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

We investigated the effect of two oral (p.o.) doses of cicletanine (5 and 30 mg/kg/day) for 4 weeks on urinary excretion (UKE), renal concentration (RKC) of kallikrein, and prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha urinary excretion of stroke-prone (SP) spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) rats submitted to a high sodium intake (1%). Both doses of cicletanine induced a significant antihypertensive effect in treated SHR as compared with hypertensive untreated controls (HC). After 4-week treatment, a significant difference in mortality was observed between normotensive controls (NC) (0%) and HC (84%). Both doses of cicletanine reduced the mortality of hypertensive animals (8% SHR with 5 mg and 24% SHR with 30 mg vs. 84% in HC). Whereas UKE and RKC were decreased in HC during the progression of untreated hypertension from week 1 to week 4, both doses of cicletanine administration significantly prevented this decrease. Consistently with maintenance of UKE during the course of hypertension, the level of tissue kallikrein was higher in hypertensive cicletanine-treated than in untreated SHR. This increased RKC was associated with a significantly higher rate of kallikrein biosynthesis. The increased level of the urinary excretion and tissue concentration of PGE2 and 6-keto-PGF1 alpha in cicletanine-treated SHR as compared with untreated animals was also of interest. This protective effect on PG excretion correlated with that on kallikrein excretion. The results confirm the efficiency of cicletatine as an antihypertensive treatment. The antihypertensive action includes protective effects on potential vasodepressor kallikrein-kinin and prostaglandin systems.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992 Oct
PMID:Protective effect of cicletanine on hypertension-induced decreases in the renal kallikrein-kinin and prostaglandin systems in stroke-prone spontaneously hypertensive rats. 128 Jul 17

alpha-Chloralose is an anesthetic commonly used in cardiovascular research. Using a chronically instrumented neonatal lamb model, we previously determined that chloralose has important effects on basal hemodynamics and arterial oxygen tension as compared with those of paired conscious control lambs. We wished to determine whether beta-adrenergic receptor stimulation accounted for chloralose-induced hemodynamic effects and to investigate the influence of chloralose and beta-adrenergic receptor antagonism on oxygen metabolism. In paired studies, five lambs were given chloralose intravenously (30 mg/kg i.v.) after propranolol (1 mg/kg i.v.) or saline control. The group pretreated with propranolol had reduced heart rate (HR 206 +/- 12 vs. 244 +/- 10 beats/min, p = 0.04) and cardiac output (CO 253 +/- 29 vs. 302 +/- 40 ml/min/kg, p = 0.005) 30 min after chloralose as compared with control; pretreatment with propranolol also attenuated the systemic hypertensive response to chloralose (77 +/- 8 vs. 89 +/- 5 mm Hg, p = 0.055). No difference in the response of stroke volume (SV), atrial or pulmonary arterial pressures, or pulmonary and systemic vascular resistances (PVR, SVR) were observed between treatment groups. No differences between propranolol and saline treatment groups were observed in arterial and mixed venous oxygen contents, arteriovenous (A-V) oxygen difference, oxygen extraction, or oxygen consumption; a reduction in oxygen delivery observed after propranolol as compared with saline was not altered by chloralose. We conclude that tachycardia and increase in CO induced by chloralose in lambs probably are mediated by beta-adrenergic receptor stimulation, which may be direct or indirect.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992 Dec
PMID:Effect of beta-adrenergic receptor antagonism on chloralose-induced hemodynamic changes in newborn lambs. 128 4

The major target organs that suffer from sustained hypertension are the heart, kidneys, and brain. Cardiac adaptation to arterial hypertension consists of left ventricular hypertrophy (LVH) of the concentric type, that is, an increase in wall thickness at the expense of chamber volume. However, LVH can no longer be considered a simple adaptive myocardial process serving to compensate for the increase in afterload and bring left ventricular wall stress back to normal. Data from the Framingham cohort have shown that the occurrence of LVH drastically increases the risk of sudden death and other cardiovascular morbidity and mortality irrespective of the levels of arterial pressure. Renal adaptation to arterial hypertension consists of a decrease in renal blood flow with elevations in filtration fraction and renal vascular resistance. With progressive hypertensive cardiovascular disease, glomerular filtration rate will fall as well. Recent data in patients with mild-to-moderate hypertension demonstrate that despite "efficacious" antihypertensive therapy, one-third to one-half of hypertensive patients may experience a significant decline in renal function. Cerebrovascular adaptation to hypertension consists of micro- and macrovascular disease leading to vascular dementia, or ischemic or hemorrhagic stroke. Cerebrovascular autoregulation, the mechanism by which cerebral blood flow is maintained, despite changes in arterial pressure, may be altered in hypertension.
J Cardiovasc Pharmacol 1992
PMID:End-organ disease in hypertension: what have we learned? 128 25

The goal of antihypertensive therapy is the reduction in morbidity and mortality associated with high blood pressure. Despite our ability to reduce blood pressure, "standard" antihypertensive therapy has not produced a general decrease in coronary heart disease. This failure might be related to the adverse metabolic consequences of diuretics and beta-adrenergic receptor-blocking agents used in most clinical trials. In the hypertensive patient population, however, the principal physiologic abnormality is increased systemic vascular resistance. This increase in vascular tone leads to compensatory changes in cardiac function that result in left ventricular hypertrophy and diastolic filling abnormalities. Diastolic ventricular dysfunction is present in approximately 50% of asymptomatic hypertensive patients and might be a precursor of the syndrome of congestive heart failure with normal systolic ventricular function. In view of the prevalence of diastolic filling abnormalities in the hypertensive patient population, one should consider the effect of an antihypertensive drug on left ventricular function. In a comparison of the angiotensin-converting enzyme (ACE) inhibitors, captopril, lisinopril, and fosinopril, only fosinopril increased stroke volume, peak ejection rate, and peak filling rate, and decreased time to peak ejection rate. These favorable inotropic and lusitropic responses to fosinopril may reflect an effect on the myocardial renin-angiotensin cascade which is dependent upon the unique chemical structure of the fosinopril molecule.
J Cardiovasc Pharmacol 1992
PMID:Left ventricular hypertrophy and performance: therapeutic options among the angiotensin-converting enzyme inhibitors. 128 27

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.
J Cardiovasc Pharmacol 1992
PMID:Beta-blockers: primary and secondary prevention. 128 45

Large-scale end-point trials have demonstrated that antihypertensive treatment reverses the risk of stroke attributable to high blood pressure and probably reduces the incidence of myocardial infarction. Despite this major achievement in therapeutics, substantial goals still need to be achieved. Thus, there is a need for improvement in existing antihypertensive agents in terms of greater blood pressure-lowering efficacy and improved impact on coronary heart disease in younger subjects. There is also a pressing need for a reduction in adverse effects. The incidence of these far exceeds the potential benefit of treatment. Last, the costs of therapy are assuming growing importance in the face of tight financial constraints on health care systems throughout the world.
J Cardiovasc Pharmacol 1992
PMID:New antihypertensive agents: benefit of treatment. 128 46

The goal of this study was to assess the effect of gallopamil on left ventricular (LV) diastolic function early after acute myocardial infarction (AMI). Gallopamil was compared with placebo and atenolol in two different groups of patients. Study patients, 2 days after experiencing their first AMI, in Killip class I and stable sinus rhythm, were randomized in a crossover, double-blind sequence to receive (a) gallopamil (50 micrograms/kg over 5 min) or placebo (i.v. 10-ml bolus, with a time interval of 90 min); and (b) gallopamil (50 micrograms/kg over 5 min) or atenolol (5 mg over 5 min), with a time interval of 24 h. Group I and group II consisted of 28 patients (26 men and 2 women; mean age 55 +/- 9 years) and of 14 patients (13 men and 1 woman; mean age 56 +/- 10 years), respectively. All the patients were treated with thrombolysis within 6 h from the onset of symptoms. Doppler echocardiographic examinations were performed as follows: at baseline (B) and 15 min after administration of gallopamil bolus and placebo bolus, in group I; at baseline before gallopamil (BG) and atenolol (BA), and 15 min after each bolus in group II. The following echo-Doppler parameters were calculated, at each examination: the early and late transmitral peak velocity ratio (E/A), the early and late velocity integral ratio (Ei/Ai), the peak filling rate normalized to mitral stroke volume (nMPFR), and the LV isovolumic relaxation time (IVRT), which was normalized to an 800-ms R-R cycle length in the patients in group II. Mean blood pressure (MBP) and heart rate (HR) were also measured.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992
PMID:Diastolic ventricular dysfunction in noncomplicated acute myocardial infarction: the influence of gallopamil. 128 57

Resection of tumours associated with the extracranial internal carotid artery such as carotid body tumours and paraganglionomas carry a hazard of stroke which might occur from temporary clamping of the artery to obtain better control, or from inadvertent damage to the artery which requires ligation. Some extensive tumours have been deemed unresectable because of their extent. Intracranial extension is a further technical challenge. We describe a technique for safe resection of such tumours employing an outlying Pruitt Inihara shunt. During resection of the tumour the shunt allows safe dissection because the internal carotid artery is rendered relatively bloodless. Further, any damage to the artery can be safely repaired, and indeed if necessary the artery itself can be resected and grafted. We have employed this technique in 3 difficult case of paraganglionoma (1) and carotid body tumour (2) whilst at the same time resecting 8 other simple cases without the need for such a technique.
J Cardiovasc Surg (Torino)
PMID:A technique for safe resection of extensive tumours associated with the extracranial internal carotid artery. 128 14

Treatment of hypertension in the elderly has so far mainly been based on clinical judgment and very few large controlled trials. During the last year several large new trials have been published, the so-called STOP-Hypertension, SHEP, and MRC trials. All have shown that drug treatment of hypertension in the elderly (65-85 years) with permanent diastolic hypertension or isolated systolic hypertension reduces stroke incidence. Most patients have needed combined drug treatment with diuretics and beta-blockers. When thiazide diuretics are used, serum potassium should be followed very closely and most likely amiloride should be added to the thiazide therapy, since this was done both in the STOP and the MRC trials. Since many elderly patients with hypertension suffer from other diseases that might represent contraindications to thiazide diuretics or beta-blockers, the choice of drug must be made after careful clinical evaluation. With the newer classes of antihypertensive agents (calcium antagonists, ACE inhibitors and alpha-blockers) side effects are probably seen less often, but long-term data on morbidity and mortality are still lacking.
Cardiovasc Drugs Ther 1992 Dec
PMID:Treatment of hypertension in the elderly--what have we learned from the recent trials? 129 75

The already strong case for drug treatment of hypertensive patients aged over 60 has been reinforced by the reports on the SHEP, STOP, and, to a lesser extent, MRC trials. SHEP showed benefit in "isolated systolic" hypertension, mainly in relation to stroke, but with a strong trend towards also reducing myocardial infarction. SHEP demonstrated advantages from low-dose chlorthalidone, especially if hypokalemia was prevented. STOP in patients aged 70-84 at entry demonstrated a reduction in stroke and all-cause mortality but not in myocardial infarction; benefit was apparent in women as well as men. The MRC trial, in subjects over 65, many of whom had "isolated systolic" hypertension, found a reduction in stroke but not in coronary events or all-cause mortality. Extensive cross-contamination of allocated treatment groups restricted worthwhile evaluation of different drug regimens in MRC. Potential benefits from antihypertensive drug treatment in old people are substantial but are in danger of being discredited because of intemperate and inaccurate claims.
Cardiovasc Drugs Ther 1992 Dec
PMID:The case for antihypertensive drug treatment in subjects over the age of 60. 129 77


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