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.

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.

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.

Effects of cocaine on incremental treadmill exercise in horses

1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams
Keyword(s):  
Right Ventricular ◽  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Ventricular Pressure ◽  
Mixed Venous Blood ◽  
Work Intensity ◽  
Venous Blood Lactate ◽  
Mixed Venous

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise

2003 ◽  
Vol 94 (6) ◽  
pp. 2135-2144 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Blood Lactate ◽  
Plasma Volume ◽  
High Intensity ◽  
Maximal Exercise ◽  
Lactate Concentration ◽  
High Intensity Exercise ◽  
Hydration Status ◽  
Mixed Venous Blood ◽  
Short Term ◽  
Arterial Hypoxemia

It is reported that preexercise hyperhydration caused arterial O2 tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425–429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 ± 1.8% increase in plasma volume was induced with NaCl (0.30–0.45 g/kg dissolved in 1,500 ml H2O) administered via a nasogastric tube, 285–290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant ( P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient.

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.

Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise

1998 ◽  
Vol 85 (2) ◽  
pp. 609-618 ◽  
Author(s):  
Craig A. Harms ◽  
Thomas J. Wetter ◽  
Steven R. McClaran ◽  
David F. Pegelow ◽  
Glenn A. Nickele ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Respiratory Muscle ◽  
Maximal Exercise ◽  
Work Of Breathing ◽  
Venous Blood ◽  
Inspiratory Muscle ◽  
Mixed Venous Blood ◽  
Muscle Work ◽  
Mixed Venous

We have recently demonstrated that changes in the work of breathing during maximal exercise affect leg blood flow and leg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573–1583, 1997). Our present study examined the effects of changes in the work of breathing on cardiac output (CO) during maximal exercise. Eight male cyclists [maximal O2 consumption (V˙o 2 max): 62 ± 5 ml ⋅ kg−1 ⋅ min−1] performed repeated 2.5-min bouts of cycle exercise atV˙o 2 max. Inspiratory muscle work was either 1) at control levels [inspiratory esophageal pressure (Pes): −27.8 ± 0.6 cmH2O], 2) reduced via a proportional-assist ventilator (Pes: −16.3 ± 0.5 cmH2O), or 3) increased via resistive loads (Pes: −35.6 ± 0.8 cmH2O). O2 contents measured in arterial and mixed venous blood were used to calculate CO via the direct Fick method. Stroke volume, CO, and pulmonary O2 consumption (V˙o 2) were not different ( P > 0.05) between control and loaded trials atV˙o 2 max but were lower (−8, −9, and −7%, respectively) than control with inspiratory muscle unloading atV˙o 2 max. The arterial-mixed venous O2difference was unchanged with unloading or loading. We combined these findings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effects on the cardiovascular system: 1) up to 14–16% of the CO is directed to the respiratory muscles; and 2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.

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.

Operation Everest II: oxygen transport during exercise at extreme simulated altitude

1988 ◽  
Vol 64 (4) ◽  
pp. 1309-1321 ◽  
Author(s):  
J. R. Sutton ◽  
J. T. Reeves ◽  
P. D. Wagner ◽  
B. M. Groves ◽  
A. Cymerman ◽  
...  
Keyword(s):  
Sea Level ◽  
Blood Lactate ◽  
Venous Blood ◽  
Blood Gases ◽  
Work Load ◽  
Open Circuit ◽  
Mixed Venous Blood ◽  
O2 Uptake ◽  
Fourfold Increase ◽  
Mixed Venous

A decrease in maximal O2 uptake has been demonstrated with increasing altitude. However, direct measurements of individual links in the O2 transport chain at extreme altitude have not been obtained previously. In this study we examined eight healthy males, aged 21-31 yr, at rest and during steady-state exercise at sea level and the following inspired O2 pressures (PIO2): 80, 63, 49, and 43 Torr, during a 40-day simulated ascent of Mt. Everest. The subjects exercised on a cycle ergometer, and heart rate was recorded by an electrocardiograph; ventilation, O2 uptake, and CO2 output were measured by open circuit. Arterial and mixed venous blood samples were collected from indwelling radial or brachial and pulmonary arterial catheters for analysis of blood gases, O2 saturation and content, and lactate. As PIO2 decreased, maximal O2 uptake decreased from 3.98 ±0.20 l/min at sea level to 1.17 ± 0.08 l/min at PIO2 43 Torr. This was associated with profound hypoxemia and hypocapnia; at 60 W of exercise at PIO2 43 Torr, arterial PO2 = 28 ± 1 Torr and PCO2 = 11 ± 1 Torr, with a marked reduction in mixed venous PO2 [14.8 ± 1 (SE) Torr]. Considering the major factors responsible for transfer of O2 from the atmosphere to the tissues, the most important adaptations occurred in ventilation where a fourfold increase in alveolar ventilation was observed. Diffusion from alveolus to end-capillary blood was unchanged with altitude. The mass circulatory transport of O2 to the tissue capillaries was also unaffected by altitude except at PIO2 43 Torr where cardiac output was increased for a given O2 uptake. Diffusion from the capillary to the tissue mitochondria, reflected by mixed venous PO2, was also increased with altitude. With increasing altitude, blood lactate was progressively reduced at maximal exercise, whereas at any absolute and relative submaximal work load, blood lactate was higher. These findings suggest that although glycogenolysis may be accentuated at low work loads, it may not be maximally activated at exhaustion.

Pulmonary diffusion in the dog lung

1962 ◽  
Vol 17 (6) ◽  
pp. 885-892 ◽  
Author(s):  
Albert H. Niden ◽  
Charles Mittman ◽  
Benjamin Burrows
Keyword(s):  
Carbon Monoxide ◽  
Pulmonary Artery ◽  
Experimental Animal ◽  
Venous Blood ◽  
Whole Body ◽  
Mixed Venous Blood ◽  
Pulmonary Diffusion ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
Mixed Venous

Methods have been presented for assessing pulmonary diffusion by the “equilibration technique” in the experimental intact dog and perfused lung while controlling ventilation with a whole body respirator. No significant change in diffusion of carbon monoxide was noted between open and closed chest anesthetized animals, with duration of anesthesia in the intact dog, or with duration of perfusion of the isolated dog's lung. There was no demonstrable difference in diffusion when arterialized blood was used as the perfusate in place of mixed venous blood in the lung perfusions suggesting that within the range studied the Po2, Pco2, and pH of pulmonary artery blood does not directly affect the diffusion of carbon monoxide. Retrograde perfusions of dogs' lungs did not significantly alter diffusion, suggesting that pulmonary venous resistance was not significantly lower than pulmonary arterial resistance in the perfused dog lung at the flows and pressures studied. The equilibration technique for measuring pulmonary diffusion and assessing the uniformity of diffusion was well suited to the study of pulmonary diffusing characteristics in the experimental animal. Submitted on January 8, 1962

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