Tissue injury modifies the acute cardiovascular response to severe haemorrhage by attenuating reflex bradycardia and hypotension, likely via interaction with cardiac C fibre afferents.
Tissue injury may blunt reflex responses in haemorrhage; leaves open translation of C-fibre mechanisms to human trauma.
A moderate haemorrhage of 0.75 +/- 0.09 ml (100 g body weight)-1 (11.1 +/- 1.3% of estimated blood volume) in the conscious rat produces a tachycardia, possibly mediated by the baroreflex, which serves to maintain mean arterial blood pressure. A severe haemorrhage of 1.20 +/- 0.06 ml (100 g)-1 (greater than or equal to 19.5 +/- 1.5% of estimated blood volume) produces a bradycardia and marked hypotension. The bradycardia is reflex in nature and is due to an increased vagal efferent activity to the heart. This bradycardia is markedly attenuated in animals treated neonatally with capsaicin to render them deficient in C fibres, suggesting that peripheral C fibres (possibly cardiac C fibre afferents, Oberg & Thorén, 1972) are of importance in the bradycardic response to a severe haemorrhage. Concomitant tissue injury produced by bilateral hindlimb ischaemia in a group of animals with normal C fibre afferents markedly attenuates or abolishes the bradycardia and reduces the fall in mean arterial blood pressure produced by severe haemorrhage, although the tachycardia seen with smaller haemorrhages is affected to a much lesser degree. It is concluded that tissue injury can modify the cardiovascular response to a severe haemorrhage, possibly by interacting with the reflex effects of stimulating cardiac C fibre afferents.
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Little et al. (1989) studied this question.
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