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Biomedical subjects

H V Forster

Publications and source records attributed to H V Forster.

At least 91 records · Page 5Linked to original sources

Effect of partial spinal cord ablation on exercise hyperpnea in ponies.

We addressed the role of spinal afferent information in the exercise hyperpnea. Arterial PCO2 (PaCO2) was assessed in 10 normal ponies during low (1.8 mph 7% or 17% grade) or moderate (6 mph 7% grade) treadmill exercise. After control studies, bilateral spinal ablation (SA) of the dorsolateral sulcus and dorsolateral funiculus at L2 was performed in seven ponies. In normal ponies within the first 90 s of exercise, PaCO2 initially decreased 2.7, 4.1, and 5.2 Torr below rest at the three work loads, respectively (P less than 0.05). PaCO2 thereafter increased toward resting levels but remained 1.1, 2.9, and 4.9 Torr below rest during the steady state of exercise (P less than 0.05). One month post-SA, PaCO2 at the exercise onset decreased 1.5, 2.3, and 5.2 Torr and in the steady state was 0.7, 1.9 and 4.9 Torr below rest at the three work loads, respectively. The changes in PaCO2 from rest to exercise (delta PaCO2) were calculated for each pony in the rest to work transition and between rest and steady-state exercise and then averaged for each group of ponies. After SA, delta PaCO2's were significantly less than pre-SA only in the rest to work transition at the low work loads (P less than 0.05). No differences were found in steady-state delta PaCO2's. The modest attenuation of the exercise hypocapnia at the lower workloads in SA ponies suggests that spinal afferent information does play some role in the exercise hyperpnea in awake ponies. Our data probably underestimate this role because our SA surgery is only a partial deafferentation.

Animals↗

Attenuated Hering-Breuer inflation reflex 4 years after pulmonary vagal denervation in ponies.

The purpose of this study was to determine whether there was any recovery of the Hering-Breuer inflation reflex in ponies between 2-4 wk and 3-4 yr after hilar nerve denervation (HND). Under anesthesia and before HND, airway occlusion after a 3-liter lung inflation lengthened the subsequent occluded breath by nearly 10 times the control breath duration. Between 2 wk and 3-4 yr after HND, this maneuver increased the duration of the occluded breath by only 2.5 times the control breath duration. Also under anesthesia, the airway was occluded at end expiration. This maneuver increased the duration of the subsequent inspiratory effort by 71% in hilar nerve intact ponies but by only 20-25% 2-4 wk and 3-4 yr after HND. For both tests, the pre- and post-HND differences were statistically significant (P less than 0.05), but there were no significant differences (P greater than 0.10) between 2-4 wk and 3-4 yr post-HND. In awake ponies, at rest and during mild and moderate treadmill exercise, breathing frequency was generally lower and inspiratory time was greater after relative to before HND. The inspiratory time-to-total cycle duration ratio was consistently increased by 0.10-0.15 after HND (P less than 0.05). There was no significant change in this ratio between 2-4 wk and 3-4 yr post-HND (P greater than 0.10). We conclude that the surgical procedure for HND used in this study does not permit any significant reinnervation, and there are no significant changes within the ventilatory control system to compensate for loss of hilar nerve afferents.

Animals↗

Breathing during exercise: demands, regulation, limitations.

In humans alveolar ventilation (VA) is adjusted almost perfectly to the metabolic demands of mild and moderate exercise. For example, in exercise transitions and in the steady state, PaCO2 rarely deviates by more than 1 to 3 mmHg from the value at rest. This near-homeostasis contrasts to most other mammalian species; equines for example, demonstrate a progressive hypocapnia and alkalosis as exercise intensity is increased to moderate levels. In equines, the control systems seem programmed for a specific hyperventilation that contributes to maintenance of PaO2 homeostasis. Generally, during heavy exercise all species hyperventilate creating hypocapnia, increased PAO2, widened A-a O2 gradient, and PaO2 homeostasis. The origin of the metabolic ventilatory stimulus remains controversial. Evidence exists for: a) "neural" mediation, either central command or peripheral afferent in nature; and b) "humoral" mediation with an intra-thoracic metabolite receptor being a possibility. The mechanism of the species differences in hyperventilation during exercise does not appear to be due to species variation in chemoreceptor "fine tuning". Contrary to traditional thinking, recent findings suggest that the hyperventilation during heavy exercise might not be mediated by lactacidosis stimulation of chemoreceptors. The increase in VA during exercise is achieved efficiently in that airway diameter is modulated and the pattern of breathing and the recruitment of respiratory muscles are set to minimize the O2 cost of breathing. It has been postulated that mechanoreceptors in airways, lung parenchyma and the chest wall are important to efficient breathing. Their role and contribution to the exercise hyperpnea has been shown by reductions in respiratory neural output within breath when respiratory impedance is reduced via helium breathing. Hilar nerve afferents do not appear to be critical to this response. However, carotid chemoreceptors appear essential for "fine tuning" of VA when respiratory impedance is reduced. In most healthy exercising mammals, the efficiency component of the exercise stimulus does not compromise VA. There are two known major exceptions. One is the extremely fit human athlete during very high workloads when atypically there is minimal or no hyperventilation resulting in arterial hypoxemia. That indeed the high O2 cost of breathing compromises VA is indicated by hyperventilation and alleviation of hypoxemia with resistance unloading through helium breathing. A second example of a compromise of VA is that of a galloping racehorse at very high workloads.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Ventilatory and PaCO2 responses to voluntary and electrically induced leg exercise.

We studied the role of central command mediation of exercise hyperpnea by comparing the ventilatory and arterial CO2 partial pressure (PaCO2) responses to voluntary (ExV) and electrically induced (ExE) muscle contractions in normal, awake human subjects. We hypothesized that if central command signals are critical to a normal ventilatory response, then ExE should cause a slower ventilatory response resulting in hypercapnia at the onset of exercise. ExE was induced through surface electrodes placed over the quadriceps and hamstring muscles. ExE and ExV produced leg extension (40/min) against a spring load that increased CO2 production (VCO2) 100-1,000 ml/min above resting level. PaCO2 and arterial pH during work transitions and in the steady state did not differ significantly from rest (P greater than 0.05) or between ExE and ExV. The temporal pattern of ventilation, tidal volume, breathing frequency, and inspired and expired times, and the ventilation-VCO2 relationship were similar between ExE and ExV. We conclude that since central command was reduced and/or eliminated by ExE, central command is not requisite for the precise matching of alveolar ventilation to increases in VCO2 during low-intensity muscle contractions.

Adult↗

Is the hyperpnea of muscular contractions critically dependent on spinal afferents?

We studied the role of spinal afferent pathways in the hyperpnea of electrically induced muscle contractions (ExE). The ventilatory (VE) and arterial CO2 partial pressure (PaCO2) responses were measured at rest and during two levels of ExE in awake human paraplegic subjects with clinically complete lesions of the spinal cord (range T4-T11). We hypothesized that if peripheral neural drive is critical to a normal ventilatory response, then ExE in the absence of intact pathways should cause a lower ventilatory response resulting in hypercapnia at the onset of ExE. ExE was induced by stimulation of the quadriceps and hamstring muscles that approximately doubled the resting level of CO2 production (VCO2). PaCO2 during work transitions and in the latter stages of ExE did not differ significantly from that at rest. Arterial pH progressively declined over time during ExE (P less than 0.01) as a result of increased lactate concentration (P less than 0.01). The linear relationship between VE and VCO2 was similar to that found for normal human subjects during ExE (P = 0.73). These data suggest that VE and presumably alveolar ventilation (VA) can be appropriately matched to VCO2 during low-intensity muscle contractions of the lower extremities in the absence of intact spinal afferent pathways. Moreover, since it is unlikely that postulated "central command" mechanisms were initiated during ExE in these paraplegic subjects, the data provide support for our previous conclusion that central command is not obligatory for matching VA to VCO2 (J. Appl. Physiol. 64: 218-225, 1988).

Adult↗

Dopamine blockade alters ventilatory acclimatization to hypoxia in goats.

Dopamine (DA) is generally accepted to be an inhibitory neurotransmitter in the carotid body (CB). It is released and depleted from the CB by acute hypoxia. From this background we made the hypothesis that hypoxic depletion of CB DA could be responsible for a time-dependent increase in CB afferent output and the early phase of ventilatory acclimatization to hypoxia (VAH) in goats. We reasoned, then, that blockade of DA receptors in the CB would accelerate the time course of VAH in the goat, i.e. produce a greater acute response to hypoxia (first 15 min) followed by a reduced rate of change of the subsequent time-dependent hyperventilation. We tested this hypothesis by exposing 7 adult female goats to up to 28 h of hypobaric hypoxia (PB = 380 Torr) on 3 different occasions separated by at least 2 months. The first was as control. During the second and third exposures different doses of the DA antagonist, domperidone, were administered prior to and during the hypoxic exposure (0.5 mg/kg followed by 0.25 mg/kg every 3 h and in the second study 1.0 mg/kg followed by 0.5 mg/kg every 2 h). The time course of acclimatization was assessed by measurement of arterial blood gases and pH in the awake goats. The data obtained in the first 4-5 h of hypoxia in domperidone treated animals appeared to support the hypothesis. Domperidone treated animals had a significantly greater acute ventilatory response to hypoxia followed by a lower rate of progressive hyperventilation in this period. However, variation in control values, greater respiratory alkalosis and a secondary significant hyperventilation after 6-7 h of hypoxia in the domperidone treated animals prevents a clear conclusion as to the precise role of CB dopaminergic mechanisms in acclimatization to hypoxia. Nevertheless, peripheral DA receptor blockade with domperidone does alter the time course and magnitude of hyperventilation during the first 7 h of hypobaric hypoxia in goats.

Acclimatization↗

Role of carotid chemoreceptors and pulmonary vagal afferents during helium-oxygen breathing in ponies.

Our purpose was to assess compensatory breathing responses to airway resistance unloading in ponies. We hypothesized that the carotid bodies and hilar nerve afferents, respectively, sense chemical and mechanical changes caused by unloading, hence carotid body-denervated (CBD) and hilar nerve-denervated ponies (HND) might demonstrate greater ventilatory responses when decreasing resistance. At rest and during treadmill exercise, resistance was transiently reduced approximately 40% in five normal, seven CBD, and five HND ponies by breathing gas of 79% He-21% O2 (He-O2). In all groups at rest, He-O2 breathing did not consistently change ventilation (VE), breathing frequency (f), tidal volume (VT), or arterial PCO2 (PaCO2) from room air-breathing levels. During treadmill exercise at 1.8 mph-5% grade in normal and HND ponies, He-O2 breathing did not change PaCO2 but at moderate (6 mph-5% grade), and heavy (8 mph-8% grade) work loads, absolute PaCO2 tended to decrease by 1 min of resistance unloading. delta PaCO2 calculated as room air minus He-O2 breathing levels at 1 min demonstrated significant changes in PaCO2 during exercise resistance unloading (P less than 0.05). No difference between normal and HND ponies was found in exercise delta PaCO2 responses (P greater than 0.10); however, in CBD ponies, the delta PaCO2 during unloading was greater at any given work load (P less than 0.05), suggesting finer regulation of PaCO2 in ponies with intact carotid bodies. During heavy exercise VE and f increased during He-O2 breathing in all three groups of ponies (P less than 0.05), although there were no significant differences between groups (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

Carotid body hypercapnia does not elicit ventilatory acclimatization in goats.

The carotid body (CB) perfusion model utilizes surgical vascular ligations to allow isolated blood supply to a single in situ CB in awake goats. The contralateral CB was excised. By use of an extracorporeal pump-oxygenator system the blood gas composition perfusing the CB can be controlled independently from that of the systemic arterial system including the brain. Using this model we compared the responses of systemically normoxic goats to CB hypercapnia and CB hypoxia. In 6 goats CB stimulation with hypercapnic-normoxic blood (mean PcbCO2 = 78 Torr, mean PcbO2 congruent to 100 Torr) produced acute hyperventilation (mean decrease in PaCO2 of 5.2 Torr, P less than 0.05) which remained constant over the 4-h perfusion period. Lack of a progressively increasing hyperventilation indicates that ventilatory acclimatization did not occur with hypercapnic CB perfusion. Hypoxic-normocapnic CB stimulation (mean PcbO2 = 40 Torr, mean PcbCO2 = 39 Torr) produced an acute mean decrease in PaCO2 of 5.5 Torr (P less than 0.05) in 6 additional goats. In contrast to CB hypercapnia, the acute hyperventilation induced by CB hypoxia was followed by a progressive time-dependent additional mean decrease in PaCO2 of 5.6 Torr (P less than 0.05) over a 4-h period (ventilatory acclimatization). These data are compatible with the concept of separate receptor mechanisms for hypercapnia and hypoxia in the CB and suggest that the early phase of ventilatory acclimatization to hypoxia in goats may result from a time-dependent increase in CB afferent output.

Acclimatization↗

Temporal pattern of arterial CO2 partial pressure during exercise in humans.

The major objective of this study was to test the hypothesis that arterial CO2 partial pressure (PaCO2) does not change in transitions from rest to steady-state exercise and between two levels of exercise. Nine young adults exercised on a treadmill or a bicycle (sit or supine) for 5 min at a mild work load (heart rate = 90 beats X min-1) and then 3 min at a moderate work load (heart rate = 150 beats X min-1). In some studies the moderate work load preceded the mild work load. Arterial blood was sampled from a catheterized artery. During all exercise tasks isocapnia was not strictly maintained (F greater than 4.0, P less than 0.001). For example, a 1-to 2-Torr hypocapnia was the dominant trend during the first 15-45 s after increasing treadmill speed, and a transient hypercapnia was most prevalent when treadmill speed was decreased. During steady-state exercise PaCO2 did not deviate by more than 1-3 Torr from PaCO2 during any resting posture, and PaCO2 differences between exercise intensities and conditions did not exceed 1-2 Torr. A mouthpiece-breathing valve system was not used in most studies, but when this system was used, it did not consistently affect exercise PaCO2. Increasing inspired O2 to 40% likewise did not consistently alter exercise PaCO2. Failure to maintain isocapnia throughout exercise indicates that the matching of alveolar ventilation (VA) to lung CO2 delivery is not exquisitely precise. Accordingly it is inappropriate to base theories of the exercise hyperpnea on the heretofore contention of precise matching.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

Carotid bodies are required for ventilatory acclimatization to chronic hypoxia.

We have compared the ventilatory responses of intact and carotid body-denervated (CBD) goats to moderate [partial pressure of O2 in arterial blood; (Pao2) approximately 44 Torr] and severe (Pao2 approximately 33 Torr) many time points for up to 7 days of hypobaria. In the intact group there were significant time-dependent decreases in partial pressure of CO2 in arterial blood (PaCO2) in both moderate and severe hypoxemia (approximately-7 and -11 Torr) that were largely complete by 8 h of hypoxemia and maintained throughout. Acute restoration of normoxia in chronically hypoxic intact animals produced time-dependent increases in Paco2 over 2 h, but hypocapnia persisted relative to sea-level control. Arterial plasma [HCO3-] and [H+] decreased, and [Cl-] increased with a time course and magnitude consistent with developing hypocapnia. Chronic CBD, per se, resulted in a sustained, partially compensated respiratory acidosis, as PaCO2 rose 6 Torr and base excess rose 3 mEq/1, [Cl-] fell 1 mEq/1, and pHa fell 0.01 units. During exposure to identical levels of arterial hypoxemia as in the intact group. CBD animals showed no significant changes in PaCO2, [H+]a, or [HCO3-]a at any time during moderate or severe hypoxemia. Plasma [C1-] remained within the normal range throughout exposure to moderate hypoxia and increased in severe hypoxia. In a few instances some hypocapnia was observed, but this was highly inconsistent and was always less than one-third of that observed in intact goats. In contrast to intact goats, acute restorations of normoxia in the chronically hypoxic CBD goats always caused hyperventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

Ventilatory acclimatization to hypoxia is not dependent on cerebral hypocapnic alkalosis.

We previously demonstrated that, in awake goats, 6 h of hypoxic carotid body perfusion during systemic normoxia produced time-dependent hyperventilation that is typical of ventilatory acclimatization to hypoxia (VAH). The hypocapnic alkalosis that occurred could have produced VAH by inducing cerebral vasoconstriction and brain lactic acidosis even though systemic arterial normoxia was maintained. In the present study we tested the hypothesis that hypocapnic alkalosis is a necessary component of VAH. Goats were prepared so that one carotid body could be perfused, from an extracorporeal circuit, with blood in which gas tensions could be controlled independently from the blood perfusing the systemic arterial system, including the brain. Using this preparation we carried out 4 h of hypoxic carotid body perfusion while maintaining systemic arterial (and brain) normoxia in awake goats. Expired minute ventilation (VE) was measured while CO2 was added to inspired air to maintain normocapnia. Carotid body PCO2 and PO2 were maintained near 40 Torr during the 4-h carotid body perfusion. Control mean VE was 8.65 +/- 0.48 l/min (mean +/- SE). With acute carotid body hypoxia (30 min) VE increased to 21.73 +/- 2.02 l/min (P less than 0.05); over the ensuing 3.5 h of carotid body hypoxia, VE progressively increased to 39.14 +/- 4.14 l/min (P less than 0.05). These data indicate that neither cerebral hypoxia nor hypocapnic alkalosis are required to produce VAH. After termination of the 4-h carotid body stimulation, hyperventilation was not maintained in these studies, i.e., there was no deacclimatization. This suggests that acclimatization and deacclimatization are produced by different mechanisms.

Acclimatization↗

Independence of exercise hyperpnea and acidosis during high-intensity exercise in ponies.

We investigated arterial PCO2 (PaCO2) and pH (pHa) responses in ponies during 6-min periods of high-intensity treadmill exercise. Seven normal, seven carotid body-denervated (2 wk-4 yr) (CBD), and five chronic (1-2 yr) lung (hilar nerve)-denervated (HND) ponies were studied during three levels of constant load exercise (7 mph-11%, 7 mph-16%, and 7 mph-22% grade). Mean pHa for each group of ponies became alkaline in the first 60 s (between 7.45 and 7.52) (P less than 0.05) at all work loads. At 6 min pHa was at or above rest at 7 mph-11%, moderately acidic at 7 mph-16% (7.32-7.35), and markedly acidic at 7 mph-22% (7.20-7.27) for all groups of ponies. Yet with no arterial acidosis at 7 mph 11%, normal ponies decreased PaCO2 below rest (delta PaCO2) by 5.9 Torr at 90 s and 7.8 Torr by 6 min of exercise (P less than 0.05). With a progressively more acid pHa at the two higher work loads in normal ponies, delta PaCO2 was 7.3 and 7.8 Torr by 90 s and 9.9 and 11.4 Torr by 6 min, respectively (P less than 0.05). CBD ponies became more hypocapnic than the normal group at 90 s (P less than 0.01) and tended to have greater delta PaCO2 at 6 min. The delta PaCO2 responses in normal and HND ponies were not significantly different (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

Effect of reducing anatomic dead space on arterial PCO2 during CO2 inhalation.

Carotid body-denervated (CBD) ponies have a less than normal increase in arterial PCO2 (PaCO2) when inspired CO2 (PICO2) is increased, even when pulmonary ventilation (VE) and breathing frequency (f) are normal. We studied six tracheostomized ponies to determine whether this change 1) might be due to increased alveolar ventilation (VA) secondary to a reduction in upper airway dead space (VD) or 2) is dependent on an upper airway sensory mechanism. Three normal and three chronic CBD ponies were studied while they were breathing room air and at 14, 28, and 42 Torr PICO2. While the ponies were breathing room air, physiological VD was 483 and 255 ml during nares breathing (NBr) and tracheostomy breathing (TBr), respectively. However, at elevated PICO2, mixed expired PCO2 often exceeded PaCO2; thus we were unable to calculate physiological VD using the Bohr equation. At all PICO2 in normal ponies, PaCO2 was approximately 0.3 Torr greater during NBr than during TBr (P less than 0.05). In CBD ponies this NBr-TBr difference was only evident while breathing room air and at 28 Torr PICO2. At each elevated PICO2 during both NBr and TBr, the increase in PaCO2 above control was always less in CBD ponies than in normal ponies (P less than 0.01). The VE-PaCO2, f-PaCO2, and tidal volume-PaCO2 relationships did not differ between NBr and TBr (P greater than 0.10) nor did they differ between normal and CBD ponies (P greater than 0.10). We conclude that the attenuated increase in PaCO2 during CO2 inhalation after CBD is not due to a relative increase in VA secondary to reducing upper airway VD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Arterial vs. rectal temperature in ponies: rest, exercise, CO2 inhalation, and thermal stresses.

We assessed in ponies the adequacy of using rectal (Tre) rather than arterial temperature (Tar) under conditions common to ventilatory control experiments, i.e., CO2 breathing, thermal stress, and particularly exercise. We were interested in whether, and to what extent, Tar-Tre differences could lead to errors in arterial blood gas corrections. At control environmental temperatures (Ta) of 5 degrees C in the winter and 21 degrees C in the summer, Tar and Tre (37.1 degrees C) did not differ (P greater than 0.05). Elevating winter or summer Ta by 10-18 degrees C for 2-days or lowering summer Ta by 9 degrees C (2-days) did not change Tar or Tre (P greater than 0.05). Furthermore, elevating inspired PCO2 to 42 Torr for 15 min did not alter Tar or Tre from control (P greater than 0.05). During treadmill exercise, at 1.8 mph 5% grade, Tar and Tre did not change significantly (P greater than 0.05) from rest by 11 min of work. At 3 mph 5% grade, Tar increased progressively by 0.3 degrees C (P less than 0.05) while Tre tended to increase 0.1 degree C by 11 min. During moderate exercise at 6 mph 5% grade, Tar increased 0.9 degree C (P less than 0.05) while Tre increased 0.25 degree C (P less than 0.05). Finally, by 6 min of heavy exercise at 8 mph 20% grade, Tar increased 2 degrees C (P less than 0.05) while Tre increased 0.5 degree C (P less than 0.05). The Tar-Tre differences during the latter three work loads were statistically significant (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of altered ambient temperature on breathing in ponies.

The objective was to determine the effect of moderate changes in ambient temperature (TA) on breathing and body temperature in ponies chronically exposed to a TA of 21 degrees C in the summer and 5 degrees C in the winter. Normal (n = 6) and chronic carotid body-denervated (n = 6, 1-2 yr) ponies were studied during 1) winter months over 3-4 days at 5 (control TA) and 23 degrees C and 2) summer months over 2-4 days at 21 (control TA), 30, and 12 degrees C. Neither rectal nor arterial temperature changed with any alteration of TA (P greater than 0.10). Skin temperature (Tsk) always changed by 2-4 degrees C in the same direction as changes in TA (P less than 0.01), and Tsk was the only variable that differed between summer and winter control TA. While breathing room air 24-48 h after TA was altered, pulmonary ventilation (VE) and breathing frequency (f) were approximately 100 and 300%, respectively, above control with elevated TA and approximately 25-50% below control with reduced TA (P less than 0.01). Changes in f were closely related to changes in Tsk. Tidal volume (VT) changed inversely with changes in TA. Generally, while breathing room air, arterial PCO2 (Paco2) did not change from control during the first 48 h of altered TA. In studies when inspired CO2 was elevated VT increased by the same amount at all TA; f increased at low and control TA but decreased at elevated TA; and VE and Paco2 both increased relatively less at elevated TA, but the VE-Paco2 slope was independent of TA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of altered ambient temperature on metabolic rate during CO2 inhalation.

The purpose of this study was to determine if the changes in O2 consumption (VO2) during CO2 inhalation could in part be due to stimulation of thermogenesis for homeothermy. Twelve ponies were exposed for 30-min periods to inspired CO2 (PIco2) levels of less than 0.7, 14, 28, and 42 Torr during the winter at 5 (neutral) and 23 degrees C ambient temperatures (TA) and during the summer at 21 (neutral TA), 30, and 12 degrees C. Elevating TA in both seasons resulted in an increased pulmonary ventilation (VE) and breathing frequency (f) (P less than 0.01) but no significant increase in VO2 (P greater than 0.05). Decreasing TA in the summer resulted in a decrease in VE and f (P less than 0.01) but no significant change in VO2 (P greater than 0.05). At neutral TA in both seasons, VO2 increased progressively (P less than 0.05) as PIco2 was increased from 14 to 28 and 42 Torr. The increases in VO2 during CO2 inhalation were attenuated (P less than 0.05) at elevated TA and accentuated at the relatively cold TA in the summer (P less than 0.05). Respiratory heat loss (RHL) during CO2 inhalation was inversely related to TA. Above a threshold RHL of 2 cal X min-1 X m-2, metabolic heat production (MHP) increased 0.3 cal X min-1 X m-2 for each unit increase in RHL during CO2 inhalation at the neutral and elevated TA. However, during cold stress in the summer, the slope of the MHP-RHL relationship was 1.6, indicating an increased MHP response to RHL.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Ventilatory acclimatization to hypoxia is not dependent on arterial hypoxemia.

Goats were prepared so that one carotid body (CB) could be perfused with blood in which the gas tensions could be controlled independently from the blood perfusing the systemic arterial system, including the brain. Since one CB is functionally adequate, the nonperfused CB was excised. To determine whether systemic arterial hypoxemia is necessary for ventilatory acclimatization to hypoxia (VAH), the CB was perfused with hypoxic normocapnic blood for 6 h [means +/- SE: partial pressure of carotid body O2 (PcbO2), 40.6 +/- 0.3 Torr; partial pressure of carotid body CO2 (PcbCO2), 38.8 +/- 0.2 Torr] while the awake goat breathed room air to maintain systemic arterial normoxia. In control periods before and after CB hypoxia the CB was perfused with hyperoxic normocapnic blood. Changes in arterial PCO2 (PaCO2) were used as an index of changes in ventilation. Acute hypoxia (0.5 h of hypoxic perfusion) resulted in hyperventilation sufficient to reduce average PaCO2 by 6.7 Torr from control (P less than 0.05). Over the subsequent 5.5 h of hypoxic perfusion, average PaCO2 decreased further, reaching 4.8 Torr below that observed acutely (P less than 0.05). Acute CB hyperoxic perfusion (20 min) following 6 h of hypoxia resulted in only partial restoration of PaCO2 toward control values; PaCO2 remained 7.9 Torr below control (P less than 0.05). The progressive hyperventilation that occurred during and after 6 h of CB hypoxia with concomitant systemic normoxia is similar to that occurring with total body hypoxia. We conclude that systemic (and probably brain) hypoxia is not a necessary requisite for VAH.

Adaptation, Physiological↗

Role of hilar nerve afferents in hyperpnea of exercise.

The objective of this study was to determine the role of hilar nerve (lung vagal) afferents in the hyperpnea of exercise. Ten ponies were studied before and 2-4 wk and 3-12 mo after sectioning only the hilar branches of the vagus nerves (HND). After HND, lung volume feedback to the medullary centers was attenuated as indicated in the anesthetized state by 1) attenuation or absence of the Hering-Breuer inflation reflex (P less than 0.01) and 2) attenuation of the lengthened inspiratory time (TI) when the airway was occluded at end expiration (P less than 0.01). Moreover, after HND in the awake state, there was an increase in the ratio of TI to total cycle time (P less than 0.01). These changes verify a compromise in lung innervation comparable to cervical vagotomy. Resting arterial PCO2, PO2, and pH were not altered following HND (P greater than 0.10). Moreover, at three levels of mild and moderate treadmill exercise, no difference in either the temporal pattern or the absolute levels of arterial blood gases and arterial pH was found between pre- and post-HND studies (P greater than 0.10). In addition, minute ventilation (VE) at rest and during exercise was not altered by HND (P greater than 0.10). However, 2-4 wk after HND the increase in breathing frequency (f) during exercise was less, whereas the increase in tidal volume during exercise was greater than pre-HND (P less than 0.05). The reduced f was due to an increase in TI with no change in expiratory time. We conclude that lung afferents via the hilar nerves influence the pattern of breathing at rest and during exercise in ponies.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗