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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The developments concern methods of application and therapeutic agents. Regarding drug aplication Ocusert has to be mentioned: inserted in the cul de sac of the eye once a week it releases a low concentration of a substance continuously and with a constant rate. For acetazolamid (Diamox) it has been shown, that in long term treatment much lower concentrations than usual are effective. Efforts regarding new local agents reducing intraocular pressure are stimulating as well as inhibiting the sympathetic tone. The practically most important discovery so far is Clonidine, whose pressure lowering mechanism is not quite clarified yet and which, due to other problems, demands a very critical indication. Beta-receptor-blocking agents, such as Propranolol could become somewhat important, as well as for some special indications the chemical sympathectomy by 6-Hydroxydopamine. The sympatholytic agent Guanethidine proves to be very valuable in special cases. Besides the pressure reducing treatment medicamentally achieved increase of the blood supply to the optic nerve becomes more important. It becomes more and more evident that the elevation of the stroke volume--thus heart output--by cardiac therapy is important what demands collaboration with colleagues of other disciplines.
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PMID:[Approaches in medical treatment in glaucoma (author's transl)]. 85 80

The effects of the antihypertensive imidazoline compounds 2-(5 fluor-0-toluidine)-2-imidazoline hydrochloride (ST 600) and 2-(2, 6 dichlorophenylamine)-2-imidazoline hydrochloride (ST 155, clonidine, Catapres) on intra-arterial pressure, cardiac output, stroke volume, heart rate, total peripheral resistance, renal blood flow, glomerular filtration rate, renal vascular resistance, plasma volume, plasma renin and aldosterone concentration were studied in five patients with essential hypertension. The antihypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no significant decrease in renal blood flow and glomerular filtration rate. Plasma volume and plasma concentrations of renin and aldosterone also did not change significantly. In the face of similar reductions in blood pressure, no differences were observed between cardio-renal haemodynamic responses after ST 600 and clonidine. However ST 600 had a longer lasting effect (8-12 hours).
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PMID:Comparison between the effects of ST 600 and clonidine. 119 Sep 9

Research on antihypertensive drugs not only provides new information on presently used agents but also leads to the introduction of exciting new compounds. Several important clinical trials involving currently available drugs have been published recently. Angiotensin-converting enzyme inhibitors improved survival in patients with milder degrees of congestive heart failure, which indicates that they have become the cornerstone of treatment for this condition. Angiotensin-converting enzyme inhibitors delayed or prevented the development of diabetic proteinuria (> 200 micrograms/min) in a placebo-controlled randomized trial. Further, enalapril was more effective than metoprolol in reducing the rate of decline in renal function in patients with type I diabetes. Calcium channel blockers protected against acute renal failure in patients after renal transplantation in two separate studies. Calcium channel blockers were shown to promote natriuresis, with negative sodium balance the same as that associated with thiazide diuretics. The voltage-dependent calcium channel has been cloned, and the binding sites of the three classes of calcium channel blockers are now known. beta-Blockers and thiazide diuretics were the drug treatments in the Systolic Hypertension in the Elderly Program trial and in the Swedish Trial in Old Patients with Hypertension study (patients 65 to 85 years). In both investigations, stroke and cardiovascular events were significantly reduced by these conventional inexpensive agents. Clonidine was found to lower blood pressure primarily by its interaction with the imidazole receptor rather than the alpha 2 receptor. Elucidation of the imidazole receptor promises to shed light on physiologic mechanisms as well as lead to the introduction of new agents, such as moxonidine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New classes of antihypertensive drugs and new findings with established agents. 136 36

Clonidine, idazoxan, rilmenidine, and comparable agents bind to imidazol(in)e (IR), as well as alpha 2-adrenergic, receptors. Interaction with IRs mediates the hypotension elicited by these drugs at their site of action in the rostral ventrolateral medulla oblongata (RVL) and probably the neuroprotection in focal ischemic cerebral infarction. Unlike alpha 2-adrenergic receptors, IRs are not coupled to G-proteins. Their native ligand may be clonidine-displacing substance (CDS), a potent, partially purified adrenomedullary secretagogue, distributed regionally in brain and some peripheral organs. IRs and CDS may be important in the genesis, expression, and/or therapy of hypertension and stroke.
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PMID:Imidazole receptors and clonidine-displacing substance in relationship to control of blood pressure, neuroprotection, and adrenomedullary secretion. 159 95

Arterial hypertension complicating acute myocardial infarction (AMI) may aggravate myocardial damage, possibly through an increase in myocardial oxygen demand. This study reports the effects of clonidine in patients with hypertension complicating acute myocardial infarction. Forty patients (37 men and three women, average age 53 years) with acute myocardial infarction, admitted to the coronary care unit not more than 24 h after the onset of symptoms, were studied. Thirty-four had anterior myocardial infarction and six had inferior myocardial infarction. All patients were in Forrester I [WP less than 18 mm Hg, cardiac index (CI) greater than 2.21 L/min/m2] or II (WP greater than 18 mm Hg, CI greater than 2.21 L/min/m2) hemodynamic subset. Blood pressure limits were systolic blood pressure greater than or equal to 150 mm Hg and diastolic blood pressure greater than or equal to 95 mm Hg. Clonidine was administered intravenously in a dose of 5 micrograms/kg over a 5-min period. Hemodynamic parameters (Swan-Ganz thermodilution catheter), systolic time intervals (Weissler), and calculated hemodynamic indexes were measured both before and 60 min after cessation of intravenous injection. Blood pressure fell from 161 +/- 20 to 126 +/- 19 mm Hg (systolic) and from 105 +/- 7.6 to 84.7 +/- 9 mm Hg diastolic. Overall, clonidine produced a decrease in total systemic resistance (-21%). Cardiac index did not change significantly (-3%). Left ventricular stroke work index was significantly reduced (-21%, p less than 0.001), as was the triple product, suggesting a favorable effect of clonidine on myocardial oxygen supply/demand ratio. This may result in a reduction in infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of clonidine in patients with acute myocardial infarction complicated by hypertension. 242 10

Pharmacological differences between canine and monkey basilar arteries were studied in vitro. The constrictor response of canine basilar artery to either norepinephrine or an alpha 1-adrenoceptor agonist phenylephrine was partly inhibited by an alpha 2-adrenoceptor antagonist yohimbine but not by an alpha 1-adrenoceptor antagonist prazosin. The contraction elicited by an alpha 2-adrenoceptor agonist clonidine was inhibited by neither prazosin nor yohimbine. These results suggest that the receptors in canine basilar artery which mediate norepinephrine-induced contraction are different from classical alpha 1 or alpha 2-adrenoceptors, although they more closely resemble the alpha 2- rather than the alpha 1-subtype. Using monkey basilar artery, phenylephrine produced the same amplitude of maximum contractile response as norepinephrine, though a much higher concentration of phenylephrine than norepinephrine was needed in order to elicit that maximum response. Clonidine did not elicit contractions. The contraction induced by norepinephrine was markedly suppressed by both prazosin and yohimbine in a noncompetitive fashion. The constrictor response of monkey basilar artery to norepinephrine, therefore, appears to be mediated by alpha 1-like adrenoceptors. Comparison of ED50 values for thromboxane A2 revealed that the monkey basilar artery was more sensitive to thromboxane A2 than that of the canine. Prostaglandin F2 alpha produced a larger maximum contraction in monkey basilar arteries than in canine basilar arteries, although the ED50 values for monkey basilar arteries were larger than those for canine basilar arteries. The ED50 values for serotonin in canine basilar arteries were a little less than those for monkey basilar arteries, although both arteries produced nearly identical maximum contractions.
Stroke
PMID:Pharmacological comparison of isolated monkey and dog cerebral arteries. 286 Jul 41

The effects of prazosin, clonidine, and indoramin on central and regional hemodynamic parameters and left ventricular performance were analyzed in a congestive heart failure population to compare the pharmacodynamic responses to different levels of alpha-adrenergic interruption in this condition. The sympathetic nervous system is blocked at the peripheral alpha1-receptor by prazosin, at central nervous system alpha-receptor sites (via alpha-adrenoceptor agonism) by clonidine, and at peripheral and central sites by indoramin. Prazosin and indoramin produced reductions in total systemic and pulmonary vascular resistances, mean systemic and pulmonary artery pressures, and pulmonary capillary wedge pressure with little change in heart rate. Both agents selectively increased hepatic blood flow. Clonidine also decreased pulmonary artery pressure and vascular resistance, but evoked negative inotropic and chronotropic activity and did not alter regional blood flow. In contrast to prazosin, indoramin and clonidine did not augment cardiac output or stroke volume. In the setting of congestive heart failure, the central and regional hemodynamic effects and the responses in left ventricular performance vary considerably depending on the site of alpha-adrenergic interruption.
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PMID:Hemodynamic responses to different levels of alpha-adrenergic interruption in congestive heart failure. 290 15

The role of central pressor mechanisms in the maintenance of blood pressure in six hypertensive patients with angiographically proven unilateral renal artery stenosis was investigated by studying the haemodynamic and hormonal responses before and after central sympathetic blockade with clonidine. To assess the dependency of blood pressure on the direct effects of angiotensin II, the same patients were studied on a separate occasion after administration of the angiotensin converting enzyme (ACE) inhibitor, captopril. There was a substantial fall in blood pressure after administration of clonidine with a smaller fall after captopril. Clonidine-induced hypotension was accompanied by a fall in cardiac output, through a reduction in the stroke volume and heart rate. Forearm vascular resistance was unchanged. There was a selective decrease in digital skin vascular resistance and plasma noradrenaline, indicating reduced sympathetic activity. Plasma renin activity and aldosterone levels did not fall. After administration of captopril, there was a fall in cardiac output due to a fall in the stroke volume but not in the heart rate. Forearm vascular resistance, digital skin vascular resistance and plasma noradrenaline were unchanged. Plasma renin activity rose and plasma aldosterone fell. We conclude that in our hypertensive patients with renal artery stenosis, clonidine lowered blood pressure by a reduction in central sympathetic activity independently of renin suppression. In these patients captopril had minimal hypotensive effects, indicating a smaller role for the direct vascular effects of angiotensin II.
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PMID:Cardiovascular and neurohormonal changes following central sympathetic blockade with clonidine in human unilateral renal artery stenosis. 307 92

The effects of baseline antihypertensive drugs or sympatholytic agents on the characteristic hemodynamic response pattern (i.e. increase in blood pressure and heart rate, decrease in total peripheral resistance) during emotional stress were examined. Middle aged male caucasian patients with hitherto untreated mild essential hypertension were given nitrendipine 10-20 mg per day, oxprenolol 160 mg per day or clonidine 75-300 micrograms per day until casual blood pressure was below 140/90 mmHg for at least three months. Blood pressure, heart rate and stroke volume was assessed, at rest and during emotional stress, before and during effective antihypertensive therapy. The increase in systolic pressure during stress was not attenuated by any of the drugs. Heart rate reactivity was lowest when patients received oxprenolol, but peripheral resistance during emotional stress was significantly increased. Clonidine had no unfavorable effects on the hemodynamic pattern during emotional stress but nitrendipine decreased peripheral resistance even more than the decrease in resistance observed during stress before initiation of therapy. If one accepts that antihypertensive therapy should not alter a physiological hemodynamic pattern to an unphysiological response, psychophysiological examinations seem to be valid in selecting suitable patients for the different alternatives in antihypertensive therapy.
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PMID:Impact of antihypertensive therapy on blood pressure reactivity during mental stress. 322 74

Intravenous clonidine was used to treat systolic hypertension (systolic blood pressure greater than 160 mm Hg) in 15 patients with acute myocardial infarction and documented sympathetic overactivity (high plasma norepinephrine). Its effects on haemodynamics and blood gases were studied. After one hour, clonidine significantly reduced the systolic (195 +/- 7 to 137 +/- 7 mm Hg, p less than 0.01) and diastolic (81 +/- 4 to 60 +/- 3 mm Hg, p less than 0.01) blood pressures as well as the systemic vascular resistance (26 +/- 2 to 20 +/- 1 IU, p less than 0.01). The cardiac index was reduced from 2.8 +/- 0.2 to 2.4 +/- 0.2 l/min X m2, p less than 0.01. This change was related to a reduction of the heart rate (92 +/- 4 to 81 +/- 4 beats/min, p less than 0.01) as the stroke index was unchanged. Pulmonary wedge pressure (15 +/- 3 to 10 +/- 2 mm Hg, p less than 0.01) and rate pressure product (18.034 +/- 1.159 to 11.274 +/- 917 mm Hg, beats/min, p less than 0.01) were also significantly decreased. The arterial oxygen tension did not change significantly but there was a significant drop in the mixed venous oxygen saturation (63 +/- 2 to 61 +/- 2%, p less than 0.02) and oxygen transport (433 +/- 41 to 409 +/- 36, p less than 0.01). Clonidine is thus able to normalize blood pressure in acute myocardial infarction; this is accompanied by a reduction in myocardial oxygen requirements and pulmonary wedge pressure. Oxygen transport to the tissues, however, may be decreased.
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PMID:Central inhibition of sympathetic overdrive by clonidine in acute myocardial infarction with systolic hypertension. Haemodynamic study. 376 70


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