Effect of chronic cocaine administration and cocaine withdrawal on coronary flow rate and heart rate responses to epinephrine and cocaine in isolated perfused rat hearts

Endothelium-derived nitric oxide (NO) has recently been reported to be a mediator of ischemic preconditioning in dog hearts. The aim of the present study was to determine the role of NO in ischemic preconditioning in isolated perfused rat hearts. Rat hearts were perfused at either constant pressure (80 mmHg) or constant flow. After aerobic perfusion (37 degrees C) for 10 min, hearts were treated with N omega-nitro-L-arginine methyl ester (L-NAME; 30 microM), which is an inhibitor of NO synthase, or vehicle. Ten minutes later, the hearts were preconditioned (4 episodes of 5 min of global ischemia and 5 min of reperfusion) or perfused normally before a 30-min global ischemic period. All hearts were reperfused for 30 min. Coronary flow or perfusion pressure plus heart rate and contractile function were measured continuously. Hearts perfused at constant pressure and treated with 30 microM L-NAME, a concentration that effectively inhibits endogenous NO synthesis, exhibited decreased coronary flow after 10 min, and flow remained decreased throughout the experiment. Ischemic preconditioning before 30 min of global ischemia resulted in a doubling of contractile function and a reduction of lactate dehydrogenase release at the end of the 30-min reperfusion period compared with nonpreconditioned hearts. The protective effect of preconditioning was not different in L-NAME-treated hearts. In addition, inhibition of NO synthase had no effect on the severity of ischemia in nonpreconditioned hearts. Similar results were obtained in preconditioned hearts that were perfused at constant flow, indicating that the flow reductions caused by L-NAME did not influence the results.(ABSTRACT TRUNCATED AT 250 WORDS)

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The Effect of Hawthorn Extract on Coronary Flow

Journal of Evidence-Based Complementary & Alternative Medicine ◽

10.1177/2156587213491428 ◽

2013 ◽

Vol 18 (4) ◽

pp. 257-267

Author(s):

Kenneth P. Dood ◽

Aaron D. Frey ◽

Timothy P. Geisbuhler

Keyword(s):

Nitric Oxide ◽

Coronary Flow ◽

Cell Injury ◽

Late Phase ◽

Rat Hearts ◽

Hawthorn Extract ◽

Perfused Rat Hearts ◽

Oxide Synthase ◽

Prostacyclin Production ◽

Isolated Perfused Rat Hearts

Hawthorn extract has been used for heart failure and may decrease cardiac cell injury and improve cardiac function. One proposed mechanism for hawthorn action is vasodilation. We hypothesized that hawthorn extract would increase coronary blood flow in isolated perfused rat hearts. Coronary flow was measured in nonworking perfused rat hearts (Langendorff, constant pressure) using a flow probe; data were collected electronically in real time. Hawthorn extract showed an early (30-120 seconds) vasodilation, followed by a later (3-5 minutes) decrease in coronary flow. Maximum vasodilation occurred with 240 μg/mL hawthorn extract. Hawthorn’s pattern of activity was unlike that of several known vasoactive drugs. Both nitric oxide synthase inhibitors and indomethacin abolished early vasodilation, but they had no effect on the late phase decrease in flow. We suggest that a hawthorn-induced increase in nitric oxide generation leads to an increase in prostacyclin production, thus causing early phase vasodilation.

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Anoxidative work and metabolism of isolated perfused rat hearts as influenced by artificially increased heart rate

Pflügers Archiv - European Journal of Physiology ◽

10.1007/bf01067027 ◽

1976 ◽

Vol 365 (2-3) ◽

pp. 265-267

Author(s):

E. R. M�ller-Ruchholtz ◽

R. L�ser

Keyword(s):

Heart Rate ◽

Rat Hearts ◽

Perfused Rat Hearts ◽

Isolated Perfused Rat Hearts

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Aspirate from stented aortocoronary saphenous vein grafts reduces coronary flow and left ventricular pressure in an isolated perfused rat hearts

The FASEB Journal ◽

10.1096/fasebj.29.1_supplement.953.4 ◽

2015 ◽

Vol 29 (S1) ◽

Author(s):

Petra Kleinbongard ◽

Helmut Lieder ◽

Philipp Kahlert ◽

Gerd Heusch

Keyword(s):

Saphenous Vein ◽

Coronary Flow ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Vein Grafts ◽

Saphenous Vein Grafts ◽

Rat Hearts ◽

Perfused Rat Hearts ◽

Isolated Perfused Rat Hearts

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Protective effects of histidine during ischemia-reperfusion in isolated perfused rat hearts

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.264.5.h1370 ◽

1993 ◽

Vol 264 (5) ◽

pp. H1370-H1381 ◽

Cited By ~ 3

Author(s):

R. C. Kukreja ◽

K. E. Loesser ◽

A. A. Kearns ◽

S. A. Naseem ◽

M. L. Hess

Keyword(s):

Coronary Flow ◽

Contractile Function ◽

Ischemia Reperfusion ◽

Protective Effects ◽

Oxygen Scavenging ◽

Rat Hearts ◽

Dose Dependent Fashion ◽

Perfused Rat Hearts ◽

Ultrastructural Damage ◽

Isolated Perfused Rat Hearts

We investigated the efficacy of histidine in reducing ischemia-reperfusion (I/R)-induced myocardial injury in isolated perfused rat hearts. In I/R hearts, the contractile function and coronary flow were 59 +/- 10 and 78 +/- 6% of control. Perfusion with histidine resulted in significant increase in contractility (94 +/- 4%) and coronary flow (92 +/- 4%). The incidence of arrhythmias during reperfusion was 100% (10 out of 10) in the I/R hearts with an average duration of 12.22 +/- 1.55 (SE) min. The duration of arrhythmias was shortened to 8.24 +/- 1.46, 2.15 +/- 0.9, and 2.49 +/- 1.50 min with 10, 25, and 50 mM histidine, respectively. The duration of sinus rhythm increased from 6.26 +/- 1.56 min in I/R hearts to 10.66 +/- 1.55, 14.99 +/- 1.61, and 17.18 +/- 0.95, and 11.73 +/- 0.93 min after perfusion with 10, 25, and 50 mM histidine, and superoxide dismutase (SOD)-catalase-mannitol, respectively. Electron microscopy revealed significant ultrastructural damage of myocytes in I/R hearts, which included swelling of the mitochondria and disruption of both the sarcolemma and the myofibrils. Histidine reduced the ultrastructural damage in a dose-dependent fashion. In general, the protective effect of histidine was superior than SOD-catalase-mannitol. We conclude that histidine protects myocardium against I/R damage most likely by a singlet oxygen scavenging mechanism.

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