Biomedical subjects

M A Busch

Publications and source records attributed to M A Busch.

24 records · Page 2Linked to original sources

PubMed1984

O2 transport in ponies during treadmill exercise.

We assessed cardiovascular variables and blood O2 contents in order to characterize O2 transport in ponies during treadmill exercise. In normal ponies at 1.8, 3, and 6 mph, respectively, cardiac output (Qc) increased from 12 l/min at rest to maximum levels of 19.7, 28.7, and 39.9 l/min between 30 and 60 s. Qc then decreased to steady-state levels of 18.2, 24.6, and 32.7 l/min by 4 min. Heart rate (HR) showed a similar biphasic response in the 1st min of exercise. Systolic and diastolic arterial blood pressure (BP) decreased at the onset of exercise by 20-25 Torr (P less than 0.05) and then increased to a steady-state by 60 s. Mean right ventricular pressures (MRVBP) increased from approximately 9.7 Torr at rest to 15.9 (1.8 mph), 15.2 (3 mph), and 23.6 Torr (6 mph) by 1 min and then decreased throughout the remainder of the 8 min of exercise (P less than 0.05). At 3 and 6 mph, respectively, arterial O2 content (CaO2) increased from 11.6 vol% at rest to 12.7 and 15.0 vol% by 45 s and 13.1 and 16.6 vol% by 7 min. At 7 min of 9.3 mph exercise, it increased to 20.34 vol%. Hemoglobin (Hb) at 3 mph increased from 9.6 g/100 ml at rest to 10.5 g/100 ml by 45 s and 11.7 g/100 ml by 7 min. At 6 mph, Hb increased to 12 g/100 ml at 45 s and 13.0 g/100 ml by 7 min of exercise. These data demonstrate that the rapid, work load-dependent increase in CaO2 represents an important mechanism to increase O2 transport in exercising ponies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Cardiodynamic variables and ventilation during treadmill exercise in ponies.

We assessed the relationship of ventilation (VE) to cardiodynamic variables and CO2 transport in seven normal ponies during treadmill exercise. At 1.8, 3, and 6 mph, respectively, VE increased from 15 l/min at rest to 43, 51, and 86 l/min by 1 min and 48, 68, and 125 l/min by 8 min. In three ponies at the same work loads, cardiac output (Qc) increased from approximately 12 l/min at rest to 19.7, 28.1, and 40.3 l/min between 30-60 s (P less than 0.05) and then decreased by about 20% to a steady state by 3-4 min. Heart rate (HR) shows a similar biphasic response during exercise. Mean right ventricular pressure (MRVBP) increased from 9.9 to 15.9 Torr at 1.8 mph, 15.2 Torr at 3 mph, and 23.5 Torr at 6 mph by 1 min (P less than 0.05) and then decreased to 11.8, 12.2, and 15.8 Torr by 8 min of the three respective work intensities. At all work loads, VE increased proportionately faster than these cardiovascular variables in the 1st min. For example, at 6 mph VE increased 470%, whereas Qc and HR increased only 230%. Thereafter, VE generally continued to increase at 3 and 6 mph, whereas MRVBP, Qc, and HR decreased. Therefore, the basic assumption of a cardiodynamic hyperpnea that VE and Qc are equivalently coupled at the exercise onset is rejected for this species. Mixed venous CO2 content (C-vCO2) at 3 and 6 mph, respectively, decreased slightly from 61.6 and 62.3 vol% at rest to 59.6 and 61.9 vol% by 45 s and then increased to 63.3 and 63.5 vol% by 7 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

The effects of unilateral carotid body excision on ventilatory control in goats.

The purpose of this study was to determine whether or not unilateral carotid body excision (UCBE) alters normal respiratory control in awake and otherwise intact goats. We measured resting VE and blood gas tensions and pH and ventilatory responses (VR) to NaCN, dopamine and Doxapram in awake goats before and after UCBE. Resting ventilation, blood gas tensions and pH, and the VR to the above stimuli were not altered by UCBE. During exposure to hypoxia in a hypobaric chamber (PB = 450 torr), PaCO2 decreased in UCBE goats over the first hour, indicating acute hypoxic hyperventilation. During the subsequent 8 h, PaCO2 decreased an additional 5-6 torr, suggesting ventilatory acclimatization to chronic hypoxia (VACH). The response was similar to that observed in intact goats. Acute normoxia following 6 and 8 hr did not completely alleviate the hypocapnia of prolonged hypoxia, further suggesting VACH. We conclude that sufficient redundancy exists in the inputs from the paired carotid body chemoreceptors so that normal ventilatory responsiveness to acute and chronic stimuli is present in goats possessing only a single carotid body.

Acclimatization↗

PubMed1983

Hyperpnea of exercise at various PIO2 in normal and carotid body-denervated ponies.

We studied the effect of changes in inspired [O2] on partial pressure of CO2 in arterial blood (PaCO2) during treadmill exercise (3 mph, 3% grade) in normal, acute (+2-4 wk), and chronic (+1-2 yr) carotid body-denervated (CBD) ponies. In all studies, PaCO2 decreased (P less than 0.01) from rest during exercise, reaching a nadir usually between 15 and 30 s of exercise. During normoxia [partial pressure of O2 in arterial blood (PaO2) approximately 95 Torr], the PaCO2 nadir was 2.3 +/- 0.6 Torr below resting level in normal ponies, but the nadir was greater (P less than -0.01) in acute (delta = 6.4 +/- 0.8 Torr) and chronic (delta = -4.7 +/- 1.1 Torr) CBD ponies. Hyperoxia (PaO2 approximately 180 Torr) accentuated (P less than 0.01) the hypocapnia only in the normal ponies (delta = -6.3 +/- 1.0 Torr). In contrast, hypoxia (PaO2 48 Torr) attenuated (P less than 0.01) the exercise-induced hypocapnia by 3-5 Torr in all ponies. Usually PaCO2 gradually increased after 30 s of exercise, reaching a stable level 1-3 Torr below rest by about 2 min (P less than 0.05). Tidal volume (VT) increased from rest during the first 15 s of exercise only when there was a large decrease in PaCO2. Recovery of PaCO2 after 30 s of exercise was associated with a decrease in VT toward rest. We concluded the following. 1) The accentuated hypocapnia caused by eliminating (CBD) or reducing (hyperoxia) carotid chemoreceptor activity suggests that the chemoreceptors normally dampen alveolar ventilation (VA) at the onset of exercise. 2) Attenuation of the hypocapnia at the onset of exercise by hypoxia in CBD ponies suggests that a direct CNS effect of hypoxia dampens VA. 3) Mechanisms tending to minimize the hypocapnia during exercise appear to adjust VA by modulating VT.

Animals↗

PubMed1983

Hyperventilation in ponies at the onset of and during steady-state exercise.

We studied blood gases in ponies to assess the relationship of alveolar ventilation (VA) to pulmonary CO2 delivery during moderate treadmill exercise. In normal ponies for 1.8, 3, or 6 mph, respectively, partial pressure of CO2 in arterial blood (PaCO2) decreased maximally by 3.1, 4.4, and 5.7 Torr at 30-90 s of exercise and remained below rest by 1.4, 2.3, and 4.5 Torr during steady-state (4-8 min) exercise (P less than 0.01). Partial pressure of O2 in arterial blood (PaO2) and arterial pH, (pHa) also reflected hyperventilation. Mixed venus CO2 partial pressure (PVCO2) decreased 2.3 and 2.9 Torr by 30 s for 3 and 6 mph, respectively (P less than 0.05). In work transitions either from 1.8 to 6 mph or from 6 mph to 1.8 mph, respectively, PaCO2 either decreased 3.8 Torr or increased 3.3 Torr by 45 s of the second work load (P less than 0.01). During exercise in acute (2-4 wk) carotid body denervated (CBD) ponies at 1.8, 3, or 6 mph, respectively, PaCO2 decreased maximally below rest by 9.0, 7.6, and 13.2 Torr at 30-45 s of exercise and remained below rest by 1.3, 2.3, and 7.8 Torr during steady-state (4-8 min) exercise (P less than 0.1). In the chronic (1-2 yr) CBD ponies, the hypocapnia was generally greater than normal but less than in the acute CBD ponies. We conclude that in the pony 1) VA is not tightly matched to pulmonary CO2 delivery during exercise, particularly during transitional states, 2) the exercise hyperpnea is not mediated by PaCO2 or PVCO2, and 3) during transitional states in the normal pony, the carotid bodies attenuate VA drive thereby reducing arterial hypocapnia.

Animals↗

PubMed1982

Regional myocardial blood flow and coronary vascular reserve in unanesthetized young calves exposed to a simulated altitude of 3500 m for 8--10 weeks.

We determined regional myocardial blood flow (15-micrometer tracer microspheres) and hemodynamics in nine normal calves, seven calves with right ventricular (RV) hypertrophy induced by pulmonary artery banding (PAB) at sea level, and five calves exposed to simulated high altitude (HA) of 3,500 m (PB = 500 mm Hg) for 8--10 weeks. Progression of RV hypertrophy was very rapid in HA calves. RV weight:body weight ratio of 2.74 +/- 0.20 g/kg at 8--10 weeks of sojourn at HA significantly exceeded that in PAB calves (1.98 +/- 0.11 g/kg) 20 weeks post-banding. All calves were studied unanesthetized at sea level before (control) and during maximal coronary vasodilation (iv adenosine; 4 microM/kg per min). Normal and HA calves were also studied during acute hypoxemia (PaO2: 42 +/- 1 mm Hg) induced by administration of 12--13% O2 + N2 in the inhaled gas. RV myocardial blood flow was significantly increased only in PAB calves, whereas in HA calves it was similar to that in normal calves. Left ventricular (LV) mass and blood flow were identical in three groups of calves. Polycythemia did not occur in HA calves. Minimal coronary vascular resistance per unit weight of the hypertrophied RV was identical to that in the normal RV myocardium. This suggested that, despite very fast progression of RV hypertrophy in HA calves, functional cross-sectional area of the RV coronary vascular bed kept pace with the increase in cardiac mass. Minimal coronary vascular resistance per unit weight of the left ventricular myocardium was also identical in three groups of calves. This suggested that chronic hypoxemia by itself did not cause an increase in the functional cross-sectional area of the LV coronary vascular bed. Acute hypoxemia resulted in a significant increase in myocardial blood flow in all calves, but in HA calves, RV endo:epi perfusion ratio decreased below 1.00. Transmural RV myocardial blood flow and RV systolic pressure in HA calves during acute hypoxemia significantly exceeded that in normal calves.

Altitude Sickness↗