Volume-controlled irreversible haemorrhagic shock in rats produced by blood withdrawal until stabilisation of critical mean arterial pressure (MAP)20-25 mmHg is associated with an extreme decrease in cardiac index (CI)and an increase in total peripheral resistance index (TPRI),with reductions in renal (RBF),hindquarters (HBF)and mesenteric blood flow (MBF),and leads to the death of all control animals within 30 min.Histamine (100 nmol)injected intracerebroventricularly (i.c.v.)in the early phase of critical hypotension produces a prompt and long-lasting increase in MAP and heart rate,with a 100%survival for 2 h after treatment.The effects are associated with the rise in the circulating blood volume and CI,and the decrease in TPRI,with the increase in RBF and HBF,and persistently lowered MBF.Both splenectomy and ligation of the suprahepatic veins inhibit histamine-induced increase in circulating blood volume as well as cardiac and regional haemodynamic effects.It can be concluded that histamine administered icv activates central endogenous compensatory mechanisms,which leads to the reversal of haemorrhagic shock conditions due to the mobilisation of blood from venous reservoirs,the increase in circulating blood volume and its redistribution.Moreover,histamine evokes the rises in CI and perfusion of the renal and skeletal muscle vascular regions.
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Oxytocin (OT) is a peptide involved in several physiological functions in the central nervous system including central cardiovascular regulation. To clarify the role of endogenous OT in cardiovascular control, one group of anesthetized rats received unilateral microinjections of the OT receptor antagonist [d(CH2)5,Tyr(Me)2,Orn8]-vasotocin (OTA) in the nucleus tractus solitarii (NTS) and a second group was injected with specific OT antiserum (Anti-OT). Moreover, the modulation of the cardiovascular effect of L-glutamate (GLU) by OT was also evaluated by cardiovascular analysis using effective and threshold doses of GLU. Mean arterial pressure (MAP) and heart rate (HR) were measured from a femoral catheter. OTA significantly (p<0.01) decreased the vasopressor and tachycardiac long-lasting response elicited by an effective dose of OT. Microinjections of Anti-OT antibody did not modify the values of MAP and HR compared with the control group. With regard to the OT/GLU coinjections, a subthreshold dose of OT significantly (p<0.001) counteracted the vasodepressor and bradycardiac responses induced by GLU. The coinjection of subthreshold doses of OT and GLU did not produce a change in MAP or in HR. These findings seem to exclude an endogenous tonic action of OT on central regulation of MAP and HR, although they confirm the significant role of OT on central cardiovascular control within the NTS. In fact, the modulation of GLU responses by OT supports the importance of OT on the central cardiovascular adjustments likely acting on the baroreceptor reflex sensitivity.
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