Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0600097 (Sedation)
 1,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonidine hydrochloride (Catapres), a potent antihypertensive agent, has been in clinical use since 1974 in the United States. Clonidine, an alpha-adrenergic receptor agonist, stimulates central alpha receptors in the depressor site of the vasomotor center of the medulla oblongata and hypothalamus, which diminishes efferent sympathetic tone to the heart, kidneys, and peripheral vasculature with a concomitant increase in vagal activity. Hemodynamic and renal effects include reduction in supine and erect blood pressure, heart rate, total peripheral resistance, plasma renin activity, and urinary aldosterone and catecholamine excretion, with little effect on resting cardiac output, response to exercise, and preservation of renal function. Clonidine alone produces a significant reduction in mean arterial pressure in all degrees of hypertension during acute and chronic administration, with little or no tendency toward tolerance or postural hypotension. Its antihypertensive potency is enhanced with the concomitant use of a diuretic or vasodilator, and it may be used in place of a beta blocker with equal efficacy in the diuretic plus vasodilator combination. Serious adverse effects are uncommon, with more than 93% of patients tolerating the drug well. Sedation and dry mouth, the most common adverse effects, are usually related to dose and duration and are minimized by gradually increasing the dose and by taking the major portion of the twice-daily schedule at bedtime. Clonidine may be safely given to patients with congestive heart failure, ischemic heart disease, obstructive lung disease, chronic renal insufficiency, and diabetes mellitus. Clonidine is one of the most versatile and effective agents presently available for the treatment of hypertension.
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PMID:Clonidine hydrochloride. 704 65

Atrial fibrillation (AF) has been treated with DC shocks delivered transthoracically, but in 5-30% of patients, the procedures fail to restore sinus rhythm (SR). We hypothesized that applying high energy shock waves to the chest may overcome the inadequate penetration of electrical shock to the atrium. The aim of this study was to evaluate the efficacy of higher energy external DC shock for the treatment of refractory AF coexisting with cardiovascular disease using a synchronized double external defibrillator. Fifteen patients (mean age 65 +/- 8) with refractory AF to standard DC cardioversion (CV) underwent higher energy DC shock using a double external defibrillator. Concomitant heart disease was present in all patients. Warfarin and amiodarone (600 mg/day), were administered for at least three weeks duration before DC CV. Sedation was performed with IV midazolam. Two defibrillator paddles were positioned on the anterior and posterior chest wall in a right lateral decubitus position. Defibrillators were synchronized to the R waves and simultaneously 720 joules of energy was administered to the patients. Amiodarone (200 mg/day) was continuously administered after DC shock to maintain SR. Sinus rhythm was obtained in 13 patients. Sinus rhythm was persistent in 11 patients for six months duration. Creatine kinase MB fractions were normal at 4 (22 +/- 4 IU/L) and 12 hours (18 +/- 4 IU/L). None of the patients developed significant hemodynamic compromise or congestive heart failure, higher AV block, stroke, or transient ischemic cerebral events. The results indicate that higher energy DC shock application using a double external defibrillator is an effective and safe method for the cardioversion of refractory AF. We believe this procedure should be performed before internal atrial cardioversion.
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PMID:Simultaneous double external DC shock technique for refractory atrial fibrillation in concomitant heart disease. 1565 68