Drugs online research references
Acta Cient Venez. 1996;47(1):17-23.
[Direct negative inotropic effect of cocaine in rat ventricle strip]
[Article in Spanish]
Romero-Vecchione E, Vasquez J, Rosa F.
Laboratorio de Estudios Cardiovasculares, Escuela de Medicina Jose Maria Vargas, UCV, Caracas, Venezuela.
Cocaine, when used as a recreative drug, can induce cardiovascular toxic effects such as acute reduction of left ventricle ejection fraction, which indicates a negative inotropic effect of the drug. The purpose of this study was to clarify the direct negative inotropic effect of cocaine in in vitro conditions. Rat right ventricle strips were incubated in Krebs solution gassed with 95% O2 and 5% CO2 at 37 degrees, and electrically driven with 2 ms square pulses, 17 mA, at 110 systoles/min. Separate experiments were conducted to study cocaine effect at 210 and 310 systoles/min. The contractile force was recorded through a strain-gauge isometric transducer. Cocaine increased contractile force at doses of 0.3-10.0 micrograms/ml, up to 53% over basal contraction. In the presence of 4 x 10(-8) M atenolol, low doses of cocaine did not increase contractile force and at doses between 3.0-10.0 micrograms/ml revealed a depressant activity on heart muscle contractions. Doxazosin (1.0 microM) and yohimbine (0.1 microM) did not modify the positive inotropic effect of cocaine, showing that alpha 1 and alpha 2 adrenergic receptors were not involved in this cocaine ventricle action. Increasing ventricle strip stimulation rate to 210 and 310 systoles/min for 30 seconds, the contractile force was risen by 55% and 95%, respectively. Cocaine at doses 1.0-3.0 micrograms/ml did not modify the physiological increase of contractile force seen upon ventricle rate increase. The mechanism involved in the contractile force increment after ventricle rate increase is a transient rise of cytosolic Ca2+, mainly derived from the sarcoplasmic reticulum and from extracellular fluid. Atenolol (4 x 10(-8) M) exposure of the right ventricle strip intensified the negative inotropic effect of cocaine (3.0-10 micrograms/ml) seen by ventricle stimulation at 210 and 310 systoles/min. The myocardial direct depressant effect of cocaine, in the presence of atenolol, was gradually reversed by extracelular Ca2+ increase at 3.2 and 5.0 mM, respectively. In conclusion, the mechanism of myocardial direct depressant effect of cocaine is related to the beating frequency of the ventricle, which may be associated to interference with the Ca2+ release process from the myocite sarcoplasmic reticulum, and not to calcium entry blockade from extracellular fluid. However, a dpressant effect of cocaine on phase "0" of depolarization, related to its local anesthetic properties can not be ruled out.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9334447&dopt=Abstract
bham.ac.uk
In those aged 65-85 years, the major causes of death and disability are cardiovascular diseases (myocardial infarction, sudden death and stroke). Clinical trials in elderly patients have demonstrated unequivocally that effective blood pressure reduction in hypertensive patients up to the age of 85 years significantly reduces this mortality and morbidity. The larger trials are referred to as the SHEP trial (chlorthalidone), the STOP trial (beta-blockers and/or diuretics), the MRC Elderly Trial (atenolol or diuretic) and the SYST-EUR trial (nitrendipine). Patients entered into clinical trials are a selected population; those with serious coexisting diseases and with a poor prognosis are usually excluded. For this reason one has to carefully consider whether the results of these trials would provide the best treatment for the next patient the doctor sees who would probably not meet the entry criteria. Elderly hypertensives may fall into one of three categories. The sick elderly with serious disorders such as cancer or dementia have a poor quality of life and a bad prognosis. They should not be given antihypertensive drugs. The medically complicated elderly have serious disorders, which usually require drug therapy and the medical condition and the drugs used in treatment may complicate the choice of antihypertensive drugs. The potential adverse effects of adding another form of drug treatment may outweigh the potential benefits. The fit elderly do derive considerable benefit from adequate blood pressure control and need an effective, well-tolerated antihypertensive drug. The choice of drug to control blood pressure in the elderly is difficult. An effective, well-tolerated antihypertensive with little potential to interact with coexisting disorders and other drugs is needed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9833161&dopt=Abstract
Cardiovasc Drugs Ther. 1992 Oct;6(5):475-9.
Intravenous atenolol in elderly patients in the early phase of acute myocardial infarction.
Kyriakides ZS, Kremastinos D, Karavolias G, Papadopoulos C, Apostolou T, Paraskevaidis J, Toutouzas P.
Department of Cardiology, Athens General Hospital, Greece.
The aim of this study was to assess the hemodynamic response to intravenous atenolol in elderly patients with acute myocardial infarction. We studied 14 elderly men, aged 64-85 years, and 14 younger men, aged 29-48 years, in the early postfibrinolytic phase of acute myocardial infarction. All the patients were in Killip class I. A triple-lumen Swan-Ganz thermodilution catheter was introduced into the right heart chambers. The patients received 5 mg intravenous atenolol over 5 minutes. All hemodynamic parameters were measured before and 10 minutes after atenolol. The hemodynamic characteristics and the location and extent of acute myocardial infarction were the same in both groups before atenolol. The hemodynamic changes after atenolol administration were the same in the two groups, but the stroke volume and cardiac indexes decreased to a greater extent in the elderly (p = .01 and p = .0001, respectively). These results indicate that intravenous atenolol in the early postfibrinolytic phase of acute myocardial infarction is safe in Killip class I elderly patients, although the cardiac and stroke volume indexes decrease, and the increase in the total systemic resistance is more in older than in younger patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1450092&dopt=Abstract
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