The effect of venous stasis of 40 mmHg upon blood flow in human skeletal muscle was studied in four normal subjects and in two chronically sympathectomized patients. Blood flow in skeletal muscle was measured by the local 133Xenon washout technique. Blood flow decreased about 30 per cent during venous stasis of 40 mmHg. In a "passive vascular bed" induced by means of histamine, blood flow decreased only by 16 per cent, indicating that the decrease in blood flow is due to a vasoconstrictor response to increase in vascular transmural pressure. The vasoconstrictor response was unaffected by a spinal sympathetic blockade, but was blocked in areas infiltrated with lidocaine or with phentolamine. The vasoconstrictor response was present in the nonoperated limbs used as a control, but abolished in the denervated arms in the two chronically sympathectomized patients. The findings strongly suggest that the vasoconstrictor response in skeletal muscle is due to a local nervous mechanism involving adrenergic fibres. Thus a local reflex mechanism, most likely a sympathetic axon reflex, seems to be present in human skeletal muscle as in cutaneous and subcutaneous tissue. This indicates that about 45 per cent of the change in total vascular conductance, when a person changes from supine to upright position, is due to this local reflex mechanism operating independently of the central nervous system.

Previous studies on intact human subcutaneous tissue have shown, that blood flow remains constant during minor changes in perfusion pressure. This so-called autoregulatory response has not been demonstrable in isolated preparations of adipose tissue. In the present study on isolated, denervated subcutaneous tissue in female rabbits only 2 of 12 expts. revealed an autoregulatory response during reduction in arterial perfusion pressure. Effluent blood flow from the tissue in the control state was 15.5 ml/100 g-min (S.D. 6.4, n = 12) corresponding to slight vasodilatation of the exposed tissue. Following total ischemia all experiments showed a period with reactive hyperemia, and both duration of hyperemia and excess flow was related to the duration of the ischemia. This response therefore seems more resistant to the experimental procedure, while autoregulation of blood flow to lowered pressure is more susceptible to surgical exposure of the tissue. During elevation of arterial perfusion pressure blood flow in the isolated tissue showed a transient increase and then almost returned to the level during normotension, indicating an elevated vascular resistance. Raising of venous pressure elicited vasoconstriction with pronounced flow reduction. These two reactions may be important for local regulation of blood flow in subcutaneous tissue during orthostatic changes in arterial and venous pressure. It is concluded that the response in adipose tissue to changes in arterial pressure (autoregulation), venous pressure and total ischemia appear to be elicited by different mechanisms.

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