Left-ventricular endomyocardial biopsy.
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Biomedical subjects
Publications and source records attributed to M M Webb-Peploe.
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1. Reflex changes in wall tension of the lateral saphenous vein of one hind limb, the splenic veins and capsule, and the resistance vessels of the other hind limb caused by changes in baroreceptor activity were measured in vagotomized dogs under thiopentone-chloralose anaesthesia.2. Three different methods were used to alter pressure in one or both carotid sinuses. (1) Both carotid sinuses were vascularly isolated and filled with fully oxygenated Krebs-Ringer bicarbonate solution (pH 7.4) from a reservoir in which the pressure could be altered at will. (2) One sinus was denervated, and the contralateral sinus was perfused with arterial blood at different flow rates. (3) One sinus was denervated, and the innervated sinus was perfused with arterial blood at constant flow, the pressure being altered by changing the outflow resistance.3. The left saphenous vein was perfused at constant flow with autologous blood; changes in perfusion pressure were used as a measure of changes in veno-motor activity. The right common iliac artery was perfused at constant flow to measure changes in resistance vessel activity. Blood flow through the spleen was temporarily arrested, trapping a fixed volume of blood in the organ. Under these conditions, changes in splenic vein pressure were a measure of changes in smooth-muscle tension in the splenic capsule and veins.4. In order to assess the responses to baroreceptor stimulation in terms of alterations in sympathetic nerve traffic to different components of the peripheral vascular system, ;frequency-response curves' were constructed for spleen, saphenous vein, and limb resistance vessels by electrical stimulation of the splenic nerves and lumbar sympathetic chains.5. The saphenous vein showed no consistent response to changes in baroreceptor activity. Reduction in carotid sinus pressure from 180 to 100 mm Hg caused an increase in venous pressure in the isovolumetric spleen and in the iliac artery perfusion pressure. These results were confirmed by electrical stimulation of the carotid sinus nerve. Whereas the peak responses of the limb resistance vessels corresponded to an increase in lumbar sympathetic nerve traffic of 6-10 c/s, the maximal splenic responses were equivalent to an increase in splenic nerve traffic of 1-4 c/s. These results are consistent with selective autonomic nervous control of different components of the peripheral vascular system.
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The lateral saphenous vein of dogs was perfused at constant flow with autologous arterial blood, and perfusion and femoral vein pressures were monitored; changes in the difference between these pressures were due to changes in venomotor activity. Injection of isoproterenol into the perfusate caused the vein to dilate. The amount of dilatation depended on smooth muscle tension in the wall of the vein before injection. When this was minimal (after sympathectomy), isoproterenol had no effect. During venoconstriction produced by electrical stimulation of the lumbar sympathetic chain or by the infusion of venoconstrictor drugs, the dilating action of 0.1 mg of isoproterenol was measured. Expressed as a percentage of the initial constriction caused by sympathetic stimulation, 5-hydroxytryptamine, or 1 M potassium chloride, the extent of the dilatation was 86.7+/-4.3 (SE of mean), 79.7+/-4.2, and 87.7+/-3.2, respectively. With norepinephrine and epinephrine infusions, the isoproterenol dilatations were less (65.1+/-9.0 and 55.2+/-7.2, respectively), consistent with the stimulant action of these agents on both alpha and beta receptors; such action was confirmed by comparing the responses to nerve stimulation and infusions of norepinephrine and epinephrine before and after betareceptor blockade. The venoconstriction caused by sympathetic stimulation and by infusions of norepinephrine and epinephrine was greatly enhanced by cooling the vein (decreasing perfusate temperature), but the dilating action of isoproterenol appeared to be insensitive to changes in temperature. The data suggest that beta receptors are specific entities and, when maximally stimulated, are capable of causing a venous relaxation that is proportional to the initial degree of tension in the vein wall.
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