Left Ventricular Pressure -Volume Relationships and Myocardial Oxygen Consumption in the Isolated Heart

Myeloperoxidase (MPO) is involved in myocardial ischemia–reperfusion (IR) injury and vascular peroxidase (VPO) is a newly identified isoform of MPO. This study was conducted to explore whether VPO is involved in IR-induced cardiac dysfunction and apoptosis. In a rat Langendorff model of myocardial IR, the cardiac function parameters (left ventricular pressure and the maximum derivatives of left ventricular pressure and coronary flow), creatine kinase (CK) activity, apoptosis, VPO1 activity were measured. In a cell (rat-heart-derived H9c2 cells) model of hypoxia–reoxygenation (HR), apoptosis, VPO activity, and VPO1 mRNA expression were examined. In isolated heart, IR caused a marked decrease in cardiac function and a significant increase in apoptosis, CK, and VPO activity. These effects were attenuated by pharmacologic inhibition of VPO. In vitro, pharmacologic inhibition of VPO activity or silencing of VPO1 expression significantly suppressed HR-induced cellular apoptosis. Our results suggest that increased VPO activity contributes to IR-induced cardiac dysfunction and inhibition of VPO activity may have the potential clinical value in protecting the myocardium against IR injury.

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Effects of Preload on Left Ventricular Pressure-Derived Indices of Contractility and Oxygen Consumption: Relationships with Direct Invasive Measurements in Anesthetized Sheep

Journal of Pharmacological and Toxicological Methods ◽

10.1016/j.vascn.2017.09.193 ◽

2017 ◽

Vol 88 ◽

pp. 227

Author(s):

Erin Ferris ◽

Shaylyn Bennett ◽

Carlos del Rio ◽

Gail Geist ◽

Bradley Youngblood ◽

...

Keyword(s):

Oxygen Consumption ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure

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Nicotine increases heart adenosine release, oxygen consumption, and contractility

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1985.249.3.h463 ◽

1985 ◽

Vol 249 (3) ◽

pp. H463-H469 ◽

Cited By ~ 1

Author(s):

R. A. Fenton ◽

J. G. Dobson

Keyword(s):

Oxygen Consumption ◽

Cardiac Contractility ◽

Left Ventricular Pressure ◽

Physiological Saline ◽

Left Ventricular ◽

Ventricular Pressure ◽

Adenosine Release ◽

Adenosine Uptake ◽

Pressure Development ◽

Transient Elevation

The effect of nicotine on adenosine release, oxygen consumption, and contractility was investigated in perfused rat hearts. Continuous infusion of nicotine into the perfusing physiological saline (PS) elicited a propranolol (10(-6) M) sensitive transient elevation of developed left ventricular pressure (LVP) and maximum rates of left ventricular pressure development and relaxation (+/- dP/dtmax) within 20 s, which subsequently declined to maintained elevated plateau levels by 1 min. The continuous infusions of nicotine to achieve PS concentrations of 5 X 10(-4), 1 X 10(-4), or 5 X 10(-5) M, respectively resulted in significant increases in the mean plateau levels of LVP (33.4, 10.1, or 6.3%), +dP/dtmax (26.3, 10.8, or 6.9%) and-dP/dtmax (35.0, 11.9, or 9.0%) at 1 min. The inclusion of propranolol (10(-6) M) with or without atropine (10(-6) M) did not alter these maintained plateau responses to nicotine. During the plateau phase of the contractile response oxygen consumption of the hearts was significantly elevated by 36, 19, or 11%, and mean levels for adenosine in the coronary effluent rose by 261, 76, or 74% in response to 5 X 10(-4), 1 X 10(-4), or 5 X 10(-5) M nicotine, respectively. Nicotine did not influence [14C]adenosine uptake by the hearts. These results suggest that nicotine is capable of 1) augmenting cardiac contractility and oxygen consumption independent of beta-adrenergic or muscarinic influence, and 2) elevating the appearance of adenosine in the coronary circulation presumably by enhancing myocardial production of the nucleoside.

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Abstract 253: Complete Reversal of Xylazine-induced Bradycardia With Intralipid in Female Mice

Circulation Research ◽

10.1161/res.119.suppl_1.253 ◽

2016 ◽

Vol 119 (suppl_1) ◽

Author(s):

Negar Motayagheni ◽

Mansoureh Eghbali

Keyword(s):

Heart Rate ◽

Cardiac Arrest ◽

Isolated Heart ◽

Ischemia Reperfusion ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Control Group ◽

Heart Rates ◽

Female Mice

Sudden cardiac arrest accounts for 300 000 to 400 000 deaths annually in united states both in men and women. Cardiac arrest could be due to abnormally slow heart rate known as bradycardia. Bradycardia is a catastrophic event which is associated with significant mortality and morbidity. We have previously shown that Intralipid, an emulsion of soy bean oil, egg yolk phospholipids and glycerol, protects the heart against ischemia/reperfusion injury as well as Bupivacaine induced cardiotoxicity. Here we examined whether intralipid can protects the heart against bradycardia. Wild type female mice C57/Bl6 (2-4 month old) were anesthetized by isoflurane after heparinization. The heart was removed immediately and placed in cold Krebs-Henseleit buffer. The aorta was cannulated and the isolated heart (Langendorff) was perfused with Krebs-Henseleit at 37°C for 15 min for stabilization. Xylazine (100-300 mg) was directly applied to the heart surface for 1-2 min until bradycardia was achieved. The heart was then perfused with either Krebs-Henseleit (KH) solution (control group), or 1% ILP (intralipid group). Hemodynamic parameters and heart rates were recorded with a catheter directly inserted into left ventricle (n=5-8 per group). The heart rates at the baseline before inducing bradycardia was 224±7 beats/min and the left ventricular pressures was 64±4 mmHg. Administration of Xylazine decreased the heart rate significantly to 81±9 beats/min and left ventricular pressure to 5±2 mmHg (p<0.001). Perfusion of the heart with intralipid rapidly restored the heart rate to 209±30 and left ventricular pressure to 59±4 which were not significantly different than their values before inducing bradycardia at the baseline. In the hearts that received Krebs-Henseleit after bradycardia, the heart rate (81±10 beats/min) and left ventricular pressure (20±8 mmHg) were significantly lower than intralipid group. In conclusion Intralipid has the ability to rapidly reverse bradycardia in female mice.

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Effects of Intraduodenal Administration of "Kyushin," a Senso (Toad Venom)-Containing Drug, on Systemic Hemodynamics, CardiacFunction and Myocardial Oxygen Consumption in Anesthetized Dogs

The American Journal of Chinese Medicine ◽

10.1142/s0192415x93000030 ◽

1993 ◽

Vol 21 (01) ◽

pp. 7-16 ◽

Cited By ~ 2

Author(s):

Matao Sakanashi ◽

Katsuhiko Noguchi ◽

Takao Chibana ◽

Yoshihiko Ojiri ◽

Masamichi Shoji

Keyword(s):

Oxygen Consumption ◽

Myocardial Oxygen Consumption ◽

Diastolic Pressure ◽

Left Ventricular Pressure ◽

Cardiovascular Effects ◽

Left Ventricular ◽

Toad Venom ◽

The Relationship ◽

Cardiotonic Effect ◽

Intraduodenal Administration

The effects of "Kyushin" (KY), a Senso (toad venom)-containing drug, on the cardiovascular system were examined by intraduodenal administration of KY in anesthetized open-chest dogs. KY (3 or 10 mg/kg) dose-dependently increased the peak positive first derivative of left ventricular pressure ((+)LVdP/dt) and mean aortic pressure, and decreased the left ventricular end-diastolic pressure (LVEDP). Myocardial oxygen consumption (MVO2) and heart rate (HR) were not significantly influenced by KY. KY produced a cardiotonic effect without any increase in MVO2, because the increase in MVO2 due to the cardiotonic effect of KY may have been cancelled by a decrease in MVO2 due to reduction of preload and the lack of increase in HR. In order to clarify the relationship between the cardiovascular effects of KY and the drug concentration in plasma, the concentration of anti-bufalin IgG reactive substance (BRS) in plasma was measured by enzyme immunoassay. The maximum BRS concentrations 20 min after administration of 3 and 10 mg/kg KY were dose-dependent. From the relationship between changes in (+)LVdP/dt and changes in BRS concentration after administration of KY, it is inferred that the effective concentration of BRS in plasma at which KY produces a cardiotonic effect in dogs is approximately 2-3 ng/ml.

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