Effects of serotonin on pulmonary blood volume in the dog

A B S T R A C T A new method has been described for measuring the pressure and resistance to blood flow in the pulmonary arteries, capillaries, and veins. Studies were performed in dog isolated lung lobes perfused at constant flow with blood from a donor dog. Pulmonary artery and vein volume and total lobar blood volume were measured by the ether plethysmograph and dyedilution techniques. The longitudinal distribution of vascular resistance was determined by analyzing the decrease in perfusion pressure caused by a bolus of low viscosity liquid introduced into the vascular inflow of the lobe.The pulmonary arteries were responsible for 46% of total lobar vascular resistance, whereas the pulmonary capillaries and veins accounted for 34 and 20% of total lobar vascular resistance respectively. Vascular resistance was 322 dynes * sec* cm-5/ml of vessel in the lobar pulmonary arteries, 112 dynes sec.cm-5/ml in the pulmonary capillaries, and 115 dynes-sec* cm5/ml in the lobar pulmonary veins. Peak vascular resistivity (resistance per milliliter of volume) was in an area 2 ml proximal to the capillary bed, but resistivity was high throughout the pulmonary arterial tree. The pulmonary arteries accounted for approximately 50% of vascular resistance upstream from the sluice point when alveolar pressure exceeded venous pressure.The method described provides the first measurements of pulmonary capillary pressure. Midcapillary pressure averaged 13.3 cm H2O, pulDr. Brody is a postdoctoral fellow of the National Institutes of Health.

Section: Resultssupporting

confidence: 73%

Longitudinal distribution of vascular resistance in the pulmonary arteries, capillaries, and veins

Brody¹,

Stemmler²,

DuBois³

1968

“…In the dose employed by Shepherd, Donald, Linder, and Swan (2) and by us, no change in total pulmonary blood volume was demonstrated, whereas an increase in serotonin dose of some 15-fold, as used by McGaff and Milnor (29), produced a significant fall in pulmonary blood volume. Pulmonary capillary blood volume measured during a comparable dose given to our dogs rose 29%o with a wide degree of scatter (30).…”

Section: Resultsmentioning

confidence: 67%

“…Previous investigators have shown that serotonin administered to dogs produces a slight increase of cardiac output, a marked rise of pulmonary arterial pressure and pressure in the small pulmonary veins, and little alteration of pressure in the large pulmonary veins or left atrium (2,3,29).…”

Section: Resultsmentioning

confidence: 99%

The site of pulmonary vasomotor activity during hypoxia or serotonin administration.

Sackner¹,

Will²,

DuBois³

1966

Pulmonary arterial pressure increases in dogs exposed to alveolar hypoxia or intravascular infusion of 5-hydroxytryptamine (serotonin). Although most investigators believe that this increase in pressure reflects a vasoconstriction in the pulmonary vascular bed, the site of vasoconstriction, whether venular, capillary, or arteriolar, is controversial. Interpretations have been based previously upon measurements of pressure and flow at various sites in the pulmonary circulation and have been handicapped by the inability to measure the volumes of the segments under study (1-3). MethodsEleven mongrel dogs weighing 12.3 to 17.7 kg were used in the experiments. They were anesthetized with sodium pentobarbital in a dosage of 26 mg per kg body weight. An 8F or 9F Cournand cardiac catheter 1 was introduced into the external jugular vein, and under fluoroscopic guidance its tip was placed within the pulmonary artery. A second catheter was placed so that its tip lay within the superior vena cava. A pediatric 7F Brockenbrough left heart catheter 1 was introduced into the femoral vein and the atrial septum punctured so that the tip of the catheter lay free in the left atrial cavity. The femoral artery was cannulated with polyethylene tubing 25 cm in length and 2 mm in diameter in such a way that its tip lay in the distal aorta. The animal was enclosed within a horizontal Plexiglas body plethysmograph (4), then paralyzed with succinylcholine and ventilated with a Starling pump. Intravascular pressures were measured by strain gauges 2 balanced to a reference pressure level 9.8 cm above the surface of the dog board. Plethysmographic pressure was measured by a differential strain gauge.3 A direct-writing instrument 4 recorded pressures from the strain gauges, the electrocardiogram, and dye concentration from a cuvette densitometer.5The plethysmograph was calibrated by injection and withdrawal of 10 ml of air with a syringe, and this produced a deflection of 20 to 30 mm on the record. The pulmonary arterial pressure was monitored while the catheter was pulled back slowly until a ventricular pressure tracing was recorded, and then the tip of the catheter was advanced to the point where a pulmonary arterial pressure tracing was again recorded from a position just beyond the pulmonic valve. A 0.5-ml volume of solution, containing 0.1 ml of ether in 0.4 ml of alcohol, was instilled into the catheter to be flushed into the animal by 5 ml of saline. In several experiments designed to determine whether C02 evolution rate was affected, 0.5 ml of a 0.5 M lactic acid solution was instilled into the catheter to be flushed into the animal by 5 ml of saline, or 5 ml of a 0.9 M sodium bicarbonate solution was placed into the catheter and connecting tubing, and this was also ad-

“…Introduction 5-Hydroxytryptamine (serotonin) contracts canine and human isolated intrapulmonary vascular preparations (1)(2)(3)(4) and elevates pulmonary vascular resistance in intact organisms (5)(6)(7)(8)(9)(10) or vascularly isolated perfused lungs (1 1-13). Microembolization or in situ aggregation of platelets produces an elevation of pulmonary vascular resistance, leading to pulmonary hypertension, which can be attributed in part to the release of vasoactive substances (5,(14)(15)(16)(17)(18)(19).…”

mentioning

confidence: 99%

Aggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamine.

McGoon¹,

Vanhoutte²

1984

Abstract. To examine the effect of platelets and 5-hydroxytryptamine on pulmonary arterial smooth muscle, rings of canine pulmonary arteries, with and without endothelium, were studied under isometric conditions in physiological salt solution. 5-Hydroxytryptamine, but not the thromboxane-like endoperoxide analogue U-466 19, produced concentration-dependent contractions of the rings with a maximum averaging 93% of that obtained with KCL. Autologous platelets in concentrations comparable to that in plasma caused contractions averaging 70% of the maximal responses to KCL. Solution withdrawn from baths containing platelet-contracted rings, but not the supernatant from nonaggregated platelets, also caused contraction. The serotonergic antagonists cyproheptadine, ketanserin, and methysergide caused concentration-dependent inhibition and eventually abolition of contractions evoked by platelets and 5-hydroxytryptamine. Phentolamine and prazosin produced significantly less inhibition of the contractile response to platelets. Pretreatment of the platelets with indomethacin or meclofenamate reduced thromboxane release but had no effect on plateletinduced contractions. Removal of the endothelium did not affect contractile responses to platelets or 5-hydroxytryptamine. These experiments demonstrate that in the canine pulmonary artery: (a) 5-hydroxytryptamine is the predominant mediator of the contractile response triggered by platelet aggregation; and (b) unlike in other blood vessels, the endothelium cannot curtail the contractile response to aggregating platelets.A preliminary report of these findings was published in abstract form (1983. Fed. Proc. 42:593). Introduction 5-Hydroxytryptamine (serotonin) contracts canine and human isolated intrapulmonary vascular preparations (1-4) and elevates pulmonary vascular resistance in intact organisms (5-10) or vascularly isolated perfused lungs (1 1-13). Microembolization or in situ aggregation of platelets produces an elevation of pulmonary vascular resistance, leading to pulmonary hypertension, which can be attributed in part to the release of vasoactive substances (5,(14)(15)(16)(17)(18)(19)