Why the study?
What are the mechanisms of respiratory stimulation during severe hemorrhage in dogs?
What are the mechanisms of respiratory stimulation during severe hemorrhage in dogs?
Respiratory stimulation during severe hemorrhage in dogs is not solely dependent on sino-aortic reflexes or decreased blood flow to the respiratory center.
Answers are grounded in this paper and cite their sources.
Respiratory stimulation in hemorrhage may involve non-sino-aortic mechanisms in dogs; leaves open central or alternative pathways for mechanistic study.
The immediate effects of severe hemorrhage on respiratory rate and amplitude were determined in dogs before and after bilateral vagotomy and isolation of the carotid sinuses. The animals were anesthetized with morphine (3 mg/kg) intramuscularly and sodium pentobarbital (15 mg/kg) intravenously. The sino-aortic denervated animals showed no respiratory responses to 1–2 mg of sodium cyanide. Most of the animals showed immediate respiratory stimulation in response to hemorrhage before denervation, and in a large percentage of these the stimulation still could be elicited by hemorrhage after sino-aortic denervation. The rapid onset of the stimulation in the denervated animals and the fact that slow withdrawal of blood to produce a certain level of hypotension caused less stimulation than rapid withdrawal would indicate that decreased blood flow through the respiratory center may not be the basis for the response.
No takes yet. Share an insight, caveat, or question.
Schopp et al. (1957) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: