Bradycardia during reversible haemorrhagic shock - A forgotten observation?
Available from: Peter Nissen
- "It is probably without exception that HR is monitored during OLT and deviations in HR in response to variation in CBV are therefore of interest. In textbook descriptions of hypovolaemic shock it is stated often that tachycardia is the arterial baroreceptor response to a low blood pressure (Secher & Bie, 1985). Yet the common, both experimental and clinical finding is that the HR response to central hypovolaemia encompasses three stages (Secher et al., 1992) (Fig. 6). "
Available from: Johannes J Van Lieshout
- "It remains, therefore, perplexing that medical textbooks (and the Advanced Trauma Life Support guidelines; www.atls.dk) do not regularly provide an accurate description of the heart rate (HR) and blood pressure responses to haemorrhage (Secher & Bie, 1985). "
Available from: onlinelibrary.wiley.com
- "In contrast to this study, high doses of naloxone administered centrally have been shown to delay the decompensatory phase of the response to haemorrhage in conscious sheep (Frithiof & Rundgren, 2006; Frithiof et al. 2007) and rabbits (Evans et al. 1989). However, haemorrhage-induced bradycardia is much smaller in these species compared with the rat (Ohnishi et al. 1997) and man (Barcroft et al. 1944; Secher & Bie, 1985). "
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ABSTRACT: Severe haemorrhage leads to a reflex bradycardia and hypotension. This is thought to be protective, but is attenuated by both concomitant musculoskeletal injury and exogenous morphine. The aim of this study was to determine whether the injury-induced attenuation of the response to severe haemorrhage could be blocked by naloxone. Male Wistar rats, terminally anaesthetized with alphadolone/alphaxalone (19-20 mg kg(-1) h(-1)I.V.), were randomly allocated to one of four groups. In groups I and IV, haemorrhage was simple [40% of estimated total blood volume (BV)], while in groups II and III it was initiated 10 min after the onset of bilateral hindlimb ischaemia (a model of musculoskeletal injury). Groups I and II received 20 microl of 0.9% saline intracerebroventricularly (I.C.V.) immediately before haemorrhage, while groups III and IV received 20 microg of naloxone I.C.V., in the same volume. In group I, the bradycardia reached its peak after the loss of 32.8 +/- 0.3% BV (mean +/- S.E.M.). Blood pressure did not fall significantly until the loss of 15.0 +/- 3.0% BV. The response in group IV was not significantly different from group I. By contrast, the bradycardia was absent after similar blood losses in groups II and III, while hypotension was attenuated. These results indicate that naloxone, at a dose known to be effective in blocking mu-opioid receptors and preventing other aspects of the response to injury, does not prevent the injury-induced attenuation of the response to severe haemorrhage. Thus the attenuation of the response to blood loss by injury is unlikely to be mediated via the mu-opioid receptors.
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