Autonomic cardiovascular control during hypoxia in the dog.

Hammill, Stephen C.; Wagner, Wiltz W.; Latham, L. P.; Frost, W W; Weil, John V.

doi:10.1161/01.res.44.4.569

Cited by 30 publications

(13 citation statements)

References 32 publications

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“…In the measurement of [3H]NE turnover, l-[(N)-7,8-3HjNE (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) Ci/mmol sp act; New England Nuclear, Boston, MA) was purified before use by column chromatography with alumina as described below. The [3H]NE was diluted to an appropriate concentration with isotonic saline and injected into the tail veins of unanesthetized animals in a total volume of 1.0 ml.…”

Section: Methodsmentioning

confidence: 99%

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

1983

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A B S T R A C T The sympathoadrenal responses to acute and chronic hypoxic exposure at 10.5 and 7.5% oxygen were determined in the rat. Cardiac norepinephrine (NE) turnover was used to assess sympathetic nervous system (SNS) activity, and urinary excretion of epinephrine (E) was measured as an index of adrenal medullary activity. The responses of the adrenal medulla and SNS were distinct and dependent upon the degree and duration of hypoxic exposure. Chronic hypoxia at 10.5% oxygen increased cardiac NE turnover by 130% after 3, 7, and 14 d of hypoxic exposure. Urinary excretion of NE was similarly increased over this time interval, while urinary E excretion was marginally elevated. In contrast, acute exposure to moderate hypoxia at 10.5% oxygen was not associated with an increase in SNS activity; in fact, decreased SNS activity was suggested by diminished cardiac NE turnover and urinary NE excretion over the first 12 h of hypoxic exposure, and by a rebound increase in NE turnover after reexposure to normal oxygen tension. Adrenal medullary activity, on the other hand, increased substantially during acute exposure to moderate hypoxia (2-fold increase in urinary E excretion) and severe hypoxia (>10-fold). In distinction to the lack of effect of acute hypoxic exposure (10.5% oxygen), the SNS was markedly stimulated during the first day of hypoxia exposure at 7.5% oxygen, an increase that was sustained throughout at least 7 d at 7.5% oxygen. These results demonstrate that chronic exposure to moderate and severe hypoxia increases the activity of the SNS and adrenal medulla, the effect being

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Section: Methodsmentioning

confidence: 99%

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

1983

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“…8,10,11 Furthermore, studies on parasympathetic neural control of HR in hypoxia have yielded discrepant findings. 4,12,13 The functional significance of vagal control of HR at altitude for systemic oxygen transport and hemodynamic responses has also never been studied. In this regard, a reduction in maximal cardiac output (Q) and oxygen delivery during exercise has also been documented with altitude acclimatization, 3,14 -17 yet it is unknown whether this is a result of parasympathetic neural control of HR.…”

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confidence: 99%

Parasympathetic Neural Activity Accounts for the Lowering of Exercise Heart Rate at High Altitude

et al. 2001

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Background-In chronic hypoxia, both heart rate (HR) and cardiac output (Q) are reduced during exercise. The role of parasympathetic neural activity in lowering HR is unresolved, and its influence on Q and oxygen transport at high altitude has never been studied. Methods and Results-HR, Q, oxygen uptake, mean arterial pressure, and leg blood flow were determined at rest and during cycle exercise with and without vagal blockade with glycopyrrolate in 7 healthy lowlanders after 9 weeks' residence at Ն5260 m (ALT). At ALT, glycopyrrolate increased resting HR by 80 bpm (73Ϯ4 to 153Ϯ4 bpm) compared with 53 bpm (61Ϯ3 to 114Ϯ6 bpm) at sea level (SL). During exercise at ALT, glycopyrrolate increased HR by Ϸ40 bpm both at submaximal (127Ϯ4 to 170Ϯ3 bpm; 118 W) and maximal (141Ϯ6 to 180Ϯ2 bpm) exercise, whereas at SL, the increase was only by 16 bpm (137Ϯ6 to 153Ϯ4 bpm) at 118 W, with no effect at maximal exercise (181Ϯ2 bpm). Despite restoration of maximal HR to SL values, glycopyrrolate had no influence on Q, which was reduced at ALT. Breathing FIO 2 ϭ0.55 at peak exercise restored Q and power output to SL values. Conclusions-Enhanced parasympathetic neural activity accounts for the lowering of HR during exercise at ALT without influencing Q. The abrupt restoration of peak exercise Q in chronic hypoxia to maximal SL values when arterial PO 2 and SO 2 are similarly increased suggests hypoxia-mediated attenuation of Q. Key Words: heart rate Ⅲ cardiac output Ⅲ hypoxia Ⅲ nervous system, autonomic Ⅲ exercise A cclimatization to high altitude induces alterations in autonomic neural control of the cardiovascular system, exemplified by a marked reduction in maximal heart rate (HR). [1][2][3][4] Christensen and Forbes 1 first described the reduction in peak exercise HR at high altitude in 1937, yet the mechanism underlying this response has remained elusive for Ͼ60 years. Adaptations in both parasympathetic and sympathetic neural tone have been implicated in the relative bradycardia response to exercise in chronic hypoxia. A progressive influence of parasympathetic activity on HR occurs with duration of altitude exposure either via a central effect of hypoxia, 4,5 by greater influence at the cardiac receptor level, 6 -8 or by cholinergic antagonism. 9 It has not been clearly shown whether enhanced vagal tone actually causes the lower HR, ie, by a direct adaptation to hypoxia, or whether a greater vagal influence is exhibited due to a lowering of HR by another mechanism, eg, lower sympathetic activation, reduced cardiac sensitivity to adrenergic stimulation, or modulation by other (eg, adenosinergic) receptors. 8,10,11 Furthermore, studies on parasympathetic neural control of HR in hypoxia have yielded discrepant findings. 4,12,13 The functional significance of vagal control of HR at altitude for systemic oxygen transport and hemodynamic responses has also never been studied. In this regard, a reduction in maximal cardiac output (Q) and oxygen delivery during exercise has also been documented with altitude acclimatization, 3,14 -...

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“…Changing the concentrations of AII and BK can be expected to initiate altered concentrations of other mediator substances; the observed circulatory effects result from a new balance among these various mediators. Acute hypoxia stimulates the release of catecholamines from the adrenal medulla (25) and affects the balance between the parasympathetic and sympathetic limbs ofthe peripheral autonomic nervous system (26). In hypoxic states there are multiple points of interaction between the kallikrein-kinin and reninangiotensin systems and autonomic cardiovascular control.…”

Section: Resultsmentioning

confidence: 99%

Impaired Angiotensin Conversion and Bradykinin Clearance in Experimental Canine Pulmonary Emphysema

Stalcup¹,

Leuenberger²,

Lipset³

et al. 1981

J. Clin. Invest.

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A B S T R A C T Chronic hypoxic lung diseases are associated with abnormal blood pressure regulation. Because the lung is the principal site of angiotensin conversion and because hypoxia decreases converting enzyme activity, we examined whether angiotensin converting enzyme activity was impaired in lung disease. 12 dogs received a 6 wk course of aerosolized and intratracheal papain that produced moderate panlobular emphysema. These dogs and 24 control dogs were anesthetized and sampling catheters were placed under fluoroscopic control. Angiotensin conversion was measured by a blood pressure response bioassay. Pulmonary converting enzyme activity was also assessed by infusing bradykinin (BK) and using radioimmunoassay to measure the instantaneous clearance of BK and the concentration of BK in the pulmonary artery which first produced spillover of BK into left atrial blood. Angiotensin conversion was reduced in the emphysematous dogs to 81.1% (13.2 SD) from 92% (6 SD) in the control dogs (P < 0.01). Instantaneous clearance of BK in the emphysematous dogs was only slightly reduced (93%), despite reduction in their Pao2 to 75 mm Hg, indicating that the greatest proportion of the perfused vascular bed was exposed to alveolar Po2 of >90 mm Hg. However, the barrier to BK passage provided by the lung, and measured by the spillover level, was reduced Y4 to ½2 that observed in control animals. That the defect was promptly corrected by supplemental oxygen indicates that regional pulmonary vascular converting enzyme activity had been impaired by regional alveolar hypoxia, which permitted some peptide to pass through the lungs (2). In men with lung disease sufficient to reduce arterial Po2 below 60 Torr, the same defects were observed and were reversed when supplemental oxygen was provided (3). Cohn and Luria (4) found that men with pulmonary emphysema failed to demonstrate increased systemic vascular resistance in response to shock, regardless of the precipitating event. Anderson et al. (5) found that the resting blood pressures of 30 men with mild to severe emphysema were significantly lower than controls. Other studies suggest that the defect is not exclusive for emphysema, but extends to other lung disease. In patients with cystic fibrosis, whether mild or severe, Lieberman and Rodbard (6) observed lower blood pressure; these patients also had a lower pressor response to exercise. The underlying mechanisms contributing to all ofthese conditions remain unknown, but they raise the possibility ofan interplay between disease ofthe lung parenchyma and control of systemic blood pressure in the whole organism.We have shown that acute hypoxia reduces the activity of angiotensin converting enzyme (7-9). pressor response to injected angiotensin I, as well as pulmonary bradykinin clearance, was reduced in hypoxic animals. We speculated that injury to the pulmonary vascular bed, occurring as a consequence ofthe development of pulmonary emphysema, could interfere with converting enzyme activity and blood pressure regulation in two ...

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Autonomic cardiovascular control during hypoxia in the dog.

Cited by 30 publications

References 32 publications

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

Sympathoadrenal responses to acute and chronic hypoxia in the rat.

Parasympathetic Neural Activity Accounts for the Lowering of Exercise Heart Rate at High Altitude

Impaired Angiotensin Conversion and Bradykinin Clearance in Experimental Canine Pulmonary Emphysema

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