Fractional Distribution Of Cardiac Output Research Articles

Pathophysiology of shock.

Pathophysiology of shock was fundamentaly investigated in several different ways. 1. Fractional distribution of cardiac output was measured, using radioactive microsphere technique. Hemorrhagic, endotoxin and trime-thapan hypotension were compared to each other in their fractional distribution of cardiac output. As a whole, cardiac output was distributed in the way to maintain cerebral or coronary blood flow, whatever the cause of shock may be. This centralization was rather well maintained even shock progressed. Splanchinic blood flow, especially the pancreas flow were decreased significantly. This may be related to the production of vasoactive or toxic substances from these organs. 2. Myocardial depressant factor was identified both in plasma and pancreas in advanced shock. Gel-chormatographic analysis was applied to separate the myocardial depressant factor. It is also demonstrated that myocardial depressant factor was produced in pancreas, transported via blood stream to the hear and caused cardiac depression. 3. In vivo cardiac contractility was measured by the change of Vmax sequentially as shock advanced. Left ventricular pressure was measured, using catheter tip transducer. In hemorrhagic shock, cardiac contractility began to decrease 4 hours after bleeding and continued to deteriorate progressively thereafter. 4. Regional coronary blood flow distribution was also measured by radioactive microsphere method. 2 hours after bleeding, endocardial fractional distribution already began to decrease and remained in the same distributional pattern even 4 hours after bleeding, while the myocardial contractility did not show any deterioration in 2 hours after bleeding. So it may be said that endo-cardial ischemia had no significant relationship with this cardic dysfunction. 5. Phagocytic function was decreased progressively when shock advanced. Reticuloendothelial depressing substance was also analyzed using gel-chromatographic method. Bioassay of RDS was shown by the decrease of phagocytic index after administering this fraction to healthy rats. 6. Closed loop, negative feed back mechanism (Fig.24) was suggested with relation to the above mentioned results. Decrease of cardiac output, followed by decrease of splanchinic blood flow, might cause the production of myocardial depressant factor. And this MDF might exert again decrease of cardiac contractility, thus closed negative feed-back loop was established. This mechanism might be called as peripheral theory for cardiac deterioration in shock. MDF, lysozomal enzymes or other vasoactive substances could not be phagocytized because of the reticuloendothelial system dysfunction, which may be caused by the decrease in opsonin activity or the release of reticuloendothelial depressing substance.

The effect of hypoxia on the regional distribution of cardiac output in the dog.

Twenty-one dogs were studied under conditions of normal oxygenation and hypoxia with the microsphere distribution method to determine the effect of arterial oxygen saturation on the regional distribution of cardiac output. The dogs were anesthetized and artifically ventilated. Cannulas were placed in the left ventricle to administer microspheres and in a peripheral artery to determine cardiac output. Each dog received two microsphere injections: (1) while normally oxygenated (room air), and (2) under hypoxia (10% oxygen-90% nitrogen in 10 dogs and 5% oxygen-95% nitrogen in 11 dogs). Absolute cardiac output increased from 87 +/- 15 ml/min per kg to 101 +/- 14 ml/min per kg during mild hypoxia (10% oxygen) (P less than 0.05), and from 73 +/- 17 ml/min per kg to 120 +/- 24 ml/min per kg during severe hypoxia (5% oxygen) (P less than 0.01). Absolute blood flows increased to all organs except skin and muscle during hypoxia, although there were decreases in the fractional distribution of cardiac output to the splanchnic bed and kidney. Striking changes were found in coronary, hepatic, and cerebral circulation, and the organ with, greatest response to hypoxia was the heart, with increased coronary flow of 37% and 285% during exposure to 10% and 5% oxygen, respectively. Hence, low oxygen levels in blood cause redistribution of cardiac output and arterial content plays an important role in blood flow regulation.

Effects of acute administration of isoproterenol on the systemic and regional blood flow in the dog

Abstract The effects of isoproterenol on cardiac output and the blood flow to various parts of the body have been investigated in pentobarbital-anaesthetized dogs, by the microsphere method. Arterial and venous catheterizations were performed for haemodynamic measurements, drug infusions and blood samples. After a stabilization period, control measurements were carried out on the cardiac output, heart rate, blood pressure, expiratory minute volume and blood gases. Radioactive microspheres of 50 μm diameter, labelled with either 85 Sr or 141 Ce, were then injected into the left ventricle. Thereafter the intravenous infusion of isoproterenol (0.5 μg min −1 kg −1 was started. Fifteen minutes after initiation of the drug infusion, the same parameters as in the control period were measured and the injection of radioactive microspheres into the left ventricle was repeated. At the end of the experiment, various organs and tissues were removed and weighed and their radioactivity was determined. The fractional distribution of cardiac output and the blood flow to various organs and tissues were calculated by the method after Rudolph & Heymann (1967). The infusion of isoproterenol resulted in an increase of 57% in cardiac output but changes in regional blood flow varied. The fraction of cardiac output to the myocardium, skeletal muscle and skin were increased, whereas that to the kidney, pancreas and brain decreased. The fraction to the bronchial arteries and splanchnic organs except for the pancreas remained unchanged. The uneven distribution of cardiac output to the various areas may be due mainly to the differences in direct and indirect responses of individual vascular beds to isoproterenol.

Trapping of radioactive microspheres in the pregnant and non-pregnant rabbit.

AbstractWe injected radioactive microspheres, 15, 25 and 50 μn in diameter in the left ventricle or the lower aorta of rabhits and counted the radioactivity in the lungs to estimate the fraction of microspheres shunted through the systemic circulation. The degree of microsphere shunting was inversely proportional to microsphere diameter. The maximum fraction of 15 μm micro‐spheres shunted after an aortic injection was 8.8 % as compared with 6.2 % with 25 μm spheres and 1.2 % with 50 μm spheres. There was no statistically significant change in the fraction of microspheres shunted in pregnancy or with anesthesia. Shunted microspheres may continue to arrive in the lungs for up to 15 min following aortic injection. Microspheres at least 25 μm in diameter should he employed to measure the fractional distribution of cardiac output in rahbits although it may he preferable to use smaller microspheres to measure blood flow within certain organs.

The effects of melatonin and serotonin on blood flow fraction and testosterone metabolism in selected organs of the male rat.

The fractional distribution of cardiac output to the testes, adrenals, liver, and kidneys and the conversion of testosterone to 4-androstenedione by hepatic and renal homogenates in vitro were measured 4 weeks after implantation of male rats with melatonin and serotonin. The fractional blood flow to these organs was not significantly influenced by the indoles. There was, however, a tendency for the adrenal fraction to be lower in indole-treated rats. Blood levels of corticosterone in these animals were reduced, but significantly so only in the rats implanted with serotonin. The ability of liver preparations to metabolize testosterone in the presence of excess nicotinamide–adenine dinucleotide was enhanced after treatment with both indoles suggesting that at least one of the 17β-hydroxysteroid dehydrogenases had been stimulated. In the case of the kidney, melatonin administration gave rise to depression of the NAD-linked conversion whereas serotonin treatment caused reductions in testosterone conversions in the presence of either NAD or NADP.

Cardiac output and organ blood flow in warm- and cold-acclimated rats exposed to cold

Cold acclimation increased the cardiac output of unanesthetized rats when measured at 30 °C. After exposure to 9 °C for 70 min cardiac output further increased by 46% in both warm- and cold-acclimated rats. From the changes in the fractional distribution of cardiac output after cold exposure it was shown that the blood flow increased significantly in muscular organs (heart, diaphragm, skeletal muscles) and in the adrenals of warm-acclimated rats. In cold-acclimated rats the blood flow to the brown and white adipose tissues, pancreas, kidney, intestine, liver, and other internal organs was also increased in a cold environment, and accounted for 65% of the increase in blood flow during exposure to cold compared with only 36% in warm-acclimated rats. It is estimated that the extramuscular thermogenesis can account for a greater proportion of the total nonshivering thermogenesis in cold-acclimated rats. The contribution of brown adipose tissue is estimated not to exceed about 6% of the total heat production increase in cold-acclimated rats during exposure to cold.