The Effect of Ethanol and Acetaldehyde on the Metabolism and Vascular Resistance of the Perfused Heart

1971 ◽  
Vol 49 (2) ◽  
pp. 227-233 ◽  
Author(s):  
L. Gailis ◽  
M. Verdy
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Anaerobic Glycolysis ◽  
Appreciable Effect ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Perfused Heart ◽  
Perfused Rat Heart ◽  
Ethanol Ethanol

The effect of ethanol and acetaldehyde on the perfused nonworking rat and guinea pig hearts was studied. Ethanol (100 mM) initially increased the coronary vascular resistance, but had no appreciable effect on oxygen consumption, glucose-U-14C oxidation, or anaerobic glycolysis. Acetaldehyde (1 mM) increased the heart rate and oxygen consumption, and decreased the coronary vascular resistance. The decrease in coronary resistance was not affected by propranolol but the increase in heart rate was partially blocked. The loss of amino acids or aspartate transminase activity from the heart was not affected by the presence of ethanol. Ethanol-1-14C, either at 10 or 100 mM, was not oxidized by the perfused rat heart.

Assessment of donor heart viability during ex vivo heart perfusion

2015 ◽  
Vol 93 (10) ◽  
pp. 893-901 ◽  
Author(s):  
Christopher W. White ◽  
Emma Ambrose ◽  
Alison Müller ◽  
Yun Li ◽  
Hoa Le ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Ex Vivo ◽  
Lactate Concentration ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Myocardial Performance ◽  
Donor Heart ◽  
Functional Parameters ◽  
Heart Perfusion

Ex vivo heart perfusion (EVHP) may facilitate resuscitation of discarded donor hearts and expand the donor pool; however, a reliable means of demonstrating organ viability prior to transplantation is required. Therefore, we sought to identify metabolic and functional parameters that predict myocardial performance during EVHP. To evaluate the parameters over a broad spectrum of organ function, we obtained hearts from 9 normal pigs and 37 donation after circulatory death pigs and perfused them ex vivo. Functional parameters obtained from a left ventricular conductance catheter, oxygen consumption, coronary vascular resistance, and lactate concentration were measured, and linear regression analyses were performed to identify which parameters best correlated with myocardial performance (cardiac index: mL·min–1·g–1). Functional parameters exhibited excellent correlation with myocardial performance and demonstrated high sensitivity and specificity for identifying hearts at risk of poor post-transplant function (ejection fraction: R2 = 0.80, sensitivity = 1.00, specificity = 0.85; stroke work: R2 = 0.76, sensitivity = 1.00, specificity = 0.77; minimum dP/dt: R2 = 0.74, sensitivity = 1.00, specificity = 0.54; tau: R2 = 0.51, sensitivity = 1.00, specificity = 0.92), whereas metabolic parameters were limited in their ability to predict myocardial performance (oxygen consumption: R2 = 0.28; coronary vascular resistance: R2 = 0.20; lactate concentration: R2 = 0.02). We concluded that evaluation of functional parameters provides the best assessment of myocardial performance during EVHP, which highlights the need for an EVHP device capable of assessing the donor heart in a physiologic working mode.

Neuropeptide Y and coronary vasoconstriction: role of thromboxane A2

1992 ◽  
Vol 263 (4) ◽  
pp. H1045-H1053
Author(s):  
S. E. Martin ◽  
J. T. Kuvin ◽  
S. Offenbacher ◽  
B. M. Odle ◽  
R. E. Patterson
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Neuropeptide Y ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Thromboxane A2 ◽  
Coronary Resistance ◽  
Txa2 Receptor

We previously reported that coronary constriction following neuropeptide Y (NPY) was alleviated by cyclooxygenase blockade. To determine the role of thromboxane A2 (TxA2), anesthetized dogs received two paired doses of NPY given 2 h apart. Nine control dogs received NPY alone. Nine test dogs received one of three TxA2 receptor antagonists given between the doses of NPY. Also, five dogs received NPY during which prostaglandins were measured. In controls, NPY decreased coronary blood flow and increased aortic pressure; coronary resistance was increased significantly. Heart rate fell, and myocardial oxygen consumption was unchanged. Thromboxane receptor blockers significantly relieved the coronary constrictor effect of NPY. The reduction in coronary blood flow was blunted, while heart rate, first derivative of left ventricular pressure, and myocardial oxygen consumption were unchanged. Alleviation by TxA2 receptor blockade paralleled that reported for cyclooxygenase inhibitors. Also, significant increases in coronary venous TxA2 were seen at the time of maximal increases in coronary resistance, while prostacyclin was unchanged. In summary, TxA2 appears to mediate part of the coronary constrictor effect of NPY.

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.

scholarly journals Effects of Acetylstrophanthidin on Coronary Vascular Resistance and Myocardial Oxygen Consumption

1965 ◽  
Vol 16 (3) ◽  
pp. 203-209 ◽  
Author(s):  
JOHN A. WALDHAUSEN ◽  
JAMES W. KILMAN ◽  
THOMAS L. HERENDEEN ◽  
FRANCIS L. ABEL
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Myocardial Oxygen Consumption ◽  
Coronary Vascular Resistance

Intramyocardial distribution of blood flow in hemorrhagic shock in anesthetized dogs

1976 ◽  
Vol 230 (1) ◽  
pp. 41-49 ◽  
Author(s):  
EL Carlson ◽  
SL Selinger ◽  
J Utley ◽  
JI Hoffman
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Anesthetized Dogs ◽  
Diastolic Coronary Flow

In 34 anesthetized, open-chest dogs aortic blood pressure was kept at 35-40 mmHg for 3 h to determine if maldistribution of coronary blood flow (CBF) could contribute to the irreversibility of hemorrhagic shock. Six dogs were pretreated with phenoxybenzamine (PBZ) and 11 dogs (3 with PBZ) received hypertonic mannitol infusions in late hemorrhage. Changes of heart rate, cardiac output, and peripheral resistance were similar to those described by others. In untreated dogs total and left ventricular CBF fell, as did coronary vascular resistance. However, minimal coronary resistance after transient ischemia rose progressively and the ratio of subendocardial:subepicardial flow fell, as did the percentage of diastolic coronary flow. Mannitol infusion returned CBF and steady-state and minimal postischemic coronary resistance to control values and also returned to normal the increased myocardial water content found in late hemorrhage. Phenoxybenzamine delayed but did not prevent the rise of coronary vascular resistance or decreased subendocardial flow. These studies suggest that there may be subendocardial ischemia, possibly due to myocardial edema, in hemorrhagic shock.

Abstract 2085: Increased Regional Coronary Vascular Resistance During Hyperemia in Hypertrophic Cardiomyopathy Is Associated with Reduced Myocardial Blood Volume

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Hiroshi Komatsu ◽  
Satoshi Yamada ◽  
Masanao Naya ◽  
Hisao Onozuka ◽  
Taisei Mikami ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Contrast Echocardiography ◽  
Interventricular Septum ◽  
Power Doppler ◽  
Doppler Imaging ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Myocardial Blood Volume

Introduction: In patients with hypertrophic cardiomyopathy ( HCM ), myocardial blood flow ( MBF ) is decreased during hyperemia because of high coronary vascular resistance. Recently myocardial blood volume ( MBV ) can be estimated in vivo using myocardial contrast echocardiography ( MCE ) with the compensation for acoustic field inhomogeneity. The relationship between MBV and coronary resistance, however, has not been investigated. We thus assessed the hypothesis that increased regional coronary vascular resistance during hyperemia in HCM is associated with reduced MBV. Methods: In 13 patients with HCM ( H , 53±16 years) with asymmetric septal hypertrophy and 9 normal volunteers ( N , 54±11 years), MCE was performed under infusion of Levovist at rest and during hyperemia induced by ATP. Apical 4-chamber views of intermittent harmonic power Doppler imaging were acquired at end-diastole of every sixth beat. MBV was calculated as 10 X/10 ×100%, where X was myocardial contrast intensity minus contrast intensity of the adjacent intracavity blood pool in dB. 15 O-water PET was performed to measure regional MBF. These parameters were measured in the interventricular septum ( IVS ) and LV posterolateral ( PL ) wall. Regional coronary vascular resistance was calculated as (mean blood pressure)/MBF. Results: Wall thickness was significantly greater in H than in N (IVS: 19±4 vs 10±1 mm, p<0.0001; PL: 10±1 vs 9±1 mm, p<0.05). MBV of IVS was lower in H than in N (rest: 2.1±0.7 vs 3.5±1.1%, p<0.01; hyperemia: 2.1±1.3 vs 4.3±1.7%, p<0.01), whereas MBV of PL wall did not differ between groups. Coronary resistance at rest did not differ between groups, but the resistance during hyperemia was significantly greater in H than in N (IVS: 59±16 vs 31±14 mmHg·min·g·ml −1 , p<0.001; PL: 40±10 vs 30±11 mmHg·min·g·ml −1 , p<0.05). Coronary resistance at rest did not correlate with MBV, whereas that during hyperemia inversely correlated with MBV during hyperemia (r=−0.77, p<0.0001) as well as MBV at rest (r=−0.65, p<0.0001). Conclusions: Increased coronary vascular resistance during hyperemia in HCM was significantly associated with reduced MBV. MCE is useful for assessing the dynamic function of coronary circulation in the clinical setting.

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