1. Central and local regulation of skeletal muscle blood flow in the leg was studied in the acute phase of myocardial infarction. 2. Blood flow was measured by the local 133 Xe washout technique in the anterior tibial muscle. 3. The vasoconstrictor response to increase in venous transmural pressure was not present on day 1 after coronary occlusion but gradually returned during days 2, 3 and 7. 4. A normal response to decrease in arterial perfusion pressure was observed, suggesting that intrinsic vascular reactions responsible for autoregulation of blood flow were not affected in the acute phase of myocardial infarction. 5. Passive head-up tilt (30°) induced vasoconstriction in skeletal muscle tissue. There were no differences in this response at any time during the course of acute myocardial infarction. 6. The abolition of the vasoconstrictor response to increase in venous transmural pressure on day 1 is most likely due to centrally elicited increase in sympathetic activity as a normal vasoconstrictor response was obtained the following days. Decrease in baroreceptor activity induced by head-up tilt enabled a marked neurogenically mediated vasoconstriction in skeletal muscle tissue which was almost unaffected during the course of myocardial infarction.
1. The effect of head-up tilt upon subcutaneous blood flow in the distal arm and leg was studied in 12 patients with complete traumatic spinal cord transection at the cervical level. 2. Blood flow was measured by the local 133 Xe washout technique. 3. Leg lowering induced a 47% decrease in blood flow in the distal leg. During head-up tilt (45°) blood flow in the leg decreased by 48%. In the arm remaining at heart level blood flow decreased by 37% during tilt and this vasoconstriction could be prevented by nervous blockade with lignocaine injected subcutaneously 5 cm proximally to the labelled area. Leg blood flow was unaltered by proximal blockade but could be blocked by local infiltration in the labelled area with lignocaine in low doses. 4. Head-up tilt of tetraplegic patients induced vasoconstriction in the subcutaneous tissue of the forearm, which could be prevented by proximal blockade. Thus the vasoconstriction could be due to a spinal sympathetic reflex mechanism. This as well as local mechanisms including the veno-arteriolar reflex may play a role in recovery of arterial blood pressure during head-up tilt in the tetraplegic patient.
1. Local regulation of subcutaneous blood flow in the forearm was studied in the acute phase of myocardial infarction. Blood flow was measured by the local 133 Xe-washout technique. 2. Plasma concentrations of noradrenaline and adrenaline were increased on day 1, suggesting an increase in sympathetic neuronal activity, but gradually returned to normal thereafter. 3. Subcutaneous blood flow on day 1 was far below normal (38%) and steadily increased to reach normal at day 7 after coronary occlusion. The sympathetic vasoconstrictor activity that caused the initial reduction in flow could be blocked by proximal nervous blockade, increasing the subcutaneous blood flow by 130, 63 and 14% on days 1, 3 and 7 respectively after coronary occlusion. A normal response to decrease in arterial perfusion pressure was observed, suggesting that intrinsic vascular reactions responsible for autoregulation of blood flow were not affected by the increase in sympathetic vasoconstrictor activity. The vasoconstrictor response to increase in venous transmural pressure could not be demonstrated on day 1 after coronary occlusion but gradually reappeared during the following days. 4. Abolition of the vasoconstrictor response is most likely to be due to a centrally elicited increase in sympathetic activity, as a normal vasoconstrictor response was obtained after proximal nervous blockade. Thus the local sympathetic reflex mechanism underlying the vasoconstrictor response appears to be suppressed by a centrally elicited increase in sympathetic discharge rate.