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Biomedical subjects

H V Forster

Publications and source records attributed to H V Forster.

At least 109 records · Page 6Linked to original sources
PubMed1985

Effect of hilar nerve denervation on breathing and arterial PCO2 during CO2 inhalation.

We determined the effects of denervating the hilar branches (HND) of the vagus nerves on breathing and arterial PCO2 (PaCO2) in awake ponies during eupnea and when inspired PCO2 (PICO2) was increased to 14, 28, and 42 Torr. In five carotid chemoreceptor-intact ponies, breathing frequency (f) was less, whereas tidal volume (VT), inspiratory time (TI), and ratio of TI to total cycle time (TT) were greater 2-4 wk after HND than before HND. HND per se did not significantly affect PaCO2 at any level of PICO2, and the minute ventilation (VE)-PaCO2 response curve was not significantly altered by HND. Finally, the attenuation of a thermal tachypnea by elevated PICO2 was not altered by HND. Accordingly, in carotid chemoreceptor-intact ponies, the only HND effect on breathing was the change in pattern classically observed with attenuated lung volume feedback. There was no evidence suggestive of a PCO2-H+ sensory mechanism influencing VE, f, VT, or PaCO2. In ponies that had the carotid chemoreceptors denervated (CBD) 3 yr earlier, HND also decreased f, increased VT, TI, and TT, but did not alter the slope of the VE-PaCO2 response curve. However, at all levels of elevated PICO2, the arterial hypercapnia that had persistently been attenuated, since CBD was restored to normal by HND. The data suggest that during CO2 inhalation in CBD ponies a hilar-innervated mechanism influences PaCO2 by reducing physiological dead space to increase alveolar ventilation.

Animals↗
PubMed1985

Changes in breathing when switching from nares to tracheostomy breathing in awake ponies.

We assessed the consequences of respiratory unloading associated with tracheostomy breathing (TBr). Three normal and three carotid body-denervated (CBD) ponies were prepared with chronic tracheostomies that at rest reduced physiological dead space (VD) from 483 +/- 60 to 255 +/- 30 ml and lung resistance from 1.5 +/- 0.14 to 0.5 +/- 0.07 cmH2O . l-1 . s. At rest and during steady-state mild-to-heavy exercise arterial PCO2 (PaCO2) was approximately 1 Torr higher during nares breathing (NBr) than during TBr. Pulmonary ventilation and tidal volume (VT) were greater and alveolar ventilation was less during NBr than TBr. Breathing frequency (f) did not differ between NBr and TBr at rest, but f during exercise was greater during TBr than during NBr. These responses did not differ between normal and CBD ponies. We also assessed the consequences of increasing external VD (300 ml) and resistance (R, 0.3 cmH2O . l-1 . s) by breathing through a tube. At rest and during mild exercise tube breathing caused PaCO2 to transiently increase 2-3 Torr, but 3-5 min later PaCO2 usually was within 1 Torr of control. Tube breathing did not cause f to change. When external R was increased 1 cmH2O . l-1 . s by breathing through a conventional air collection system, f did not change at rest, but during exercise f was lower than during unencumbered breathing. These responses did not differ between normal, CBD, and hilar nerve-denervated ponies, and they did not differ when external VD or R were added at either the nares or tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1985

Effect of upper airway CO2 on breathing in awake ponies.

We determined whether the [CO2] in the upper airways (UA) can influence breathing in ponies and whether UA [CO2] contributes to the attenuation of a thermal tachypnea during periods of elevated inspired CO2. Six ponies were studied 1 mo after chronic tracheostomies were created. For one protocol the ponies were breathing room air through a cuffed endotracheal tube. Another smaller tube was placed in the tracheostomy and directed up the airway. By use of this tube, a pump, and prepared gas mixtures, UA [CO2] was altered without affecting alveolar or arterial PCO2. When the ponies were at a neutral environmental temperature (TA) and breathing frequency (f) was 8 breaths X min-1, increasing UA [CO2] up to 18-20% had no effect on f. However, when TA was increased 20 degrees C to increase f to 50 breaths X min-1, then increasing UA [CO2] to 6% or to 18-20% reduced f by 5 +/- 1.7 (SE) and 12 +/- 1.6 breaths X min-1, respectively (t = 3.3, P less than 0.01). These data suggest that in the pony there exists a UA CO2-H+ sensory mechanism. For a second protocol the ponies were breathing a 6% CO2 gas mixture for 15 min in the normal fashion over the entire airway (nares breathing, NBr) or they were breathing this gas mixture for 15 min through the cuffed endotracheal tube (TBr). At a neutral TA, increasing inspired [CO2] to 6% resulted in a 6-breaths X min-1 increase in f during both NBr and TBr.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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↗
PubMed1984

Temporal pattern of pulmonary gas exchange during exercise in ponies.

We characterized the temporal patterns of pulmonary O2 consumption (VO2) and CO2 excretion (VCO2) in exercising ponies. We also assessed the cardiac, ventilatory, and hematologic contributions to the VO2-VCO2 changes during exercise. At five moderate treadmill work loads in normal ponies, VO2 and VCO2 generally increased progressively throughout the 1st min reaching, respectively, approximately 95 and 80% of steady state by 45-60 s. Between 1 and 1.5 min, Vo2 and Vco2 were either stable or they decreased 300-500 ml, but then each increased slightly, reaching steady-state levels between 3 and 5 min. The increases to steady-state VO2 and VCO2 were clearly not monoexponential. Arterial O2 content (CaO2) increased during exercise, presumably because of mobilization of stored splenic erythrocytes. For example, after 1 and 6 min at 6 mph 3% grade, CaO2 had increased above rest by 3.2 and 4.9 vol%, respectively (P less than 0.05). Hyperventilation during exercise decreased arterial CO2 content (CaCO2) below rest. For example, after 1 and 6 min at 6 mph 3% grade, CaCO2 had decreased below rest by 2.8 and 1 vol%, respectively (P less than 0.05). At all work loads, heart rate (HR) and presumably cardiac output increased rapidly during the 1st min, reaching a maximum by approximately 45 s. HR then decreased (P less than 0.05), reaching a steady state by 3 min of exercise. During the first 1.5 min of exercise in carotid body-denervated (CBD) ponies, the changes in VO2, HR, and CaO2 were temporally delayed relative to the normals, whereas the changes in VCO2 and CaCO2 were relatively augmented.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Independence of exercise hypocapnia and limb movement frequency in ponies.

The objective of this study was to determine whether changes in limb motion per se influence arterial CO2 partial pressure (PaCO2) during muscular exercise in ponies. Fifteen ponies were studied at rest and during 8 min of treadmill exercise when the work load was constant or when the work load was increased after the 4th min. Five different treadmill settings were selected to provide for a range of metabolic rate achieved with primary changes in either speed or grade (1.8 mph at 3, 8, and 15% grade; or 3 and 6 mph at 3% grade). The ponies exercised either on all four legs or on only the hindlegs. Step frequencies were 49, 66, and 99 at 1.8, 3, and 6 mph, respectively. During all work tasks PaCO2 decreased maximally 30-60 s after the work task was initiated from rest or from a less intense level of exercise. This nadir in PaCO2 was followed by some recovery with a stable level of mild hypocapnia (delta PaCO2) maintained after 3-4 min. The delta PaCO2 was directly related to O2 consumption (VO2) (P less than 0.01). The delta PaCO2-VO2 regression slopes did not differ between speed and grade VO2 changes nor between four- and two-legged exercise (P greater than 0.10). These data suggest that neither frequency of limb movement nor the number of limbs moving are major factors in the PaCO2 (and alveolar ventilation) response to exercise in ponies. We conclude that the apparent difference in PaCO2 regulation during exercise between ponies (hypocapnia) and humans (isocapnia during walking and bicycling) is not related to a species difference in the number of limbs employed in the exercise task.

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

Measurement of ventilation using digitally filtered transthoracic impedance.

A seven-stage low-pass digital filter was used to remove the cardiac artifact and motion interference from a respiratory transthoracic impedance signal in human subjects. After removal of these artifacts, the mean difference from a conventional gasometer technique fell from 5% to 1.6%. When the impedance technique was used to measure ventilation during air breathing, the addition of a breathing valve with a mouthpiece and noseclip induced the following changes in ventilatory parameters: 7% drop in frequency, 24% increase in tidal volume, 49% increase in inspiratory time, 56% increase in expiratory time, 10% decrease in inspiratory flow rate, and 4% decrease in ratio of respiratory time to total breath duration. These alterations were not significant at elevated inspired CO2 levels. The digitally filtered transthoracic impedance technique provides an accurate technique for measuring ventilatory parameters without the perturbations induced by using a conventional breathing valve technique even when cardiac and motion artifacts were prominent.

Adult↗
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

Regulation of PaCO2 and ventilation in humans inspiring low levels of CO2.

This study was designed to determine whether 1) arterial PCO2 (PaCO2) increases when inspired PCO2 (PICO2) is increased from less than 0.4 Torr (eupnea) to 7 or 14 Torr, and 2) ventilatory sensitivity to CO2 (delta VE/ delta PaCO2) is greater at low levels of PICO2 (7-21 Torr) than it is at higher levels (28-42 Torr). Human subjects were studied while seated in an environmental chamber that permitted alteration of PICO2 by changing the chamber PCO2. In study 1, arterial blood was sampled over the final 5 min of a eupneic period and again 10-15 min later when PICO2 was 7 or 14 Torr. With this protocol, PACO2 was increased above eupnea by 0.7 (P less than 0.02) and 0.9 Torr (P less than 0.01) when PICO2 was 7 and 14 Torr, respectively. In study 2, arterial blood was sampled every 5 min during two 1-h periods of eupnea that were separated by 3 h during which PICO2 was increased by 7 Torr each 0.5 h. With this protocol there was no consistent difference in PACO2 between eupneic periods and periods when PICO2 was 7-14 Torr. There was a progressively increased hypercapnia as PICO2 was increased from 7 to 42 Torr. The delta VE/ delta PaCO2 was less than half for data obtained at low relative to high PICO2. The two studies demonstrated that measurement error and physiologic variation necessitate using a "powerful" experimental design (study 1) to detect small increases in PaCO2. On the basis of these results, we have concluded that there is no apparent reason to postulate a sensory mechanism other than the carotid and intracranial chemoreceptors to account for the hyperpnea during CO2 inhalation. Specifically, isocapnic hyperpnea probably does not occur.

Adult↗
PubMed1982

Role of the carotid body in hyperpnea of moderate exercise in goats.

In the present study the ventilatory response to exercise was measured in goats before and after carotid body excision (CBE) (n = 7) or sham operation (n = 1). Nine-minute periods of moderate treadmill walking were carried out under three conditions: 4.8 kph, 0% grade during normoxia and hypoxia (arterial O2 tension approximately 43 Torr) and 4.8 kph, 5% grade during normoxia. Ventilatory variables, metabolic rate, and arterial blood acid-base and blood gases were measured at 30-s intervals for the first 3 min and again during the 6th and 9th min of exercise. In normal goats during exercise in normoxia, ventilation changed in proportion to changes in metabolic rate resulting in arterial CO2 tension (PaCO2) and arterial pH (pHa) homeostasis throughout exercise. CBE resulted in nearly equivalent hypoventilation during steady-state rest and exercise (delta PaCO2 approximately equal to 5--7 Torr) during normoxia and loss of the positive interaction between hypoxia and exercise. There was also a significant disruption of PaCO2-pHa homeostasis during the first 30 s of exercise after CBE when PaCO2 was 3 Torr below rest and pHa was 0.03 units above rest. Our data indicate: 1) that the carotid chemoreceptors may contribute a similar proportional drive to breathe during rest and exercise; 2) that transient hyperventilation at the onset of exercise after CBE may indicate an important neural drive to breathe that is normally damped by intact peripheral chemoreceptors; and 3) that the mechanism linking ventilation to CO2 production remains intact after CBE.

Animals↗
PubMed1982

Ventilatory response to inspired CO2 in normal and carotid body-denervated ponies.

The purpose of these studies was to gain insight into mechanisms regulating pulmonary ventilation (VE), arterial CO2 partial pressure (PaCO2), and arterial pH (pHa) in ponies when inspired CO2 partial pressure (PICO2) is above normal. Ponies were studied four times daily each weekday for 2 wk in an environmental chamber. Each study consisted of a 15-min control period (PICO2 = 0.7 Torr) followed by a 15- to 30-min experimental period during which PICO2 in the chamber was 0.7, 7, 14, 21, 28, or 42 Torr (PIO2 = 147 Torr throughout). Between 11 and 15 min of each period, four 3-ml samples of arterial blood were drawn, each over 45 s. In 12 normal ponies, elevation of PICO2 to 7 Torr caused PaCO2 to increase approximately 0.4 Torr (P less than 0.01) and pHa to decrease approximately 0.003 (P less than 0.02) relative to control. The hypercapnia and acidosis increased progressively as PICO2 was increased in 7- to 14-Torr increments to 42 Torr (P less than 0.02). Accordingly, the hyperpnea in these ponies during CO2 inhalation could have been mediated by carotid and intracranial chemoreceptors. One month after carotid body denervation (CBD) in nine ponies, PaCO2 during control conditions was 6 Torr above normal, but during CO2 inhalation, PaCO2 changed less from control than during CO2 inhalation before CBD (P less than 0.01). The delta VE/ delta PaCO2 near eupneic PaCO2 appeared to be above normal 1 mo after CBD (P less than 0.01). The mechanism of this increase was not discernible from our data. Finally, our data indicated that the magnitude of the hypercapnia and acidosis during CO2 inhalation was inversely related to PaCO2 and breathing frequency during control conditions.

Acid-Base Equilibrium↗
PubMed1982

Effect of elevated PICO2 on metabolic rate in humans and ponies.

The primary purpose of this study was to determine the effect of acute (20-30 min) elevations of inspired CO2 partial pressure (PICO2) on whole-body O2 consumption (VO2). In human subjects, VO2 increased approximately 15 ml.min-1.m-2 with each 7-Torr increment in PICO2 from 0.4 to 28 Torr (P less than 0.05), but VO2 did not change significantly when PICO2 was increased from 28 to 35 and 42 Torr (P greater than 0.05). In ponies, VO2 did not change when PICO2 was increased from 0.7 to 7 Torr (P greater than 0.05), but it increased about 6 ml.min-1.m-2 with each 7-Torr increment in PICO2 from 7 to 28 Torr, and it increased 18 ml.min-1.m-2 when PICO2 was increased from 28 to 42 Torr (P less than 0.05). At low PICO2 the delta VO2/ delta VE was 25 and 7 ml/l for humans and ponies, respectively, where VE is pulmonary ventilation. These values exceeded the expected O2 cost of breathing; hence, some factor, such as shivering or nonshivering thermogenesis, contributed to the elevated VO2. At high PICO2, VE increased without a proportional increase in VO2; thus the delta VO2/ delta VE decreased to about 2.5 ml/l in ponies and to near 0.0 in humans. Accordingly, at high PICO2 some VO2-suppressing factor partially counteracted those factors stimulating VO2. The maximum decrease from control pHa was 0.061 and 0.038 in humans and ponies, respectively. It is questionable whether this mild acidosis was sufficient to suppress VO2. In both species, pulmonary excretion of metabolic CO2 and the respiratory exchange ratio were below control during CO2 inhalation (P less than 0.01), which suggested an increased tissue storage of CO2.

Adult↗
PubMed1981

Effect of peripheral chemoreceptor denervation on acclimatization of goats during hypoxia.

The purpose of this study was to determine the effect of peripheral chemoreceptor denervation on ventilatory acclimatization of goats during chronic hypoxia. After 1 h of stimulated altitude (PB 450 Torr), arterial O2 tension (PaO2) in seven normal goats averaged 42 Torr, and arterial CO2 tension (PaCO2) was 1.3 Torr below control (P less than 0.001). In these goats nearly 66% of the increase in alveolar ventilation (VA) associated with acclimatization occurred between 1.5 and 4 h of hypoxia. Acclimatization was complete by the 3rd day of hypoxia, and it caused 1) a 23% increase in VA/CO2 output (P less than 0.001); 2) a 5-Torr increase in PaO2 (P less than 0.001); and 3) a 6.5-Torr decrease in PaCO2 (P less than 0.001). Denervation of the carotid chemoreceptors in seven goats caused hypoventilation during eupnea at sea level (PaCO2 change from control +7 Torr, P less than 0.001). Denervation also attenuated but did not eliminate peripheral chemoreceptor responsiveness. No additional changes were observed following attempted denervation of the aortic chemoreceptors. After 1 h of simulated altitude (PB 530 Torr), PaO2 in the denervated goats averaged 46 Torr, and PaCO2 was increased 1.1 Torr above control (P less than 0.001). In these goats VA did not change significantly during the subsequent 3 days of hypoxia. Accordingly, we conclude that the peripheral chemoreceptors are essential for ventilatory acclimatization of goats during chronic hypoxia.

Acclimatization↗
PubMed1980

Depression of ventilation by dopamine in goats--effects of carotid body excision.

Dopamine (DA) given IV by bolus injection (5, 10, 20 micrograms/kg) and by slow IV infusion (20 micrograms . kg . min) depressed VE significantly in awake normoxic goats. These responses were attenuated but not eliminated during hypoxia (FIO2 = 0.14) and hyperoxia (FIO2 = 1.0). After administering haloperidol (0.3 mg/kg) or removing the carotid bodies (CBE) there was greater attenuation of the response to DA. In normal goats haloperidol also caused a significant increase in ventilatory response to acute hypoxia and exaggerated depression of VE after 3--5 breaths O2 during steady-state hypoxia. After CBE haloperidol caused mild hypoventilation (delta PaCO2 = +2.5 Torr). CBE induced hypoventilation in goats (delta PaCO2 = +7.8 Torr) and reduced, but did not totally eliminate, peripheral chemoreceptor responses to acute stimuli (NaCN injection, transient N2 and transient O2 breathing). Attempted aortic body denervation did not eliminate these residual responses. We conclude: (1) DA may function as a modulator of carotid body (CB) function in the goat, (2) there may be central excitatory DA receptors in the goat, (3) the CB is important in regulating resting ventilation in the goat.

Animals↗