Why the study?
Does interruption of sympathetic pathways alter cardiac and catecholamine responses during hemorrhagic hypotension in dogs?
Does interruption of sympathetic pathways alter cardiac and catecholamine responses during hemorrhagic hypotension in dogs?
Sympathetic pathway interruption during hemorrhagic hypotension in dogs blunts the rise in heart force and catecholamines while preserving responsiveness to exogenous norepinephrine.
Answers are grounded in this paper and cite their sources.
Sympathetic interruption may blunt compensatory responses in canine hemorrhage; leaves open translation to human hypovolemic shock.
Hemorrhagic hypotension was observed for several hours in open-chest dog preparations under pentobarbital anesthesia. Heart force, as recorded from a strain gage arch on the right ventricle, followed a pronounced upward trend above control levels in some cases while in others there were variable grades of cardiac depression. Plasma epinephrine levels progressively increased, reaching extreme values at terminal stages; norepinephrine levels were only moderately increased. Force and pressor responses to injected norepinephrine progressively decreased in association with progressive acidosis. Following interruption of sympathetic pathways with extradural procaine infusions or with ganglionic blocking agents, hemorrhage caused less pronounced increments in heart force and catechol amine levels while responsiveness to injected norepinephrine was better maintained.
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Walton et al. (1959) studied this question.
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