Attenuation of the Acute Cardiovascular Responses to Haemorrhage by Tissue Injury in the Conscious Rat

Abstract

SUMMARYA moderate haemorrhage of 0-75 + 0-09 ml (100 g body weight)-1 (I 111 + 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 120 + 006 ml (100 g)-1 (> 195 + 1[5 % of estimated blood volume) produces a bradycardia and mnarked 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 & Thoren, 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.

Acute hemorrhagic shock decreases airway resistance in anesthetized rat

“…In humans, parasympathetic activation has been shown to be involved in the bradycardia associated with lower body negative pressure-induced hypovolemia (32). Previous studies in the literature suggest that reflex vagal activation is involved in the bradycardia associated with hypovolemia in the rat model of hemorrhagic shock (18,21). Parasympathetic activation is a possible mechanism for the overshoot observed in Raw on blood volume restoration.…”

The Effects of Primary Thoracic Blast Injury and Morphine on the Response to Haemorrhage in the Anaesthetised Rat

“…inhibition) and maintenance of blood pressure via the arterial baroreceptor reflex (Secher & Bie, 1985;Little et al 1989). As haemorrhage progresses, and blood loss exceeds 20-30 % of total blood volume, a depressor phase becomes apparent.…”

“…As haemorrhage progresses, and blood loss exceeds 20-30 % of total blood volume, a depressor phase becomes apparent. This involves a vagally mediated bradycardia (inhibited by atropine, Little et al 1989), a reduction in peripheral vascular resistance (Barcroft et al 1944;Evans & Ludbrook, 1991) and a marked fall in arterial blood pressure. This second phase is not due to a failure of the baroreflex, since the latter's sensitivity is increased at this stage (Little et al 1984), nor is it a preterminal event (Hoffman, 1972;Sander-Jensen et al 1986), but rather it is due to the activation of additional reflex(es).…”

“…The response to musculo-skeletal injury reduces or abolishes the bradycardia and delays the onset of hypotension (Little et al 1989). However, the interaction, if any, of blast injury with haemorrhage is unknown.…”

Ethanol augments the baroreflex‐inhibitory effects of sciatic nerve stimulation in the anaesthetized dog

“…Furthermore, it appears that the element of neural activity involved in producing the 'injury'-like effects of sciatic stimulation are mediated via small diameter fibres (possibly C fibres); recent studies have shown that stimulation of the sciatic nerve attenuates the vagal bradycardia seen when cardiac afferent fibres are activated. This mimics the effects of real injury on the bradycardia associated with a severe haemorrhage (Little, Marshall & Kirkman, 1989), and is dependent on small, rather than large, somatic afferent fibre activity in the sciatic nerve since it cannot be abolished by cooling the sciatic nerve to 3°C, which blocks transmission in large myelinated fibres (E. Kirkman, J. R. Banks, H. W. Marshall & R. A. Little, unpublished observations).…”