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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurologic and abdominal complications can occur in the postoperative period of aortic coarctation repair, ischemia being the pathogenic factor most likely to be involved. This study was designed to evaluate the extent of the hemodynamic changes proximal and distal to the coarctation at the time of cross-clamping, as well as the effects of pentolinium and isoproterenol upon the hemodynamic changes. Included in the study were 17 patients with adult type coarctations who had dual hemodynamic monitoring. During cross-clamping, there was an increase in the gradient between proximal and distal pressures, with severe distal hypotension (< 50 mm Hg) occurring in six patients. Isoproterenol corrected the hypotension in five patients, but the sixth required a surgical shunt. Pentolinium was effective for the treatment of proximal hypertension; however, it also decreased distal pressure. The ligation of collateral vessels was associated with a decrease in distal pressures as well. During cross-clamping, pentolinium was useful for the management of proximal hypertension and isoproterenol increased the distal pressures in some of the patients who presented distal hypotension. However, because of the difficulties in predicting the individual response, their administration would be best guided by dual pressure monitoring. It is postulated that the recognition and proper treatment of distal hypotension may be an important factor in the prophylaxis of postoperative complications.
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PMID:Technical and pharmacologic management of distal hypotension during repair of coarctation of the aorta. 740 68

The experience derived from the administration of isoproterenol in six patients with pulmonary hypertension of unknown etiology (PAH-UE) is presented. The diagnosis was made after exclusion of other known diseases capable of producing hypertension in the pulmonary circuit. Catheterization was performed, and basal cardiopulmonary parameters, mean pulmonary artery pressure (PAP), pulmonary arteriolar resistance (PAR), cardiac index (CI), alveolar-arterial oxygen tension difference P(A-a)O2, and PaO2 were investigated. The effect of infusing 3 micrograms/min of isoproterenol into the pulmonary artery was studied in five cases. Isoproterenol was given sublingually to one patient who had previously received it intravenously; in another case it was given only sublingually. Significant P values (P less than .05) as a group were obtained, in relation to heart rate, CI, PAR, and mean PAP after isoproterenol. A favorable effect on the heart and lungs was seen in two cases, maintained for three years with sublingual isoproterenol with a favorable cardiorespiratory effect. Use of isoproterenol in PAH-UE is justified at present in those cases with a favorable cardiopulmonary response while no specific therapy is available.
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PMID:The role of isoproterenol in pulmonary artery hypertension of unknown etiology (primary): short- and long-term evaluation. 747 61

A chronically increased rate of catecholamine release has various deleterious actions. Isoproterenol injections (80 mg/kg body weight) resulted in depressed Ca2+ transport in the sarcolemma (ATP-dependent Ca2+ uptake, Na(+)-dependent Ca2+ uptake) and sarcoplasmic reticulum (Ca2+ uptake) of rat heart. The formation of malondialdehyde owing to lipid peroxidation was increased. Pretreatment with vitamin E (10-25 mg/kg/day) strongly inhibited the membrane damage. The toxic effects of catecholamines arise most probably from their oxidation, and it is therefore important either to reduce the central sympathetic outflow or to prevent the oxidation. An inappropriately high sympathetic outflow is a typical feature of Western affluent societies, and is linked to psychosocial stress and hypercaloric nutrition. However, established pharmacologic interventions to reduce sympathetic outflow have proven not practicable because of marked side effects. Using radiotelemetry for monitoring cardiovascular parameters of spontaneously hypertensive rats treated with clonidine or moxonidine, we showed that clonidine, unlike moxonidine, resulted in rebound hypertension after drug withdrawal. Because the rebound blood pressure and the typical side effects of clonidine associated with low patient compliance are mainly mediated by alpha-adrenoceptors, it can be inferred that the I1-imidazoline agonist moxonidine does not exhibit the side effects commonly seen with clonidine and therefore represents a promising approach for reducing an inappropriately high central sympathetic outflow.
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PMID:Mechanisms of cardiac cell damage due to catecholamines: significance of drugs regulating central sympathetic outflow. 753 22

71 patients with unexplained syncope was examined by 60 grade of head up tilt table test with or without administration of isoproterenol during 25 minutes interval. The mean age of patients was 71.44 +/- 16.40 (12-86) years. 38 (54%) were female and 33 (46%) were male. The underlying heart disease were 27 (38%) coronary artery disease, 12 (17%) arterial hypertension, 6 (8%) diabetes mellitus, 3 (4%) valvular heart disease and 14 (20%) patients had other diseases. Nine (13%) patients had no organic disease. During head up tilt table test positive reaction was found in 13 (18%) patients. Four (6%) patients were vaso-vagal syncope with classic signs, and 9 (13%) patients were vasodepressor type of syncope, without changes in the heart rate. Isoproterenol was given to 16 (23%) patients, and in 4 (6%) (2 vasodepressor and 2 mixed type of syncope) patients occurred the positive test during isoproterenol administration. Orthostatic reaction occurred during head up tilt table test in 14 (20%) patients. Normal was the result of tilt table test in 42 (59%) patients, and two (3%) patients had autonome neuropathy. The vasovagal syncope was treated by metoprolol, atenolol and disopyramid with success. The head up tilt table testing is a good, simple, useful test for evaluation of syncope patients, especially the diagnosis of vasovagal syndrome.
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PMID:[Tilt-table test in the diagnosis of syncope of unknown origin]. 764 89

We have previously reported that addition of 8-bromocyclic AMP enhances the stimulatory effect of dexamethasone on the expression of the angiotensinogen gene in mouse hepatoma cells in vitro. Isoproterenol is known to stimulate the synthesis of hepatic intracellular cyclic AMP via beta-adrenergic receptors. To study the possible effect of beta-adrenergic receptors on the expression of the angiotensinogen gene in mouse hepatoma cells, we transiently transfected them with a fusion gene with the 5'-flanking region of the angiotensinogen gene linked to a bacterial chloramphenicol acetyltransferase coding sequence as a reporter, pOCAT (ANG N-1498/+18). The addition of isoproterenol (10(-9) to 10(-5) mol/L) alone had no stimulatory effect on the expression of pOCAT (ANG N-1498/+18). In the presence of dexamethasone (10(-6) mol/L), however, isoproterenol enhanced the stimulatory effect on the dexamethasone on the expression of pOCAT (ANG N-1498/+18). The enhancing effect of isoproterenol was inhibited by the presence of propranolol (beta 1- and beta 2-adrenergic receptor antagonist) and ICI 118,551 (beta 2-adrenergic receptor antagonist) but not by the presence of atenolol (beta 1-adrenergic receptor antagonist). Furthermore, the addition of Rp-cAMP (an inhibitor of protein kinase A I and II) blocked the enhancing effect of isoproterenol. These studies demonstrated that isoproterenol enhances the stimulatory effect of dexamethasone on the expression of the angiotensinogen gene in mouse hepatoma cells via beta 2-adrenergic receptor and cyclic AMP-dependent protein kinase pathways. Our data may be important in understanding the molecular mechanism(s) of the stimulatory effect of catecholamines/glucocorticoid-induced expression of the angiotensinogen gene in the liver.
Hypertension 1995 Jan
PMID:Beta-adrenergic receptors and angiotensinogen gene expression in mouse hepatoma cells in vitro. 784 40

A 21-year-old female patient with psychotic symptoms developed hyperthermia, muscular rigidity and hypertension after administration of haloperidol. A muscle biopsy showed some atrophic and necrotic fibers, and a great number of fibers with central cores in the oxidative enzyme preparations. A related syndrome, Malignant Hyperthermia (MH), is sometimes associated with central core disease. The present case shows an association of a hyperthermic syndrome related to haloperidol with central core disease.
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PMID:Hyperthermic reaction to haloperidol with rigidity, associated to central core disease. 785 68

1. The study was carried out in adult patients having normal cardiovascular reflexes and no brain stem lesions. They were exposed to ambient temperature of 72-74 degrees F. Injections of agonists and antagonists of receptors were made into the lateral cerebral ventricles of these patients through diagnostic burr hole in the skull. 2. Noradrenaline, adrenaline and dopamine evoked hypotension and bradycardia. While the core temperature was reduced by nor-adrenaline and adrenaline, dopamine evoked hyperthermia. Isoprenaline elicited hypertension, tachycardia and hyperthermia. Opposite cardiovascular and thermal effects were observed with blockade of alpha 1-, beta-and dopamine receptors with prazosin, propranolol and haloperidol respectively. 3. Injection of 5-hydroxytryptamine resulted in hypertension, tachycardia and hyperthermia but hypotension, bradycardia and hypothermia were seen with methysergide. 4. Similarly, carbachol injection caused initial excitatory followed by inhibitory cardiovascular responses. These were associated with hypothermia. On the contrary atropine per se elicited hypertension, tachycardia and hyperthermia. 5. Thus, alpha 1- and beta-adrenoceptors, dopaminergic, serotonergic and muscarinic cholinergic receptors are present in human brain which appear to modulate cardiovascular activity and core temperature.
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PMID:A study of effects of putative neurotransmitters injected into the lateral cerebral ventricle of man. 790 93

The objective of the present work has been to analyze the influence of endothelium, ageing and hypertension in the norepinephrine (NE)-induced responses. For this purpose we used aortic rings from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats of different ages. In rings with endothelium from 5-week-old WKY, cumulative addition of NE (0.01 and 0.1 microM) caused concentration-dependent contractions, whereas higher concentrations (1 and 10 microM) induced concentration-dependent relaxations. In 5-week-old SHR and 3-month-old WKY rats, these relaxant responses were observed only at 10 microM NE, and they disappeared in older animals from both strains. In endothelium denuded rings, NE induced only contractions, which were similar in WKY rats of different ages, but significantly increased in 6- and 12-month-old SHR. In both strains, the endothelium-dependent relaxant responses to NE were abolished by NG-nitro-L-arginine methyl ester and propranolol, but not modified by yohimbine or ouabain. Isoproterenol (0.01-10 microM) induced concentration-dependent vasodilation in rings from 5-week-old rats of both strains, precontracted with 1 microM NE. Isoproterenol-elicited responses were reduced by endothelium removal or by 0.1 mM NG-nitro-L-arginine methyl ester and abolished by 1 microM propranolol. These results suggest that: 1) in the aorta from young WKY and prehypertensive SHR rats, NE induces vasodilations mediated by activation of endothelial beta adrenoceptors and release of nitric oxide; 2) these responses are impaired during ageing and hypertension; and 3) there is an important negative endothelial modulation of NE-induced contraction in adult SHR rats.
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PMID:Norepinephrine-induced relaxations in rat aorta mediated by endothelial beta adrenoceptors. Impairment by ageing and hypertension. 807 45

A 21-year-old woman with weight loss, palpitations and facial flush was found to have hypertension (up to 200/130 mm Hg) and mild hyperkalaemia (3.4 mmol/l). Extensive diagnostic tests revealed hyperaldosteronism with contrast storing in the right adrenal gland on scintigraphy after injection of dexamethasone (2 mg daily for one week). The hyperaldosteronism could not be suppressed by dexamethasone. Analysis of venous blood separately from each side pointed to aldosterone production in the right adrenal (right renal vein: 80 ng/dl, drainage area of the right adrenal vein: 114 ng/dl, left renal vein: too low to measure). The right adrenal gland was removed. No adenoma was found histologically. After the operation the aldosterone level was reduced and the blood pressure transiently fell. But both had risen again after 3 months. Renewed tests revealed dexamethasone-remediable hyperaldosteronism. On treatment with hydrocortisone (15-5-5 mg) and 50 mg metoprolol the patient became normotensive without any other medication.
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PMID:[Unilateral autonomous aldosterone production in hyperaldosteronism suppressible by dexamethasone]. 826 28

A 21-year-old man presenting with jaundice and hypertension was found to have an extraadrenal pheochromocytoma. Cholangiography demonstrated a cavity in the head of the pancreas that was in communication with both the pancreatic and common bile ducts. Hemorrhage from the cavity led to the patient's death and postmortem examination revealed focal infarction of the pancreatic head. This case adds hemobilia, obstructive jaundice, and focal pancreatic infarction to the list of bizarre remote manifestations of pheochromocytoma.
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PMID:Focal pancreatic infarction in pheochromocytoma. 832 94


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