Cardiovascular drugs catecholamines

Cardiovascular Increased catecholamine activity results in cardiac overstimulation, which can be life-threatening if an overdose of one of the drugs is taken. The slowing of atrioventricular conduction among depressed elderly patients is of particular concern. 

Donnelly, M., Zametkln, A.J., Rapoport, J.L., Ismond, D.R., Wein-gartner, H., Lane, E., Oliver, J., Linnoila, M., and Potter, W.Z. (1986) Treatment of childhood hyperactivity with deslpramlne plasma drug concentration, cardiovascular effects, plasma and urinary catecholamine levels, and clinical response. Clin Pharmacol Ther 39 72-81. 

The drug disulfiram interferes with the oxidation of acetaldehyde formed during the metabolism of alcohol. This increases the blood level of acetaldehyde which acts directly on cardiovascular system and produce these toxic reactions. Disulfiram also inhibits dopamine beta oxidase and thus interferes with the synthesis of noradrenaline, which causes depletion of catecholamines. 

The effects of sympathomimetic drugs on blood pressure can be explained on the basis of their effects on heart rate, myocardial function, peripheral vascular resistance, and venous return (see Figure 6-7 and Table 9-4). The endogenous catecholamines, norepinephrine and epinephrine have complex cardiovascular effects because they activate both and 13 receptors. It is easier to understand these actions by first describing the cardiovascular effect of sympathomimetics that are selective for a given adrenoreceptor. 

Rooke GA, EO Feigl (1982) Work as a correlate of canine left ventricular oxygen consumption, and the problem of catecholamine oxygen wasting. Circ Res 50 273-286 Scholkens BA, Becker RHA, Kaiser J (1984) Cardiovascular and antihypertensive activities of the novel non-sulfhydryl converting enzyme inhibitor 2-[N-[(S)-l-ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-(lS,3S,5S)-2-azabicyclo[3.3.0]octane-3-carboxylic acid (Hoe 498). Arzneim Forsch Drug Res 34 1417-1425... 

The cardiovascular effects of metamfetamine in 11 patients with Parkinson s disease have been described and compared with six healthy controls (5). All were tested twice, once with intravenous saline and once with intravenous metamfetamine 0.3 mg/kg. Cardiovascular measurements were taken for 15 minutes before drug administration and for 103 minutes after. Both groups had significant increases in blood pressure after metamfetamine, but the patients with Parkinson s disease had a shorter duration of increased blood pressure and a lower increase from baseline than the controls. The authors proposed that these results suggested cardiac and vascular hyposensitivity to metamfetamine in Parkinson s disease due to impaired metamfetamine-induced catecholamine release. 

Bousquet P, Feldman J, Schwartz J. Central cardiovascular effects of a adrenergic drugs differences between catecholamines and imidazolines. J Pharmacol Exp Ther 1984 230 232-236. 

Bousquet, P., Feldman, J., Schwartz, J., 1984. Central cardiovascular effects of the a-adrenergic drugs. Differences between catecholamines and imidazolines. J. Pharmacol. Exp. Ther. 230, 232-236. 

Although not strictly an adrenergic drug, dopamine is a catecholamine with properties related to the cardiovascular activities of the other agents in this chapter. Dopamine acts on specific dopamine receptors to dilate renal vessels, increasing renal blood flow. ... 

The normal additive hypotensive effects of these drugs result from the two acting in concert at different but complementary sites in the cardiovascular system. Just why antagonism sometimes occurs is unexplained. The hypertensive rebound following elonidine withdrawal is thought to be due to an increase in the levels of circulating catecholamines. With the beta (vasodilator) effects blocked by a beta blocker, the alpha (vasoconstrictor) effects of the catecholamines are unopposed and the hypertension is further exaggerated. 

Uncertain. Simple additive hypertensive effects would seem to be part of the explanation. The effects of caffeine may compound the effects of these sympathomimetic drugs on the cardiovascular and central nervous systems by blocking adenosine receptors (causing vasoconstriction) and also augmenting the release of catecholamines. ... 

In addition to studying hemodynamic changes caused by liberated histamine, plasma epinephrine and norepinephrine levels have been investigated following injection of morphine. In a study of a patient who experienced an anaphylactoid response following the intravenous injection of morphine 0.3 mg/kg, plasma catecholamines were increased and this was accompanied by decreases in systemic vascular resistance and arterial blood pressure. In another study, intravenous morphine increased cardiac output, histamine, and epinephrine plasma concentrations and decreased arterial blood pressure and systemic vasculature resistance in adult subjects with no history of drug allergy or clinical evidence of cardiovascular, pulmonary, or metabolic disease. 

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