Relationship between anaerobic energy formation and myocardial contractility during disturbance of coronary perfusion

The study was designed to assess the influence of nitric oxide (NO) on myocardial contractility in vivo. The left anterior descending coronary artery (LAD) of 28 anesthetized, open-chest dogs was perfused with arterial blood via an extracorporeal circuit. In the LAD bed, segmental shortening (SS), an index of local myocardial contractility, was measured with ultrasonic crystals. Coronary blood flow (CBF) was measured by Doppler flow transducer and used to calculate myocardial oxygen consumption (MVO2). Studies were performed with coronary perfusion pressure (CPP) constant (n = 23) or with CBF constant (n = 5). Measurements were obtained 1) during intracoronary infusions of the NO donors sodium nitroprusside (SNP, 80 ng/min) and nitroglycerin (NTG, 40 micrograms/min) and of a stimulator of endogenous NO release, acetylcholine (ACh, 20 micrograms/min), and 2) after inhibition of basal NO synthase activity with either NG-nitro-L-arginine methyl ester (L-NAME, 300 micrograms/min ic for 15 min) or NG-monomethyl-L-arginine (L-NMMA 2mg/min ic for 15 min). Decreases in SS (-38%) and MVO2 (-42%) during intracoronary isoflurane infusion verified responsiveness of preparation to negative inotropic agents. With CPP constant, SNP, NTG, and ACh caused increases in CBF (177, 28, and 280%, respectively) with no changes in SS or MVO2. Neither L-NAME nor L-NMMA affected SS, MVO2, or CBF. With CBF constant, the SNP- and ACh-induced decreases in CPP were accompanied by no changes in SS. In conclusion, NO had no direct influence on myocardial contractility or oxygen demand under baseline conditions, or when its local concentration was increased acutely with SNP, NTG, or ACh. An augmented SS secondary to increased CBF per se, i.e., Gregg's phenomenon, did not obscure potential negative inotropic effects of SNP and ACh with CPP constant.

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Effect of Coronary Perfusion on Myocardial Contractility in the Heart

Cardiac Adaptation and Failure ◽

10.1007/978-4-431-67014-8_2 ◽

1994 ◽

pp. 21-35

Author(s):

Masafumi Kitakaze ◽

Tetsuo Minamino ◽

Toshikazu Morioka ◽

Koichi Node ◽

Michitoshi Inoue ◽

...

Keyword(s):

Myocardial Contractility ◽

Coronary Perfusion

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Effects of Imposed Acid–Base Derangement on the Cardiovascular Effects and Pharmacokinetics of Bupivacaine and Thiopental

Anesthesiology ◽

10.1097/00000542-200406000-00018 ◽

2004 ◽

Vol 100 (6) ◽

pp. 1457-1468 ◽

Cited By ~ 5

Author(s):

Laurence E. Mather ◽

Leigh A. Ladd ◽

Susan E. Copeland ◽

Dennis H.-T. Chang

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Myocardial Contractility ◽

Cardiovascular Effects ◽

Whole Body ◽

Coronary Perfusion ◽

Acid Base ◽

Blood Concentrations ◽

Blood Ph

Background By changing physicochemical properties such as effective lipophilicity, changes in blood pH could alter the distribution, elimination, and effects of weakly ionizing drugs. The authors examined the outcome of imposed acid-base derangement on cardiovascular effects and myocardial and whole body pharmacokinetics of bupivacaine, a weak base, and thiopental, a weak acid. Methods Intravenous infusions of rac-bupivacaine HCl (37.5 mg) or rac-thiopental sodium (250 mg, subanesthetic dose) were administered over 3 min to previously instrumented conscious ewes with normal blood pH, acidemia imposed by lactic acid infusion, or alkalemia imposed by bicarbonate infusion. Hemodynamic and electrocardiographic effects were recorded; arterial and coronary sinus drug blood concentrations were analyzed by chiral high-performance liquid chromatography. Results Bupivacaine decreased myocardial contractility, coronary perfusion, heart rate, and cardiac output; however, cardiac output and stroke volume were not as affected by bupivacaine with acidemia. Thiopental decreased myocardial contractility and stroke volume and increased heart rate; acidemia enhanced the tachycardia and produced a greater decrease in stroke volume than with alkalemia. Taken as a whole, the cardiovascular changes were not systematically modified by acid-base derangement. Overall, the tissue distribution of bupivacaine was favored by alkalemia, but thiopental pharmacokinetics were essentially unaffected by acid-base derangement. Acid-base derangement did not influence the kinetics of either drug enantioselectively. Conclusions At the doses used, the hemodynamic and electrocardiographic effects of bupivacaine and thiopental were not systematically modified by acid-base derangement, nor were there changes in regional or whole body pharmacokinetics of either drug that were clearly related to acid-base status.

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Contribution of myocardial contractility to myocardial perfusion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1979.236.1.h121 ◽

1979 ◽

Vol 236 (1) ◽

pp. H121-H126 ◽

Cited By ~ 2

Author(s):

J. Trimble ◽

J. Downey

Keyword(s):

Myocardial Contractility ◽

Perfusion Pressure ◽

Regional Blood Flow ◽

Coronary Perfusion Pressure ◽

Ventricular Pressure ◽

Coronary Perfusion ◽

Sodium Pentobarbital ◽

Inotropic State ◽

Myocardial Layers ◽

Coronary Tone

Myocardial contractility in open-chest anesthetized (sodium pentobarbital) dogs was varied while ventricular pressure, coronary perfusion pressure, and coronary tone were held constant. Under those conditions, changes in regional blood flow should reflect changes only in intramyocardial compression related to the altered inotropic state. Increasing contractility with isoproterenol caused flow to decrease in the outer myocardial layers without change at the subendocardium. When contractility was decreased with pentobarbital, flow at the subendocardium was increased with little change in the outer layers. By manipulating perfusion pressure in the latter experiments it was demonstrated that subendocardial compression was falling from a starting value that was somewhat above peak ventricular pressure.

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Contributions of Coronary Perfusion Pressure, Metabolic Acidosis and Adrenergic Factors to the Reduction of Myocardial Contractility during Hemorrhagic Shock in the Cat

Circulation Research ◽

10.1161/01.res.27.6.875 ◽

1970 ◽

Vol 27 (6) ◽

pp. 875-889 ◽

Cited By ~ 13

Author(s):

HOWARD W. SIEGEL ◽

S. EVANS DOWNING

Keyword(s):

Metabolic Acidosis ◽

Hemorrhagic Shock ◽

Myocardial Contractility ◽

Perfusion Pressure ◽

Coronary Perfusion Pressure ◽

Coronary Perfusion

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Iron storage sites in the myocardium as revealed by cytohistochemistry

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100104030 ◽

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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