Severe hypotensive haemorrhage results in a biphasic response, characterized by an initial increase in heart rate and sympathetic vasomotor activity (phase I) followed by a life-threatening hypotension, accompanied by profound sympathoinhibition and bradycardia (phase II). The phase II response is believed to be dependent on inputs from cardiopulmonary receptors, and may be triggered by the reduction in venous return and cardiac filling associated with severe haemorrhage. In this study, we tested the hypothesis that the phase II response could be reversed by venoconstriction, which is known to enhance venous return and cardiac filling, by comparing the effects of phenylephrine (which constricts veins as well as arterioles) with that of vasopressin (which constricts arterioles but not veins). In sodium pentobarbitone-anaesthetised rats, haemorrhage evoked an initial increase in heart rate (HR) and renal sympathetic activity (RSNA) followed by a large decrease in both variables to levels below the pre-haemorrhage baseline levels (phase II response). During the phase II response, an intravenous injection of phenylephrine, sufficient to restore mean arterial pressure to the pre-haemorrhage level, resulted in a gradually developing increase (over 3-4 min) in HR and RSNA back to the baseline levels. In contrast, intravenous injection of an equipressor dose of vasopressin did not result in any increase in RSNA and only a transient increase in HR. Injection of phenylephrine, but not vasopressin, also increased the pulsatile component of central venous pressure, indicative of reduced venous capacitance. The findings indicate that venoconstriction reverses the phase II sympathoinhibition and bradycardia.
- Cardiopulmonary reflex
- Decompensatory response