Reflex changes in heart rate during chemoreceptor stimulation in monkeys.

Area of Science:

• Cardiovascular Physiology
• Neuroscience

Background:

• Arterial chemoreceptors play a role in cardiovascular regulation.
• The specific reflexes elicited by arterial chemoreceptor stimulation in nonhuman primates require further elucidation.

Purpose of the Study:

• To investigate the heart rate responses to arterial chemoreceptor stimulation via apneic asphyxia and sodium cyanide injections in anesthetized monkeys.
• To differentiate the roles of cardioacceleratory and cardioinhibitory reflexes in modulating heart rate during chemoreceptor activation.

Main Methods:

• Monkeys were anesthetized, artificially ventilated, and paralyzed.
• Apneic asphyxia and intracarotid sodium cyanide injections were administered.
• Heart rate changes were recorded, and pharmacological agents (propranolol, atropine) were used to block specific pathways.
• Phrenic efferent activity was monitored to assess central respiratory drive.

Main Results:

• Apneic asphyxia and sodium cyanide induced tachycardia, bradycardia, or both, depending on the neuromuscular blocking agent used.
• Tachycardia was abolished by propranolol, and bradycardia by atropine, indicating involvement of beta-adrenergic and cholinergic pathways.
• Prior ventilation with 100% oxygen eliminated heart rate responses.
• Increased neural discharge in phrenic efferent activity was observed, suggesting a central respiratory drive, but this did not solely determine the heart rate outcome.

Conclusions:

• Arterial chemoreceptor stimulation in nonhuman primates triggers both cardioacceleratory and cardioinhibitory reflexes.
• The observed heart rate response is a result of the interplay between these opposing reflex mechanisms.
• Central respiratory drive influences, but does not solely dictate, the net heart rate response to chemoreceptor stimulation.