenez ◽  
G. Dureau ◽  
P. Dureau ◽  
...  
Keyword(s):  
Venous Blood ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Orthotopic Heart Transplantation ◽  
Peak Exercise ◽  
Cardiac Transplant ◽  
Maximal Heart Rate ◽  
O2 Uptake ◽  
C 71 ◽  
Exercise Induced

Orthotopic heart transplantation results in cardiac denervation that can disrupt the normal regulation of hydromineral balance. This study compared the exercise-induced variations in plasma osmolality; atrial natriuretic peptide (ANP), arginine vasopressin (AVP), norepinephrine (NE), epinephrine (E), and dopamine (DA) concentrations; and plasma renin activity (PRA) of six cardiac transplant recipients (HTX) and six healthy age-matched controls (C) submitted to graded upright maximal cycling. Venous blood samples were obtained at rest, at submaximal (70% O2 uptake) and peak exercise, and after 10 and 30 min of sitting recovery. Peak O2 uptake was not different between groups despite lower maximal heart rate in HTX (136 +/- 6 vs. 183 +/- 9 beats/min). Baseline plasma ANP and PRA were higher in HTX (203 +/- 55 pg/ml and 29.9 +/- 7.4 ng.ml-1 x h-1) than in C (71 +/- 17 pg/ml and 5.4 +/- 0.96 ng.ml-1 x h-1); AVP was lower in HTX than in C (1.1 +/- 0.3 vs. 3.2 +/- 0.8 pg/ml; P < 0.05); and circulating E, NE, and DA were not different between groups. Exercise resulted in more marked increases in HTX than in C for ANP (300 vs. 100%), AVP (2,000 vs. 300%), NE (860 vs. 500%), and DA (611 vs. 187%) but not for PRA and a higher E response in C than in HTX (455 vs. 1,258%). These observations confirm that the potential for ANP release to central volume loading is independent of intact cardiac innervation. The exaggerated AVP response in HTX could, however, reflect the absence of inhibitory influences consecutive to denervation.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of blood Po2 on the stability of agitated saline contrast

2020 ◽  
Vol 129 (6) ◽  
pp. 1341-1347
Author(s):  
Lindsey M. Boulet ◽  
Tyler D. Vermeulen ◽  
Paul D. Cotton ◽  
Glen E. Foster
Keyword(s):  
Regulatory Mechanism ◽  
Venous Blood ◽  
Pulmonary Vasculature ◽  
Mixed Venous Blood ◽  
Arteriovenous Anastomoses ◽  
Stabilizing Effect ◽  
Flow Through ◽  
Exercise Induced ◽  
The Stability ◽  
Mixed Venous

Hyperoxic blood has a small stabilizing effect on agitated saline contrast compared with mixed venous blood, lending support to studies that show the reversal of exercise-induced blood flow through intrapulmonary arteriovenous anastomoses (Q̇IPAVA) with hyperoxia. These data support the possible presence of a local O2-dependent regulatory mechanism within the pulmonary vasculature that may play a role in Q̇IPAVA regulation.

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