Nitrous Oxide Added to Halothane Reduces Coronary Flow and Myocardial Oxygen Consumption in Patients with Coronary Disease

1983 ◽  
Vol 27 (5) ◽  
pp. 284
Author(s):  
E. A. MOFFITT ◽  
D. H. SETHNA ◽  
R. J. GRAY ◽  
M. J. RAYMOND ◽  
J. M. MATLOFF ◽  
...  
1960 ◽  
Vol 199 (2) ◽  
pp. 349-354 ◽  
Author(s):  
H. Feinberg ◽  
A. Gerola ◽  
L. N. Katz

The effect of hypo- and hypercapnia—induced by changing the respiratory gas mixture—on coronary flow and myocardial oxygen consumption was observed at constant cardiac output and over a broad range of pressure-loads in open-chested, anesthetized dogs. The correlation of cardiac effort (as indexed by the product of heart rate and mean aortic blood pressure) with myocardial oxygen consumption was not altered by increasing or decreasing the arterial CO2 content. Coronary blood flow was observed to be increased relative to the cardiac effort during hypercapnia but not during hypocapnia. The coronary arteriovenous oxygen difference and the percentage of oxygen extracted decreased during hypercapnia pari passu with the increase in venous oxygen content.


1985 ◽  
Vol 248 (4) ◽  
pp. H508-H515 ◽  
Author(s):  
C. S. Apstein ◽  
R. C. Dennis ◽  
L. Briggs ◽  
W. M. Vogel ◽  
J. Frazer ◽  
...  

Storage of blood can depress erythrocyte 2,3-diphosphoglycerate (DPG) levels and thereby increase oxyhemoglobin affinity and potentially decrease capillary-to-tissue oxygen transport. We measured myocardial function and metabolism in isolated rabbit hearts with fixed coronary flow under basal conditions and during isoproterenol stress at 37 and 30 degrees C, comparing high and low oxyhemoglobin affinity (OHA) erythrocytes. The high OHA state resulted from standard storage conditions, which caused depressed values of DPG and P50 (the oxygen tension at which hemoglobin is 50% saturated). The low OHA erythrocytes were initially stored and then underwent biochemical treatment to restore the DPG and P50 values to normal. The low OHA cells released more oxygen, and myocardial oxygen consumption and contractile function were increased relative to the high OHA cells during both the basal and stress states at both 37 and 30 degrees C. These observations may be relevant for patients with limited coronary flow when such patients receive large transfusions of stored blood.


1962 ◽  
Vol 64 (6) ◽  
pp. 789-795 ◽  
Author(s):  
Armand A. Lefemine ◽  
Henry B.C. Low ◽  
Manfred L. Cohen ◽  
Steven Lunzer ◽  
Dwight E. Harken

1959 ◽  
Vol 196 (4) ◽  
pp. 719-725 ◽  
Author(s):  
A. Gerola ◽  
H. Feinberg ◽  
L. N. Katz

Effects of hypothermia (at 32° and 27°C) were determined in the open-chest anesthetized dog prepared for measurement of total coronary flow and myocardial oxygen consumption. When hypothermia was induced at any fixed cardiac output, cardiac oxygen consumption and heart rate declined while blood pressure remained constant. Cardiac external mechanical efficiency increased at the same time. Hypothermia did not alter the relationship between the myocardial oxygen requirement and the total cardiac effort as indicated by the product of blood pressure times heart rate. Without regard to the large individual variability, the coronary venous O2 rose; thus the general trend during the induction of hypothermia was a decline in the coronary A-V oxygen difference, the percentage O2 extracted by the heart and the ratio: cardiac O2 consumption/O2 availability. The coronary venous O2 content and the coronary A-V O2 difference remained fairly constant as the cardiac effort and its oxygen requirement varied during hypothermia, just as in the control period. Thus coronary flow was the only means of adjusting to the altered cardiac oxygen need in both periods.


1977 ◽  
Vol 55 (3) ◽  
pp. 471-477 ◽  
Author(s):  
D. T. Zborowska-Sluis ◽  
R. R. Mildenberger ◽  
G. A. Klassen

When coronary flow was kept constant and coronary pressure increased by angiotensin or decreased by dipyridamole, myocardial oxygen consumption (MVO2) remained unchanged. When vasomotor tone was abolished by dipyridamole or was intact, changing coronary flow resulted in a change in MVO2 in the same direction as flow; this change in MVO2 was in part the result of a significant alteration in coronary oxygen extraction. These results suggest that coronary flow, but not coronary pressure is an important determinant of MVO2 both in the presence or absence of vasomotor tone.


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