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

A case of anesthesia for a heart-transplant operation on a patient on mono-amine oxidase inhibitors (M.A.O.I.) is reported. This 63-year-old farmer was in end-stage cardiac failure due to familial cardiomyopathy. For 24 hours before surgery, he was on a dobutamine infusion (3 mcg/kg/min). He had been taking nialamide (100 mg/day) for 8 years for reactional depression and had not stopped it, despite advice. Anesthesia was induced with etomidate and succinylcholine, and maintained with fentanyl (25 mcg/kg/min) and pancuronium. Cardio-vascular stability was maintained during induction and first stage of surgery, up to cardectomy. Graft ischemia was 188 minutes. Successful defibrillation occurred after verapamil 3 mg. Weaning from C.P.B. was easy with dopamine (5 mcg/kg/min) and isoprenaline (0.01 mcg/kg/min). Post-operatively, on day 1, hypertension appeared and needed a nitroprusside infusion. On day 3, the patient needed another anesthetic for removal of pericardial clots, without problems. He remained very confused and disorientated during all his stay in hospital, but improved greatly with a neuroleptic. He left the hospital on day 28 in a good shape, with an anxiolytic, captopril and immunosuppressors. One month later, he was back on nialamide. The pharmacology of the M.A.O.I. is reviewed and their interactions with anesthesia are discussed as well as the use of inotropes. In this case, the denervated heart-graft, free from M.A.O. inhibition, behaved normally when transplanted in a chronically M.A.O.I. treated recipient.
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PMID:Heart-transplant and mono-amine oxidase inhibitors. 280 Sep 99

Transmission of information among neurons is of a chemical nature. The activity of the neurotransmitter in the brain is regulated by the spontaneous activity of neurotransmitter cell body and the sensitivity of both pre- and post-synaptic receptors. Neurotransmitters are present at very early stages of brain development; they do not only mediate the behavioral-physiological responses of the immature animal, but have trophic effects on the maturation of target neurons as well. Many centrally acting drugs which are frequently used also during pregnancy for the treatment of depression, hypertension, epilepsy, asthma, insomnia, hyperkinetism and other neurological and psychiatric disorders act directly on brain neurotransmitters (in particular monoamines) and behavioral states. Chronic administration of drugs acting on monoamines (such as clonidine, imipramine, alpha-methyl-Dopa, reserpine, monoamine oxidase inhibitors, diazepam) disturb the spontaneous activity and behavioral state dependency of the monoaminergic cells, influences neurotransmitter turnover and change the sensitivity of both pre- and post-synaptic receptors. Sensory deprivation during a critical period of development is known to produce permanent effect on the brain; e.g., monocular deprivation during a particular period of development in a kitten leads to a rewiring of the connectivity in the visual system in the adult cat. Disturbances in neurotransmitter activity during early life will induce a comparable reorganization of the chemical structure of the adult brain.
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PMID:Central neurotransmitter disturbances underlying developmental neurotoxicological effects. 287 1

After ingesting 3,4-methylene-dioxy-methamphetamine (MDMA) and the monoamine oxidase (MAO) inhibitor phenelzine, a 50 year old male developed marked hypertension, diaphoresis, altered mental status, and hypertonicity lasting 5-6 hours. This clinical course is typical of interaction between MAO inhibitors and some sympathomimetics including amphetamines. Such interaction has not previously been described involving MDMA. Sympathomimetic-MAO inhibitor interactions can cause excessive release of endogenous bioactive amines (e.g. norepinephrine, serotonin). Hypertensive crisis, intracranial hemorrhage, hypertonicity, and severe hyperthermia have occurred due to sympathomimetic-MAO inhibitor interactions. MDMA shares structural and pharmacologic features with other agents capable of causing this interaction, and this case suggests that MDMA can cause significant toxicity in patients taking MAO inhibitors.
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PMID:A case of MAO inhibitor/MDMA interaction: agony after ecstasy. 288 26

Previous studies have indicated that brain noradrenaline (NA) neurons in spontaneously (genetically) hypertensive rats (SHR) are implicated in the development of hypertension. Thus, a number of biochemical aberrations in the metabolism of NA in the SHR brain have been detected although the data are not in total agreement. We report here experiments utilizing single cell recording techniques which show directly a reduction in neuronal activity of brain NA neurons in the locus coeruleus (LC) of SHR. This reduction develops gradually with age and in parellel with the increased blood pressure (BP), but is not altered by acute alterations in BP. The SHR were found to display an increased intraneuronal monoamine oxidase (MAO) activity as well as a specifically reduced sensitivity of inhibitory alpha 2-receptors within the LC. It is suggested that in SHR the LC system, in spite of a reduced basal activity displays increased responsiveness to sensory stimuli, a phenomenon that may contribute to the development of hypertension.
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PMID:Locus coeruleus neurons show reduced alpha 2-receptor responsiveness and decreased basal activity in spontaneously hypertensive rats. 303 85

The interest evoked by the Broad Breasted White Turkey (BBWT) as an animal model for studying the cardiovascular damages produced by hypertension and catecholamines is mainly due to the fact that hypertension is spontaneous and tissue and circulating catecholamines, especially norepinephrine, are extremely high. In this paper we focused our attention on three characteristic pathophysiological features displayed by these animals which are strictly related, as well as in humans, to the elevated blood pressure values and to catecholamine action. We also described the possibility of modifying the development of some of these lesions with pharmacological interventions liable to antagonize the peripheral effects of norepinephrine and epinephrine. The dissecting aneurysm of the aorta accounts for 5-10% of sudden deaths in this animal strain. It can be prevented by lowering blood pressure, especially with beta-blockers, and facilitated by MAO-inhibitors. The degree of cardiac hypertrophy is remarkably high and unexpectedly characterized by the synthesis of a "fast" V1-like isomyosin with high Ca++ activated ATPase activity, oxygen consumption and speed of muscle shortening. Neither the reduction of the degree of cardiac hypertrophy, nor treatment with labetalol alone were able to modify this peculiar pattern. In spite of having very high levels of high-density-lipoproteins, which are known to be protective against atherosclerosis, this animal develops a severe atheromatous disease especially in the abdominal aorta, where the cellular growth has also been proven to be in vitro more pronounced than in the thoracic tract. Treatment with beta-blockers reduced the severity and extent of the lesion even in absence of a significant reduction in blood pressure.
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PMID:Catecholamine-induced cardiovascular disease in the spontaneously hypertensive and atherosclerotic turkey. 304 59

The clinical features, pathogenesis, and pharmacologic management of hypertensive crises are reviewed, with emphasis on newer therapies. Hypertensive crises may be divided into hypertensive emergencies and hypertensive urgencies. Hypertensive emergencies, in which acute organ damage exists, require blood pressure reduction within one hour. In hypertensive urgencies no acute end-organ damage has yet occurred; however, blood pressure should be controlled within 24 hours. Factors that may precipitate a hypertensive crisis include renovascular hypertension, acute glomerulonephritis, head injuries, renin- or catecholamine-secreting tumors, antihypertensive-therapy withdrawal syndromes, eclampsia, and ingestion of tyramine by patients receiving monoamine oxidase inhibitors. The traditional drug of choice for therapy of hypertensive emergencies is sodium nitroprusside. Intravenous labetalol produces a prompt, controlled reduction in blood pressure and is a promising alternative. Other agents used are diazoxide, trimethaphan camsylate, hydralazine, nitroglycerin, and phentolamine. However, all these agents have disadvantages, including unpredictable antihypertensive effects, difficult blood pressure titration, and serious potential adverse effects such as profound hypotension, reduced renal blood flow, and increased myocardial workload. Most patients with hypertensive urgencies can be effectively treated with orally or sublingually administered agents. Older regimens of reserpine, methyldopa, or guanethidine, with their slow onsets and long durations of action, have been largely replaced by clonidine and nifedipine. Captopril and minoxidil have also been used with some success. Despite the lack of comparative trials with traditional agents, demonstrated efficacy and desirable pharmacologic characteristics have made several new agents acceptable for therapy of hypertensive crises.
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PMID:Drug therapy of hypertensive crises. 304 49

Antihypertensive drugs with pharmacological action due to sympatholytic activity have been second only to diuretics in their use and efficacy in normalizing blood pressure. Their pharmacological actions have resulted in the notable absence of chemical toxicity, but because of symptomatic side effects, their use has been limited relative to some of the newer antihypertensive agents. Most prominent among undesirable side effects are the central nervous system findings of sedation, altered thought process, depression, and orthostatic or exercise hypotension. Sexual problems, especially in men, are also prominent. Special toxicity is discussed with reference to methyldopa, clonidine, monoamine oxidase inhibitors, and metyrosine.
Hypertension 1988 Mar
PMID:Side effects of sympatholytic antihypertensive drugs. 328 Apr 88

'Designer drugs' are substances intended for recreational use which are derivatives of approved drugs so as to circumvent existing legal restrictions. The term as popularised by the lay press lacks precision. Contrary to the popular belief that 'designer drugs' are original creations, the majority of these agents are 'borrowed' from legitimate pharmaceutical research. They merely represent the most recent developments in the evolution of mind-altering chemicals. The most extensively studied class of psychoactive compounds is the phenylethylamines (mescaline analogues). This class includes catecholamines, therapeutic agents and numerous illicit derivatives. Subtle alterations of the phenylethylamine molecule give rise to a spectrum of pharmacological properties ranging from pure sympathomimetic stimulation to primarily psychoactive effects. Although most of these compounds are only of historical interest, amphetamine, methamphetamine, 3,4-methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA) continue to be used recreationally. Many deaths have been ascribed to this class of compounds. In overdose the differences between these compounds blur and the clinical presentation is similar to that of amphetamine overdose characterised by tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, agitation, muscle rigidity, and hyper-reflexia. Death usually results from arrhythmias, hyperthermia or intracerebral haemorrhage. Treatment is aggressive and supportive with careful attention to temperature, blood pressure and seizure control. Synthetic opioid derivatives, which represent the second major class of 'designer drugs', are derivatives of fentanyl (e.g. alpha-methylfentanyl, 3-methylfentanyl) or pethidine (meperidine) and are extremely potent compounds responsible for numerous overdose deaths. Attempts to synthesise pethidine have resulted in the accidental production of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a compound which is metabolised in the brain by the monoamine oxidase system to a toxic intermediate (MPP+) which selectively destroys the sustantia nigra, resulting in the rapid onset of severe Parkinsonian symptoms. Naloxone will antagonise the opiate effects of this drug class, although high doses may be required. Arylhexylamines constitute the third class of 'designer drugs'. The predominant member of this class is phencyclidine (PCP), a derivative of the anaesthetic ketamine. This unique class of psychoactive agents exhibits broad and complex pharmacological effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:'Designer drugs'. A problem in clinical toxicology. 328 24

Adverse systemic reactions associated with the use of topical ophthalmic timolol, chloramphenicol, phenylephrine and cyclopentolate are surveyed, with special emphasis on precautions and contraindications for these ophthalmic drug preparations. Systemic reactions secondary to timolol, a beta-adrenergic antagonist indicate that it should be used with caution in patients with asthma or a history of asthma, chronic obstructive pulmonary disease or cardiovascular disease and in those patients receiving systemic administration of beta-blockers or verapamil. Because significant blood dyscrasias or aplastic anaemia have been reported following topical ophthalmic chloramphenicol, the only absolute indication in ocular conditions is an organism that is resistant to all other antibiotics. Both 2.5% and 10% phenylephrine have been associated with cardiovascular effects and should be used with caution in selected patients on monoamine oxidase inhibitors, tricyclic antidepressants or atropine or in those with hypertension, advanced arteriosclerotic changes, aneurysms, orthostatic hypotension, long-standing insulin-dependent diabetes and in children with low bodyweights. Central nervous system toxicity secondary to cyclopentolate is dose-related and can be avoided by use of minimal concentrations and avoidance of unnecessary repetition of administration. Occlusion of the nasolacrimal passage with finger pressure immediately after instillation of any eyedrop also decreases the amount of drug that is absorbed systemically.
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PMID:Systemic reactions to ophthalmic drug preparations. 330 68

The existence of a severe toxic interaction (occasionally fatal) from the clinical use of pethidine and monoamine oxidase (MAO) inhibitors is well established. The present study evaluates the possibility of such an interaction existing for the opioid partial agonist buprenorphine. Conscious rabbits (n = 6 in each group) pretreated 18-24 h previously with physiological saline or the MAO inhibitor phenelzine 20 mg kg-1 s.c. were subsequently given physiological saline, pethidine 5 mg kg-1 i.v. or buprenorphine 0.1 or 1.0 mg kg-1 i.v. Whilst saline was without effect and phenelzine produced only a small increase in the rabbit temperature, the combination of phenelzine and pethidine produced a marked, prolonged hyperpyrexia (+4.4 +/- 0.19 degrees C; P less than 0.001), hypertension (+33.9 +/- 3.1 mm Hg; P less than 0.01) and agitation. Three rabbits died, at 35, 45 and 55 min after the pethidine-phenelzine combination. Buprenorphine was without significant effect on any parameter when given after phenelzine. In the model used buprenorphine, in contrast to pethidine, showed no interaction with the MAO inhibitor phenelzine.
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PMID:Influence of pretreatment with a monoamine oxidase inhibitor (phenelzine) on the effects of buprenorphine and pethidine in the conscious rabbit. 334 81


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