Adrenergic and vasopressinergic contributions to the cardiovascular response to acute hypoxaemia in the llama fetus

1. The effects of ft tal intravenous treatment with phentolamine or a vasop ressinergic V-1-receptor antagonist on the fetal cardiovascular responses t o acute hypoxaemia in the llama were investigated. 2. Six llama fetuses were surgically prepared between 60 and 70% of gestati on under general halothane anaesthesia with vascular catheters and transit- time ultrasonic flow probes around a carotid artery and a femoral artery. A t least 4 days after surgery all fetuses were subjected to a 3 h experiment : 1 h of normoxia, 1 h of hypoxaemia and 1 h of recovery while on slow I.V. infusion with saline. On separate days this experiment was repeated with f etal I.V. treatment with either phentolamine or a V-1-receptor antagonist d issolved in saline. 3. During saline infusion all llama fetuses responded to acute hypoxaemia w ith intense femoral vasoconstriction. Phentolamine during normoxia produced hypotension, tachycardia and vasodilatation in both the carotid and the fe moral circulations. During hypoxaemia, fetuses treated with phentolamine di d not elicit the pronounced femoral vasoconstriction and all died within 20 min of the onset of hypoxaemia. A V-1-receptor antagonist produced a femor al vasodilatation during normoxia but did not affect the fetal cardiovascul ar responses to acute hypoxaemia. 4. In conclusion, alpha-adrenergic and V-1-vasopressinergic mechanisms cont ribute to a basal vasoconstrictor tone in the femoral circulation in the ll ama fetus. The enhanced femoral vasoconstriction during acute hypoxaemia in the llama fetus is not mediated by stimulation of V-1-vasopressin receptor s, but is dependent on alpha-adrenergic receptor stimulation. Such alpha-ad renergic efferent mechanisms are indispensable to fetal survival during hyp oxaemia in the llama since their abolition leads to cardiovascular collapse and death.