Pulmonary capillary blood volume in dog: effects of 5-hydroxytryptamine

Section: Methodssupporting

confidence: 60%

Differential reactivity in the pulmonary circulation

Brody¹,

Stemmler²

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: 72%

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-

“…Excretion of CO that occurs via the lungs is principally a function of alveolar ventilation (VA), the diffusing capacity of the lung (Dco), and the mean oxygen tension in pulmonary capillary blood (12). Both Dco (31) and VA are smaller in dog than in man, and it is therefore likely that the higher [COHb] /Vco found in dogs is explainable on this basis.…”

Section: Introductionmentioning

confidence: 99%

The Production of Carbon Monoxide from Hemoglobin In Vivo*

Coburn¹,

Williams²,

White³

et al. 1967

Summary. Dogs anesthetized with pentobarbital were shown to produce carbon monoxide at an average rate of 0.21 + (SD) 0.05 ml per hour. After intravenous injection of erythrocytes damaged by incubation with N-ethylmaleimide, CO was produced in excess of base-line production for 3 to 4 hours with an average yield of 0.89 + (SE) 0.046 umole of carbon monoxide to 1 Mmole of heme degraded.After intravenous injection of N-ethylmaleimide (NEM)-treated erythrocytes containing hemoglobin labeled with 14carbon, 14CO was produced. Its specific activity was approximately one-eighth that of the injected heme. It was also produced after intravenous injection of solutions of hemoglobin-14C and of reconstituted methemoglobin containing hemin-14C, but not after injections of methemoglobin containing globin-14C. The average yields of 14CO from metabolized heme in the experiments with damaged erythrocytes and hemoglobin solutions were 89 + (SE) 4.6 and 97 + (SE) 17.0%, respectively. These results demonstrate that the CO produced during hemoglobin degradation arises from the heme moiety.The yield of 14CO after injection of hemoglobin-14C solutions decreased significantly to values of 35 and 42% in two experiments when exogenous CO was added to the body stores, resulting in blood carboxyhemoglobin levels of 11.3 and 13.2% saturation. This finding suggests that oxidative metabolism is required during catabolism of hemoglobin to CO and that carboxyhemoglobin levels in this range are sufficient to cause inhibition.After intravenous injection of either hemin-14C or protoporphyrin-14C, 14CO was also produced. After injection of protoporphyrin-14C labeled bilirubin was isolated from gall bladder bile, and labeled hemin was isolated from the liver. It is thus very likely that protoporphyrin is converted to heme before the formation of CO.There was a large difference between the maximal rates of catabolism of hemoglobin to CO observed after injection of damaged erythrocytes and hemoglobin solutions. The limiting parameters in these processes are not yet clear.