Lack of cardiovascular tolerance during intravenous cocaine infusions in human volunteers

Kumor, Karen M.; Sherer, Michael A.; Thompson, Loren K.; Cone, Edward J.; Mahaffey, John E.; Jaffe, Jerome H.

doi:10.1016/0024-3205(88)90119-1

Cited by 36 publications

(5 citation statements)

References 10 publications

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“…There are conflicting reports regarding the effect of acute and chronic cocaine treatment on the adrenergic system (Fischman et al, 1985;Kumor et al, 1988; Ambre Figure 5. Effect of double binge cocaine treatment on total plasma nitrate-nitrite level in the rat.…”

Section: Discussionmentioning

confidence: 94%

“…Following acute cocaine administration blockade of this transporter leads to increased accumulation of norepinephrine resulting in an increase in arterial pressure and total peripheral resistance (Trouve et al, 1991;Gillis et al, 1995). Although there are numerous behavioral studies on the effect of acute cocaine in animal and human subjects, there are few studies on the effect of chronic or repetitive cocaine use on the cardiovascular system (Matsuzki et al, 1976;Fischman and Schuster, 1982;Fischman et al, 1985;Tarizzo and Rubio, 1985;Foltin et al, 1988;Kumor et al, 1988;Avakian, 1990;Ambre et al, 1991;Foltin and Fischman, 1991;Katz et al, 1992), and there are conflicting data regarding the effect of chronic cocaine use on the sympathetic nervous system. Some studies suggest that acute and chronic cocaine use can induce tolerance to the cardiovascular effects (Fischman and Schuster, 1982;Fischman et al, 1985;Kumor et al, 1988;Ambre et al, 1991;Foltin and Fischman, 1991), whereas other studies suggest that chronic cocaine use can cause sensitization to the cardiovascular actions of the drug (Kumor et al, 1988;Foltin et al, 1988).…”

Section: Introductionmentioning

confidence: 98%

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Effect of binge cocaine treatment on hindlimb vascular function

Pradhan¹,

Dabisch²,

Liles³

et al. 2005

J. Appl. Toxicol.

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Chronic cocaine abuse is known to cause endothelial dysfunction and atherosclerosis. The present study investigated the effect of binge cocaine treatment, a model for chronic cocaine abuse, on the blood flow responses to the adrenergic agonists norepinephrine, phenylephrine and isoproterenol, the endothelium-dependent vasodilator acetylcholine, and the endothelium independent vasodilator sodium nitroprusside (SNP) in the hindlimb vascular bed of male Sprague Dawley rats. Rats received either single binge or double binge treatment. Each binge treatment consisted of three doses of cocaine (30 mg kg(-1) i.p.) for 3 days. For double binge treatment, there was a 4 day recovery period between the binges. At the end of the treatment the rats were anesthetized and agonists were administered into the right hindlimb circulation through a catheter in the left iliac artery and blood flow responses were measured with a flow probe around the right iliac artery. Rats receiving double cocaine binges showed a significant decrease in the magnitude and duration of the blood flow response to norepinephrine and a decrease in the duration of the blood flow response to phenylephrine, isoproterenol and acetylcholine when compared with saline controls. The blood flow response to SNP was not changed. Total plasma nitrate-nitrite levels were significantly reduced and big endothelin levels were significantly increased in rats receiving double cocaine binges. This study demonstrates that binge cocaine treatment can alter endothelial function, while not changing smooth muscle function, and impairs the adrenergic pathway.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 98%

Effect of binge cocaine treatment on hindlimb vascular function

Pradhan¹,

Dabisch²,

Liles³

et al. 2005

J. Appl. Toxicol.

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“…The peak effect of intravenous cocaine on blood pressure occurs within 1-5 min after injection (Kumor et al 1988) and was measured in this study at 2 min. The maximum effect of nifedipine after the place-bo injection, however, occurred at 30 min post-injection [50 min after oral administration of nifedipine; Kleinbloesem et al (t984)] (Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of nifedipine pretreatment on subjective and cardiovascular responses to intravenous cocaine in humans

et al. 1991

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The effects of oral nifedipine pretreatment on subjective and cardiovascular responses to intravenous cocaine infusions were studied in cocaine-using volunteers. Nifedipine, 10 mg or placebo, was administered 20-25 min before placebo, 20 mg, or 40 mg cocaine, using a repeated measures randomized double-blind design. The variables measured were self-reported subjective effects, general behavior rated by two observers, blood pressure and heart rate. Cocaine produced the expected dose-related effects on subjective and cardiovascular measures. Nifedipine pretreatment attenuated some subjective effects of cocaine. Nifedipine directly reduced blood pressure but did not antagonize the effects of cocaine on blood pressure. These findings suggest that dihydropyridine calcium channel modulators may be useful compounds in the clinical management of cocaine users.

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“…Interestingly, the Admin: time after administration; Present: time after presentation; COC: cocaine concentrations; EME: ecgonine methyl ester; CE: cocaethylene; E: ecgonine; NC: norcocaine; BE: benzoylecgonine measured half-life for cocaine and the blood concentrations observed in these two individuals were consistent with values reported from normothermic, healthy, human volunteers (0.1-0.6 mg/L). [14][15][16][17][18][19][20] If anything, the half-lives of 132 and 114 min in these patients were prolonged. This suggests that, at least in the living, cocaine metabolism is not accelerated by elevated body temperature, even in the presence of profound hyperthermia as in Case 1.…”

Section: Discussionmentioning

confidence: 99%