Circulatory Control via Vagal Afferents VI. The bleeding bradycardia in the rat, its elicitation and relation to the release of vasopressin

Abstract Sjöstrand, T. Circulatory control via vagal afferents. VI. The bleeding bradycardia in the rat, its elicitation and relation to the release of vasopressin. Acta physiol. scand. 1973. 89. 39–50. Bradycardia appears regularly in Sprague‐Dawley rats on arterial hemorrhage. It is usually preceded by an increase of the heart rate of varying duration. On an average the bradycardia starts 21s after the fall in arterial pressure. On reinfusion the bradycardia disappears during 10–20 min following a varying course. Compression of the inferior caval vein provokes bradycardia which appears and disappears similarly but starts earlier in relation to the pressure fall. If blood or saline is intravenously infused simultaneously with the hemorrhage, the bradycardia starts later and is less pronounced in relation to the fall in arterial pressure. The bradycardia is inhibited by hypophysectomy, hydration and infusion of small amounts of ethyl alcohol through the carotid artery. A similar bradycardia may be provoked by intra‐carotid infusion of vasopressin at maintained arterial pressure. It is concluded that the bleeding bradycardia is elicited by receptors on the low pressure side stimulated by a decrease of the venous return or central blood volume and is a part of a reflex control of the blood volume and distribution. The release of vasopressin is stimulated through vagal afferents and, by local transmission, exerts an excitatory effect on the depressor area in the hypothalamus. The significance of the deduced vasopressin releasing reflex under normal and pathological conditions is discussed.