CO₂asphyxia increases plasma norepinephrine in rats via sympathetic nerves

Abstract

The objective of this study was to determine whether the plasma norepinephrine (NE) increase in rats exposed to CO2 asphyxia was due to adrenal gland release or sympathetic nerve ending (SNS) release. Plasma NE was measured by high-performance liquid chromatography in hypertensive and normotensive rats using the following protocol: control session, CO2 exposure, N2 exposure, reserpine + CO2, and adrenalectomy + CO2. Four strains of male and female rats were used: spontaneously hypertensive rats, Wistar-Kyoto rats, and two congenic strains with different Y chromosomes. The same rats were used throughout the experiment ( n = 80). Blood pressure measured by aortic telemetry increased ∼50–60 mmHg in response to CO2 in all strains. CO2 increased NE 6–10× in all strains and both genders. N2 produced a significant increase in NE (73% of CO2 response). Reserpine significantly decreased (67%) plasma NE after CO2. Adrenalectomy did not significantly reduce the NE response to CO2. In conclusion, the increase in plasma NE after CO2 was associated with SNS release and not adrenal medullary release, was mainly due to hypoxia, and was not a specific response to CO2.

Chronic rosiglitazone treatment restores AMPKα2 activity in insulin-resistant rat skeletal muscle

“…Because hypoxia stimulates AMPK activity and a catecholamine response (3,15), the combination of euthanasia by CO 2 asphyxiation and the elapsed time between tissue collection and freezing might have resulted in an altered intracellular environment that could have contributed to changes in AMPK activity. These factors are potential limitations of the present study.…”

Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest

“…Sudden death induced by a life-threatening stressor is postulated to result from a generalized sympathetic storm within the autonomic nervous system (3). Consistent with this view, exposure to carbon dioxide leads to an immediate systemic surge of neurally released norepinephrine in the asphyxic rats (11); human patients with sustained ventricular arrhythmias exhibit higher levels of plasma norepinephrine levels (12). Despite the hypothesized role of brain-heart connections in sudden death, however, simultaneous and detailed analysis of the dying brain and heart has not been reported.…”

Sympathetic Neurotransmitters in Neuroblastoma – Between Physiology and Pathology

“…Phenylepinephrine, a non-vasoconstrictive -AR agonist, has been shown to induce endothelial cell proliferation and migration, as well as promote capillary formation. These effects were potentiated by hypoxia (Vinci et al, 2007), which is also a known stimulator of norepinephrine release from the sympathetic nerves (Borovsky et al, 1998). Thus, the direct angiogenic effect of norepinhephrine can be particularly pronounced in hypoxic areas of tumors.…”