Positive inotropism in hypothermia partially depends on an increase in maximal Ca(2+)-activated force

1991 ◽  
Vol 261 (4) ◽  
pp. H1005-H1010 ◽  
Author(s):  
H. Kusuoka ◽  
Y. Ikoma ◽  
S. Futaki ◽  
H. Suga ◽  
A. Kitabatake ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Oxygen Consumption ◽  
Mild Hypothermia ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Phosphorus Compounds ◽  
Resonance Spectroscopy ◽  
Positive Inotropism ◽  
Rapid Pacing ◽  
Intact Heart

We investigated the contribution of maximal Ca(2+)-activated force to the positive inotropism induced by mild hypothermia. Phosphorus-31 nuclear magnetic resonance spectroscopy revealed that neither energy-related phosphorus compounds in myocardium nor intracellular pH was responsible for the change in contractility. Maximal Ca(2+)-activated pressure (MCAP), the intact-heart correlate of maximal Ca(2+)-activated force, was determined in isolated perfused rabbit hearts by measuring isovolumic left ventricular pressure during tetani at extracellular Ca2+ concentrations greater than or equal to 10 mM. Tetani were elicited by rapid pacing after exposure to ryanodine. MCAP increased by 2.17 +/- 0.28% (mean +/- SE, P less than 0.001, n = 19) for each degree of myocardial cooling between 30 and 38 degrees C. Our results indicate that a primary change in myofilament Ca2+ responsiveness underlies the positive inotropism in hypothermia. The increase in maximal Ca(2+)-activated force may explain the observation of positive inotropism without an upward shift in the relation between oxygen consumption and pressure-volume area, as previously reported for cooled whole hearts.

Metabolic correlates of adenosine formation in stimulated guinea pig heart

1991 ◽  
Vol 260 (1) ◽  
pp. H165-H172 ◽  
Author(s):  
J. P. Headrick ◽  
G. P. Matherne ◽  
S. S. Berr ◽  
D. C. Han ◽  
R. M. Berne
Keyword(s):  
Guinea Pig ◽  
Inorganic Phosphate ◽  
Consumption Rate ◽  
Myocardial Metabolism ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Guinea Pig Heart ◽  
Norepinephrine Infusion ◽  
Myocardial O2 Consumption

Adenosine release into epicardial fluid and coronary effluent of isolated isovolumic guinea pig hearts was examined at baseline and after stimulation with norepinephrine (30 nM) during 31P-nuclear magnetic resonance spectroscopy to monitor myocardial metabolism. At baseline flow (9.6 +/- 0.3 ml.min-1.g-1), epicardial and venous adenosine concentrations were 154 +/- 40 and 17 +/- 5 nM, respectively. The phosphorylation potential (log[ATP]/[ADP][Pi]) and the phosphocreatine-inorganic phosphate ratio ([PCr]/[Pi]) were 5.26 +/- 0.04 and 8.5 +/- 0.7, respectively. Norepinephrine increased left ventricular pressure, heart rate, and myocardial O2 consumption rate by approximately 21, 70, and 45%, respectively, and increased epicardial and venous adenosine to 496 +/- 74 and 461 +/- 94 nM, respectively. Log-[ATP]/[ADP][Pi] and [PCr]/[Pi] declined to 4.57 +/- 0.06 and 1.9 +/- 0.3, respectively. Epicardial [AMP] increased from 54 +/- 13 to 123 +/- 24 nM. AMP was not detectable in the venous effluent. Coronary resistance correlated with epicardial and venous [adenosine] (r = 0.86 and 0.90). Epicardial and venous [adenosine] correlated with log[ATP]/[ADP][Pi], [PCr]/[Pi], and cytosolic [AMP]. Hence, interstitial adenosine is linked to cytosolic metabolism and may regulate coronary vascular resistance. Venous adenosine underestimates epicardial adenosine at baseline but more closely approximates epicardial adenosine during norepinephrine infusion.

Myoglobin function in the isolated fluorocarbon-perfused dog heart

1978 ◽  
Vol 234 (5) ◽  
pp. H567-H572 ◽  
Author(s):  
R. P. Cole ◽  
B. A. Wittenberg ◽  
P. R. Caldwell
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Mechanical Performance ◽  
Left Ventricular Pressure ◽  
Dry Weight ◽  
Left Ventricular ◽  
Facilitated Diffusion ◽  
Dog Heart ◽  
Before And After ◽  
Ringer’S Lactate

An isolated dog heart preparation perfused with hemoglobin-free fluorocarbon suspension has been developed to study the role of myoglobin in myocardial function. The coronary vasculature was perfused at constant flow, with oxygen consumption determined from arteriovenous PO2 differences. Muscle function was assessed by measurement of pressures generated in a latex balloon placed in the left ventricle. The perfusate consisted of 20% perfluorotributylamine and 80% Ringer's lactate with 16 mM glucose. Steady-state oxygen consumption decreased from 0.30 to 0.11 ml/min per gram dry weight left ventricle, as perfusate PO2 decreased from 690 to 150 mmHg. Left ventricular pressure generation and oxygen consumption were determined before and after addition of 8 mM sodium nitrite, which changed functional ferrous myoglobin to high-spin ferric myoglobin. Over the range of perfusate PO2 studied, nitrite addition did not alter mechanical performance or myocardial oxygen consumption. These data suggest that those conditions necessary for substantial myoglobin-facilitated diffusion of oxygen in the myocardium are not present in the isolated fluorocarbon-perfused dog heart.

Endotoxin-induced contractile dysfunction in guinea pig hearts is not mediated by nitric oxide

1995 ◽  
Vol 268 (6) ◽  
pp. H2460-H2465 ◽  
Author(s):  
U. K. Decking ◽  
C. W. Flesche ◽  
A. Godecke ◽  
J. Schrader
Keyword(s):  
Nitric Oxide ◽  
Guinea Pigs ◽  
Left Ventricular Pressure ◽  
Creatine Phosphate ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
Cardiac Depression ◽  
Organ Removal ◽  
And Control

The decreased contraction amplitude of isolated cardiac myocytes from guinea pigs exposed to lipopolysaccharide (LPS) was reported to be partially reversed by nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS) [Brady, et al., Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1963-H1966, 1992]. We have tested the potential involvement of NO formation in LPS-induced cardiac depression in the intact heart. Isolated perfused hearts of LPS-treated guinea pigs (4 mg/kg 4 h before organ removal) displayed a greatly decreased left ventricular pressure (LVP) when compared with untreated controls (48 +/- 11 vs. 93 +/- 18 mmHg, n = 6 hearts each), whereas heart rate and coronary flow were similar. Perfusion of LPS-treated hearts with L-NMMA or L-NAME (100 microM each) at constant flow did not increase LVP (50 +/- 14 and 44 +/- 11, respectively, vs. 52 +/- 14 mmHg). However, coronary resistance increased significantly. There was no difference between LPS-treated and control hearts in venous adenosine release (104 +/- 58 vs. 133 +/- 86 pmol.min-1.g-1). Measurement of the activities of the induced (iNOS) and constitutive forms of NOS revealed that there was no difference in total NOS activity (237 +/- 82 vs. 181 +/- 97 fmol.min-1.mg protein-1. There was no measurable induction of iNOS in the LPS-treated hearts either. Finally, cardiac energy status was studied by 31P nuclear magnetic resonance spectroscopy. There was no difference between LPS-treated and control hearts in myocardial ATP, creatine phosphate, pH, and free ADP (59 +/- 20 vs. 50 +/- 27 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of a Senso (Toad Venom) Containing Drug on Systemic Hemodynamics, Cardiac Function and Myocadial Oxygen Consumption in Anesthetized Dogs

1991 ◽  
Vol 19 (01) ◽  
pp. 17-31 ◽  
Author(s):  
Yoshihiko Ojiri ◽  
Katsuhiko Noguchi ◽  
Matao Sakanashi
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricular Pressure ◽  
Ventricular Myocardium ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Stroke Work ◽  
Stroke Work Index ◽  
Pressure Peak ◽  
Toad Venom

Effects of a Senso (toad venom)-containing drug, KY, on cardiovascular system were examined in anesthetized open-chest dogs. KY increased aortic pressure, peak positive first derivative of left ventricular pressure, stroke work index, percent segment shortening in left ventricular myocardium and myocardial oxygen consumption, and decreased heart rate and total peripheral vascular resistance (TPR). Propranolol augmented the increase in aortic pressure with KY, inhibited the increase in aortic flow with KY and reversed KY-induced decrease in TPR to an increase. These results indicate that KY has positive inotropic and vasodilating actions possibly originating from both digitalis- and adrenaline-like action of a Senso.

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