- Email: [email protected]
Cardiac basal oxygen consumption as a function of oxygen supply
57 OXYGEN DEMAND OF THE HEART UPON SUPPRESSION OF CARDIAC FREE FATTY ACID UPTAKE AND HYPERINSULINEMIA INDUCED BY D(-)-3-HYDROXYBUTYRATE INFUSION IN THE ANESTHETIZED INTACT DOG. J. Lamerant, T. Huynh-Thu, J. Kolanowski. Department of Physiology, School of Medicine, FNDP, B-5000 Namur, Belgium. Ketones reduce the cardiac free fatty acid (FFA) metabolism and, hence, the corresponding 02 need. They also stimulate insulin secretion. Hyperinsulinemia enhances cardiac 02 consumption (MSo2) by inducing adrenergic discharge, even when euglycemia is maintained (J. Clin. Invest., 1982, 69 : 1321). Therefore, the cardiac 02 demand per beat (Mo2/heart rate x systolic pressure) was examined in dogs infused with D(-)-3-hydroxybutyrate (30HB) iv at rates of 20 umol/kg.min (group A) and 80 umol/kg. min (group B). After 30 min infusion, the following mean values + se were observed : Art.30HB Cardiac uptake (% of control) I?GZi?lemia 1Glymmi i Dogs in) mM FFA C Zucose Lactate p u/m 1 IrM Group A (10) 1.2 + 0.1 67 + 10 87 + 17 66 + 8 17 + 3 4.9 + 0.3 Group B 181 6.4 : 0.3 5;6 76 : 29 44 i 17 58 : IO 4.4 5 0.2 Uptake of 30HB averaged 17 + I and 31 _+ 10 imol/lOO g.min in group-A and group>. respectively (control : 0.4 + 0.04 umol/lOO g.min). The 02 demand per beat decreased in group A (P < O-02), but not in group B (P > 0.5) despite suppression of FFA uptake. Stroke volume and aortic pressure did not change in group A (P > 0.1) but increased in group B (P < 0.05), suggesting an associated insulin-related adrenergic discharge.
CARDIAC BASAL OXYGEN CONSUMPTION AS A FUNCTION OF OXYGEN SUPPLY. D.S. Loiselle. Department of Physiology, School of Medicine, University of Auckland, New Zealand. Hearts of juvenile guinea-pigs were mounted in a Langendorff apparatus and the coronary circulation perfused at constant pressure (50 torr). Coronary venous effluent was sampled from a cannula placed in the right ventricle via the pulmonary The left ventricle was aspirated by a cannula inserted through the wall of artery. the left atrium and mitral valve. Oxygen consumption (VO2) was calculated as the oroduct of coronarv flow and the difference in arterial and venous oxvqen contents. Coronary vascular Resistance (Rev) was calculated as the ratio of perfision pressure to venous outflow. The Krebs perfusate contained glucose (10 M/t), insulin (20 U/e) and the colloidal plasma substitute naem~~.d (20 ml/&); it was equilibrated with either 20%. 45% or 95% oxvqen and 5% CO9 (DH = 7.4). Upon arrest in 15 mM/!J. KCl, each of six hearts was subjected (in a balanced Latin Square design) to each oxygen environment for 15 mins both in the presence and absence of the coronary vasodilator adenosine (1.5 PM/!?.). V02 fell 30% during the first half hour of arrest whereas Rev remained constant. V02 varied directly with oxygen content (doubling from 20% to 95% oxygen) while Rev was constant. Adenosine failed to stimulate oxygen consumption at any level of oxygen content despite reducing coronary vascular resistance to 40% of its control value. These results suggest that the decline in oxygen consumption with oxygen concentration is not due to a reduction of oxygen supply.
CILBBOIIP~~~L;EPID~~~SnINTIlEIiBIBTIr#DLIVEBOP~TS UNDER HXPOKIl?BBIA. Y. Zorbaa, V. Petrovak Lab., Europeau Institute 0r Environmental The rate 0r atmimilation of carbo pentow-phorrphato pathway @PP> as in B bile uere evaluated under hypokinesia (Xj on 76 rabbits weighing 2.54 . The experimental rabbits were kept in amall individual o-s mde oz plexialaee which restricted their movements in all direction6 and the con&01 laoed under ordiner viveriua condition& Olycrogen, rate of lycalm I 8. actititi of the f+PP in the liver and the heart were aalc J ated on %he iOth, 15th. 30th and 60th day of the experinent. B bile, aholeaterol, bile acids and reeidue were aleo raoured. The remlta uere proceseed statirtioally. % &creased the rate or glyoolyeis in the liver and, especially, in the heart whereae at tk mme time increased the fraction 0r carbo drak utilLation in the PPP. This wm ale0 accoqmnied by accumulat h3 on of cholesterol in the blood and tiamee in spite of imnaeed bile excretion of aholeeterol and ite derivativesbile aoidl. It was concluded that under hypokine8ia the rate accida underwend mrtial oxidation. whereaa cholesterol use wtabol I calls leee
CARDIAC BASAL OXYGEN CONSUMPTION AS A FUNCTION OF OXYGEN SUPPLY. D.S. Loiselle. Department of Physiology, School of Medicine, University of Auckland, New Zealand. Hearts of juvenile guinea-pigs were mounted in a Langendorff apparatus and the coronary circulation perfused at constant pressure (50 torr). Coronary venous effluent was sampled from a cannula placed in the right ventricle via the pulmonary The left ventricle was aspirated by a cannula inserted through the wall of artery. the left atrium and mitral valve. Oxygen consumption (VO2) was calculated as the oroduct of coronarv flow and the difference in arterial and venous oxvqen contents. Coronary vascular Resistance (Rev) was calculated as the ratio of perfision pressure to venous outflow. The Krebs perfusate contained glucose (10 M/t), insulin (20 U/e) and the colloidal plasma substitute naem~~.d (20 ml/&); it was equilibrated with either 20%. 45% or 95% oxvqen and 5% CO9 (DH = 7.4). Upon arrest in 15 mM/!J. KCl, each of six hearts was subjected (in a balanced Latin Square design) to each oxygen environment for 15 mins both in the presence and absence of the coronary vasodilator adenosine (1.5 PM/!?.). V02 fell 30% during the first half hour of arrest whereas Rev remained constant. V02 varied directly with oxygen content (doubling from 20% to 95% oxygen) while Rev was constant. Adenosine failed to stimulate oxygen consumption at any level of oxygen content despite reducing coronary vascular resistance to 40% of its control value. These results suggest that the decline in oxygen consumption with oxygen concentration is not due to a reduction of oxygen supply.
CILBBOIIP~~~L;EPID~~~SnINTIlEIiBIBTIr#DLIVEBOP~TS UNDER HXPOKIl?BBIA. Y. Zorbaa, V. Petrovak Lab., Europeau Institute 0r Environmental The rate 0r atmimilation of carbo pentow-phorrphato pathway @PP> as in B bile uere evaluated under hypokinesia (Xj on 76 rabbits weighing 2.54 . The experimental rabbits were kept in amall individual o-s mde oz plexialaee which restricted their movements in all direction6 and the con&01 laoed under ordiner viveriua condition& Olycrogen, rate of lycalm I 8. actititi of the f+PP in the liver and the heart were aalc J ated on %he iOth, 15th. 30th and 60th day of the experinent. B bile, aholeaterol, bile acids and reeidue were aleo raoured. The remlta uere proceseed statirtioally. % &creased the rate or glyoolyeis in the liver and, especially, in the heart whereae at tk mme time increased the fraction 0r carbo drak utilLation in the PPP. This wm ale0 accoqmnied by accumulat h3 on of cholesterol in the blood and tiamee in spite of imnaeed bile excretion of aholeeterol and ite derivativesbile aoidl. It was concluded that under hypokine8ia the rate accida underwend mrtial oxidation. whereaa cholesterol use wtabol I calls leee