Cocaine: Long-Term Administration Depletes Cardiac Enzymes in the Rat

Trulson, Michael E.; Epps, Lisa R.; Joe, John C.

doi:10.1159/000146394

Cited by 8 publications

(2 citation statements)

References 6 publications

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“…and isocitrate dehydrogenase (ICDH). These histochemicai techniques have previously been reported in de tail (8). The enzymes were quantified using a Leitz Data Acquisition and Dis play System (DADS).…”

Section: Methodsmentioning

confidence: 99%

Halothane Depletes Cardiac Microvasculature Enzymes in the Rat

Trulson¹,

Ulissey²

1987

Cells Tissues Organs

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Left ventricular arterioles from Sprague-Dawley rats were analyzed histochemically to determine the effects of halothane administration on key enzymes of aerobic and anaerobic metabolism, as well as on key enzymes of the hexose monophosphate shunt. Significant decreases occurred in cytochrome oxidase (–42%) and β-hydroxybuty-rate dehydrogenase (–57%). No significant changes were observed in isocitrate dehydrogenase, glucose-6-phosphate dehydrogenase, or lactate dehydrogenase. These data suggest that anesthetic levels of halothane can cause impaired metabolism in the coronary microvasculature.

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Section: Methodsmentioning

confidence: 99%

Halothane Depletes Cardiac Microvasculature Enzymes in the Rat

Trulson¹,

Ulissey²

1987

Cells Tissues Organs

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“…Exposure of cardiac myocytes to cocaine for 24 hours is sufficient to induce the release of lactate dehydrogenase (LDH, a marker for cell damage) and to produce clear evidence of morphological alterations (Welder et al, 1988;Welder, 1992a). Exposure of myocytes also alters the metabolic activity of these cells (Trulson, Epps & Joe, 1987) and alters their ability to accumulate and release calcium (Tomita et al, 1993). Thus, the morphological changes observed in cardiac myocytes is correlated with functional changes in those cells.…”

Section: Pathological Changes With Long-term Usementioning

confidence: 99%

Cocaine and cardiovascular toxicity

Schindler

1996

Addiction Biology

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Over the past 10 years a great deal has been learned about the cardiovascular effects of cocaine. In particular, the acute effects of cocaine have been studied extensively. Upon acute administration cocaine increases blood pressure and heart rate, primarily through an action on the sympathetic nervous system. Cocaine also suppresses the baroreflex response and vagal tone, further contributing to its effects on heart rate. At the same time cocaine is increasing the work-load on the heart it induces coronary artery vasoconstriction, potentially leading to cardiac ischemia. At higher doses cocaine can depress ventricular function and slow electrical conduction in the heart. Both these effects appear to be mediated by cocaine's local anesthetic action. The effects of cocaine mediated by the sympathetic nervous system are greatly reduced in anesthetized animals. Further, when cocaine is administered repeatedly over a short period of time, acute tolerance can develop to the sympathomimetic effects of cocaine. In contrast, the effects of cocaine mediated by its local anesthetic action do not appear blunted by anesthesia or susceptible to acute tolerance. With chronic administration, higher doses appear to induce tolerance while lower doses may induce sensitization to cocaine's sympathomimetic effects. Cocaine also induces a variety of pathological changes in the heart, including myocardial contraction band necrosis and ventricular hypertrophy. These effects of cocaine on the heart can all contribute to potentially lethal cardiovascular events. In addition to the effects of cocaine alone, the metabolites of cocaine may also contribute to cocaine's cardiovascular toxicity, and both licit and illicit drugs used in combination with cocaine might potentially alter its cardiovascular effects.

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