SUMMARY1. The cardiovascular responses to voluntary isometric contractions performed by human subjects are determined by the proportion of maximal tension achieved by the muscles contracting, and not by the mass of the contracting muscles, nor by the absolute tension achieved (Lind & McNicol, 1967; confirmed here). When two or more muscle groups contract simultaneously at different relative tensions, the increments in heart rate and blood pressure are the same as when the muscle group at the higher relative tension contracts alone at that tension (Lind & McNicol, 1967). It is known that there are both central and reflex stimuli to the cardiovascular system in exercise, and the present study examines whether the muscular reflex stimuli are related to the proportion of maximal tension achieved or to the mass of contracting muscle. 3. When human subjects perform isometric contractions, a pressor response can be maintained beyond the conclusion of the exercise by occluding muscle blood flow. This response is generally attributed to a reflex set up in the muscle by the action of chemical factors on afferent nerves. When comparable pressor responses were evoked by comparable proportional efforts with either the whole hand or the little finger, it was found here that the pressor responses remaining during the period of post-exercise occlusion were greater when the greater mass of muscle had been exercised.4. It is concluded that the muscular reflex drive in isometric exercise is related to the bulk of contracting muscle.

Isometric hindlimb contractions were induced in anaesthetised dogs by stimulation of appropriate spinal ventral roots. During such contractions there were appreciable reflex systemic pressor responses accompanied by small increases in heart rate. The heart rate responses during contractions were small because the primary cardioacceleratory reflexes from muscle were partly masked during contractions by opposing baroreceptor-cardiodepressor reflexes.

Correspondence decreased intracellular calcium availability which is necessary for the secretion of kallikrein [2].The exact mechanisms whereby adrenaline causes the release of kallikrein is unknown, but it is known that it acts via adrenoceptors [3]. If adrenaline acts via cyclic AMP as a second messenger it would suggest that adrenaline is safer when given with somatostatin than when given alone. In the case described, when there was difficulty weaning the patient from cardiopulmonary bypass, it may have been the somatostatin itself which gave rise t o the need for adrenaline, for it has recently been shown that in an animal model [4], somatostatin is a negative inotrope.The use of adrenaline, and particularly an adrenaline infusion, should be considered part of a rational approach to weaning from cardiopulmonary bypass in those patients with the carcinoid syndrome who are also receiving somatostatin. Northwick Park Hospital, Harrow, Middlesex HA1 3UJ M.H. CROSS ReferencesLEVINE J, SJOERDSMA A. Pressor amines and the carcinoid flush.

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