Folkow, B., R. R. Sonnenschein, and D. L. Wright, Loci of neurogenic and metabolic effects on precapillary vessels of skeletal muscle. Acta physiol. scand. 1971. 81. 459–471. By cannulation of a branch of the proximally clamped sural artery of the anesthetized cat, distal arterial pressure (DAP) in the gastrocnemius muscle was recorded. Measurement of blood flow, femoral arterial pressure and DAP allowed calculation of total resistance (Rt) and its partition into a distal component (Rd) which included precapillary sphincters and the smaller arterioles, and a proximal component (RP) which included the larger arteries. With sympathetic vasoconstriction, the initial increase in Rt was accounted for mainly by constriction of the distal vessels which then tended to relax; progressive constriction of proximal vessels accounted for most of the elevated Rt during the steady state; subsequent reactive hyperemia mainly involved distal vessels. Rt was less affected by sympathetic stimulation during exercise than when the muscle was at rest; constriction of distal vessels was more markedly reduced than that of proximal vessels. Ascending dilatation was evident during exercise. Sympathetic cholinergic vasodilatation mainly involved vessels more proximal to those which were dilated early in exercise. The findings are compatible with the concept that capillary flow distribution, as a function of terminal arterioles and precapillary sphincters, is adjusted by local factors towards an optimum for the prevailing metabolic level of the tissue.

No abstract

Cerebral blood flow (CBF) was estimated from measurements of internal carotid blood flow and sagittal sinus blood flow in mechanically ventilated rabbits under 70% N2O-30% O2. Intravenously administered physostigmine, a cholinesterase inhibitor, increased CBF under normocapnia and enhanced the cerebral vasodilatation of hypercapnia, but did not alter the cerebral metabolic rate of oxygen (CMRO2). The cerebrovascular effects of physostigmine were antagonized by atropine but not by dihydro-beta-erythroidine, a nicotinic blocker. Neostigmine, a quaternary cholinesterase inhibitor that does not cross the blood-brain barrier, showed no cerebrovascular effects. It is concluded that the cholinergic cerebral vasodilatation does not depend on cerebral metabolic activation, and that the cholinergic receptors involved are muscarinic and located beyond the blood-brain barrier.

The relationships between blood flow and contraction force in intermittently contracting eat skeletal muscle during alterations of flow by various procedures were studied. When flow only to the active gastrocuemiussoleus was measured, mechanical reduction in perfusion pressure, sympathetic chain stimulation and intra-arterial norepinephrine and epinephrine infusion were found to have esscritially identical effects in producing reduction in muscle force proportionate to that in blood flow. When flow in the whole leg musculature was measured while either the gastrocnemius-soleus or the quadriceps was active, varying results were obtained with these procedures which could be ascribed to differenees in response of vessels in active and resting muscles. During the carotid sinus reflex some vasoconstrictor activity occurred in active muscle. On the assumption that the maximal, muscle force is an index of the nutritional component of the flow, it may be inferred that, in general, those procedures in which total flow was restricted produced no alteration in distribution of nutritional and non-nutritional flow within the active muscle. Blood flow and muscle force were generally unaffected by concomitant stimulation in the hypothalamus of the sympathetic vasodilator system. An increase in flow and force occasionally was observed whien these were at low levels, or when a rise in arterial pressure occurred. The sympathetic vasodilator system produces no alteration in distibution of flow and would seem to play no role in the maintenance of blood flow and performance of normal active muscle. A fundamental difference appears to exist in the responses of the vasculature of resting and active skeletal muscle; this difference is related to the interplay of specialized effects of the vasomotor innervations and the action of vasodilator metabolites.

The vasoconstrictor response to “diving” was simulated in pentobarbital‐anesthetized ducks by administration of 20 % CO2 combined with vagotomy and controlled bleeding. Muscle blood flow, 30–50 ml/min ×. 100 g, at rest, could by reflex vasoconstriction be almost stopped and was then barely increased by exercise; in the absence of vasoconstriction, however, exercise increased flow to about 150 ml. In cats exercise produced considerable flow increases also during vasoconstriction; further, maximal flow reached only some 50 ml. Simultaneous recordings of venous outflow and pressures in the femoral artery and a small (0.3–0.5 mm) extramuscular artery revealed that large extramuscular arteries constrict far more in ducks than in cats and then fail to manifest ascending dilatation. The femoral artery has a far richer supply of adrenergic nerve terminals in ducks than in cats. In all the above respects, turkeys were more similar to cats than to ducks. In duck muscles maximal contractile force increased during CO2 breathing due to augmentation via the sympathetic innervation (Orbeli effect), an effect mimicked by intra‐arterial catechol amines. The ability of diving animals to maintain muscle vasoconstriction during exercise while diving may well reside in the differently balanced vascular innervation with intense constrictions of extramuscular vessels. The sympathetic augmentation of contractility may partly compensate for the effect of flow reduction. The larger maximal flow capacity and capillary area in duck muscles facilitates rapid post‐dive restitution.