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Oxygen consumption after massive sympathetic nervous system discharge.
S A Lang1, M B Maron, S A Signs
1Department of Physiology, Northeastern Ohio Universities, College of Medicine, Rootstown 44272.
The American Journal of Physiology
|March 1, 1989
Summary
Massive sympathetic nervous system activation increases oxygen demand, potentially due to adrenal hormones. This heightened metabolic rate may challenge oxygen balance in patients with neurogenic pulmonary edema.
Area of Science:
- Physiology
- Cardiovascular Research
- Pulmonary Medicine
Background:
- Sympathetic nervous system (SNS) activation is implicated in neurogenic pulmonary edema (NPE).
- The impact of SNS activation on oxygen demand (VO2) requires further elucidation.
- Calorigenic agents like epinephrine (EPI) and norepinephrine (NE) may play a role.
Purpose of the Study:
- To investigate whether massive SNS activation increases oxygen consumption (VO2).
- To determine the role of adrenal catecholamines in mediating elevated VO2 during SNS activation.
- To assess the implications for oxygen supply-demand balance in NPE.
Main Methods:
- Measurements of VO2 and plasma EPI/NE concentrations in alpha-chloralose-anesthetized dogs.
- Administration of intracisternal (ic) veratrine to stimulate SNS, intravenous (iv) veratrine, or ic saline.
- Comparison between intact animals and those with clamped adrenal blood vessels.
Main Results:
- Intracisternal veratrine significantly increased VO2 by 31.7% and elevated plasma EPI and NE levels.
- Adrenal clamping abolished VO2 increases and EPI elevation, while attenuating NE increase.
- Neither ic saline nor iv veratrine administration altered VO2 or catecholamine levels significantly.
Conclusions:
- Elevated VO2 during SNS activation appears to be mediated by adrenal catecholamines.
- Increased metabolic rate due to SNS activation may impair oxygen supply-demand balance in severe NPE patients.