Oxygen consumption of the myocardium in conditions of normo- and hypothermic coronary perfusion and a general artificial circulation

1966 ◽  
Vol 61 (6) ◽  
pp. 624-627
Author(s):  
D. D. Bershadenko ◽  
E. N. Ashcheulova
Keyword(s):  
Oxygen Consumption ◽  
Coronary Perfusion ◽  
Artificial Circulation

Dynamics of myocardial oxygen consumption and coronary vascular resistance

1977 ◽  
Vol 233 (1) ◽  
pp. H34-H43 ◽  
Author(s):  
F. L. Belloni ◽  
H. V. Sparks
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Time Course ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Constant Flow

Coronary vascular resistance may be regulated in part by substances whose concentrations are determined by or reflect the rate of myocardial oxygen consumption (e.g., adenosine, vessel wall PO2). We tested this hypothesis by comparing the time course of changes in myocardial oxygen consumption and coronary vascular resistance following 20 beat/min changes in heart rate. Main left coronary arteries of in situ dog hearts were perfused with blood at constant flow. Coronary sinus O2 content was monitored continuously with a densitometer and reflected the time course of changes in oxygen consumption and also the effects of vascular transit between tissue and the coronary sinus. These transit effects were estimated from dye transit curves and added to the time course of changes in coronary perfusion pressure which was proportional to coronary vascular resistance at constant flow. Coronary sinus O2 content changes preceded the adjusted time course of vascular resistance. This supports the hypothesis that coronary vascular resistance is regulated in part by factors closely linked to oxidative metabolism.

Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion

1985 ◽  
Vol 249 (6) ◽  
pp. H1070-H1077 ◽  
Author(s):  
I. Y. Liang ◽  
C. E. Jones
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Adrenergic Blockade ◽  
Adrenergic Antagonist

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6–8 min of prazosin infusion (0.6–0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

Endogenous nitric oxide modulates myocardial oxygen consumption in canine right ventricle

2001 ◽  
Vol 281 (2) ◽  
pp. H831-H837 ◽  
Author(s):  
Srinath Setty ◽  
Xiaoming Bian ◽  
Johnathan D. Tune ◽  
H. Fred Downey
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Right Ventricular ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Aortic Pressure ◽  
Coronary Perfusion ◽  
Endogenous Nitric Oxide ◽  
The Right

The role of endogenous nitric oxide (NO) in modulating myocardial oxygen consumption (MV˙o 2) is unclear, in part because of systemic and coronary hemodynamic effects of blocking NO release. This study evaluated the effect of NO on right ventricular MV˙o 2 under controlled hemodynamic conditions. In 12 open-chest dogs, N ω-nitro-l-arginine methyl ester (l-NAME, 150 μg/min), a NO synthase (NOS) blocker, was infused into the right coronary artery. Heart rate and mean aortic pressure were constant. Right coronary blood flow and right ventricular MV˙o 2 were measured at normal and elevated right coronary perfusion pressures (RCP) before and afterl-NAME. To avoid effects of NO synthesis blockade on right coronary blood flow, which might have altered right ventricular MV˙o 2, experiments, were conducted during adenosine-induced maximal coronary vasodilation. l-NAME did not affect right coronary blood flow ( P = 0.51). However,l-NAME significantly increased right ventricular MV˙o 2 (6% at RCP 100 mmHg, and 21% at RCP 180 mmHg). Right coronary blood flow varied with perfusion pressure ( P < 0.02), and the elevation of MV˙o 2 produced by l-NAME increased at higher flows ( P < 0.04), consistent with the greater shear stress-mediated release of NO. These findings indicate that endogenous NO limits right ventricular MV˙o 2.

Coronary pressure-flow autoregulation protects myocardium from pressure-induced changes in oxygen consumption

1994 ◽  
Vol 266 (6) ◽  
pp. H2359-H2368 ◽  
Author(s):  
X. J. Bai ◽  
T. Iwamoto ◽  
A. G. Williams ◽  
W. L. Fan ◽  
H. F. Downey
Keyword(s):  
Oxygen Consumption ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Coronary Perfusion ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Anesthetized Dogs ◽  
Induced Changes

Pressure-flow autoregulation minimizes changes in coronary blood flow (CBF) when coronary perfusion pressure (CPP) is altered. This investigation determined if autoregulation also minimizes CPP-induced changes in coronary vascular volume (CVV) and CVV-dependent changes in myocardial oxygen consumption (MVO2). In 11 anesthetized dogs, the left anterior descending coronary artery was cannulated, and responses to 20-mmHg changes in CPP were examined over a range of CPP from 60 to 180 mmHg. Changes in CPP had no significant effect on systemic hemodynamics or on left ventricular end-diastolic segment length, end-systolic segment length, or percent segment shortening. In hearts with effective pressure-flow autoregulation [closed-loop gain (GC) > 0.4], CVV increased 0.06%/mmHg change in CPP. For the same hearts, MVO2 increased 0.04%/mmHg change in CPP. In hearts with ineffective autoregulation (GC < 0.4), CVV increased 0.97%/mmHg (P < 0.001 vs. autoregulating hearts), and MVO2 increased 0.41%/mmHg (P < 0.001 vs. autoregulating hearts). MVO2 and CVV were correlated (r = 0.69, P < 0.0001) independently of autoregulatory capability, but only when autoregulation was poor and capacitance was elevated did CPP significantly affect MVO2. We conclude that pressure-flow autoregulation protects myocardium from CPP-induced changes in CVV, which in turn produces changes in oxygen consumption.

Effect of varying coronary perfusion on ventricular function in isolated dog hearts

1964 ◽  
Vol 207 (3) ◽  
pp. 683-690 ◽  
Author(s):  
N. M. Buckley ◽  
E. P. Porter ◽  
L. A. Jedeikin
Keyword(s):  
Oxygen Consumption ◽  
Ventricular Function ◽  
Oxygen Content ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Arterial Oxygen ◽  
Coronary Perfusion ◽  
Stroke Work ◽  
Arterial Oxygen Content

The effects of coronary perfusion on ventricular function have been studied in isolated ventricle preparations working under different conditions. Coronary flow, oxygen consumption, ventricular stroke work, rate of ventricular pressure change during isovolumetric contraction (dPC), and diastolic ventricular pressure (DVPm) and pressure/inflow ratio were determined. Maintenance of coronary flow and oxygen consumption in 5 experiments did not prevent irreversible changes in DVPm, stroke work, and dPC when the right ventricle was acutely overloaded. These ventricles did not accumulate water. Decreasing coronary perfusion pressure at constant arterial oxygen content in 11 experiments led to inconsistent changes in DVPm, stroke work and dPC. Decreasing arterial oxygen content at constant coronary perfusion pressure in 10 experiments led to increased DVPm but inconsistent changes in stroke work and dPC. There was an inverse relationship between DVPm and oxygen consumption in the variable perfusion experiments, but not in the overloading experiments. Ventricular function did not change significantly with time in 6 experiments in which the conditions of workload and coronary perfusion were kept constant. It was concluded that irreversible changes in performance of acutely overloaded ventricles could be independent of coronary flow, myocardial water content, or duration of experiment.

Effect of hyperosmotic mannitol on myocardial oxygen consumption

1977 ◽  
Vol 233 (4) ◽  
pp. H444-H450
Author(s):  
G. J. Vlahakes ◽  
W. J. Powell
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Tension Time ◽  
Anesthetized Dogs ◽  
Myocardial Efficiency ◽  
Experimental Myocardial Ischemia

Hyperosmotic mannitol produces salutary hemodynamic and histologic effects during experimental myocardial ischemia. However, the administration of hyperosmotic mannitol is associated with a positive inotropic influence. Positive inotropic interventions, which increase myocardial oxygen consumption (MVO2), also tend to increase the extent of ischemic myocardial injury. Thus, the purpose of this study was to determine the effect of mannitol on MVO2. Anesthetized dogs on right-heart bypass under conditions of controlled hemodynamics were studied. Both coronary arteries were perfused; mannitol was infused via the coronary perfusion cannulas to produce a 35 mosmol increase in osmolality. Heart rate was maintained constant. Cardiac output was held constant or deliberately increased so that left ventricular end-diastolic pressure and tension-time index, two other hemodynamic correlates of MVO2, remained constant or increased. MVO2 significantly decreased under conditions of decreased myocardial perfusion (P less than 0.025). This was in spite of a significant increase (P less than 0.001) in the peak rate of rise of left ventricular pressure (LV dP/dt), a hemodynamic correlate of MVO2. Thus, hyperosmotic mannitol under conditions of reduced coronary perfusion increases myocardial efficiency.

Transmural gradient of adenosine in canine heart during functional hyperemia

1991 ◽  
Vol 260 (3) ◽  
pp. H671-H680 ◽  
Author(s):  
A. Deussen ◽  
C. Walter ◽  
M. Borst ◽  
J. Schrader
Keyword(s):  
Oxygen Consumption ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Atrial Pacing ◽  
Canine Heart ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Transmural Gradient

Effects of beta-adrenergic stimulation and atrial pacing on the transmural gradient of intracellular free adenosine were assessed in dog hearts in vivo by measurement of the accumulation of S-adenosylhomocysteine (SAH) in the presence of homocysteine (1.6 mg.kg-1.min-1 iv). Isoproterenol (0.3-0.5 micrograms.kg-1.min-1 iv for 30 min) consistently enhanced left ventricular dP/dtmax (86%), heart rate (38%), and myocardial oxygen consumption (MVO2; 62%) within 3 min while formation and release of adenosine transiently increased. Diastolic aortic pressure fell from 107 +/- 12 to 58 +/- 5 mmHg, and the transmural gradient of SAH was 1.6-, 2.5-, and 4.4-fold increased in subepi-, mid- myo-, and subendocardial layers, respectively. Adenosine formation was inversely related to diastolic aortic pressure. Maintaining aortic pressure greater than 65 mmHg only slightly enhanced venoarterial difference of adenosine despite a greater augmentation of MVO2. Pacing the heart at 209 +/- 4 beats/min enhanced MVO2 by 42% and increased subepi-, midmyo-, and subendocardial levels of SAH by 1.5-, 3.3- and 1.9-fold, respectively. These results demonstrate that in the in situ heart 1) beta-adrenergic stimulation and pacing cause an inhomogeneous transmural increase in free intracellular adenosine mainly affecting the subendocardial and midmyocardial layers; 2) diastolic aortic pressure as the driving force of coronary perfusion is of critical importance for cardiac adenosine formation; and 3) the kinetics of oxygen consumption and adenosine formation are clearly dissociated during beta-stimulation.

Iron storage sites in the myocardium as revealed by cytohistochemistry

1988 ◽  
Vol 46 ◽  
pp. 394-395
Author(s):  
M. Ashraf ◽  
F. Thompson ◽  
S. Miki ◽  
P. Srivastava
Keyword(s):  
Cardiac Tissue ◽  
Coronary Perfusion ◽  
Intracellular Iron ◽  
Ether Anesthesia ◽  
Intense Staining ◽  
Iron Storage ◽  
Thin Sections ◽  
Rat Hearts ◽  
Cacodylate Buffer ◽  
Made In

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).

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