Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with a toxic adenoma, already reduced in size by TSH, presented on the third day after treatment of a common cold by phenylpropanolomine, a severe pain in the thyroid gland. 4 weeks later, the nodule, which measured 3 x 4 cm. had clinically disappeared and the scan returned to normal. The disappearance 5 months later of the antithyroid antibodies confirmed the cure. Catecholamines, stimulating the production of thyroid hormone and producing temporary ischemia of the gland, phenylpropanolamine, a sympathomimetic drug, may have caused hemorrhagic necrosis of the adenoma and its disappearance.
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PMID:[Evanescent toxic thyroid adenoma. Possible role of phenylpropanolamine]. 20 Oct 31

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

The effects of pindolol and timolol on ischemia reperfusion damage were studied in isolated working rat hearts. Ischemia (15 min) decreased the mechanical function and the energy state, and increased the tissue levels of free fatty acids (FFA). During reperfusion (20 min), the mechanical function did not recover, but the energy state recovered incompletely, whereas FFA increased further. Pindolol (50 microM) accelerated recovery of the mechanical function and the energy state that had been decreased by ischemia during reperfusion, and inhibited the accumulation of FFA during ischemia and reperfusion, especially when it was applied during the whole period of reperfusion. Timolol (50 microM), however, did not accelerate recovery of the mechanical function and the energy state during reperfusion, although it attenuated FFA accumulation during reperfusion. The pindolol-induced recovery of the mechanical function during reperfusion was reduced by timolol. The results suggest that the intrinsic sympathomimetic activity of pindolol may play an important role, at least in part, in producing the cardioprotective effect, especially during reperfusion.
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PMID:Cardioprotective effect of pindolol in ischemic-reperfused isolated rat hearts. 152 58

Although beta-sympathomimetic tocolytic therapy has been associated with transient subendocardial ischemia, magnesium sulfate has rarely been noted to cause acute chest pain and is, in fact, known to improve myocardial perfusion in patients with variant angina. We believe this report represents the first case in which intravenous magnesium sulfate administered as a tocolytic agent caused acute chest pain accompanied by transient electrocardiographic evidence of subendocardial ischemia.
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PMID:Transient symptomatic subendocardial ischemia during intravenous magnesium sulfate tocolytic therapy. 173 14

We report a case with focal neurological deficits suggesting vertebro-basilar system ischemia, in the course of pre-eclampsia. An early CT scan showed a large hypodensity throughout the midbrain. Brainstem auditory evoked potentials initially showed an abolition of III and V pikes suggesting brainstem injury. Two days later both neurological examination and brain stem auditory evoked potentials returned to normal. A CT scan performed three weeks after the onset was normal. These findings suggest a vasospasm which may have been due to sympathomimetic agents given two weeks before the onset of toxemia for preterm labor.
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PMID:[Neurologic manifestations in the vertebro-basilar system revealing pregnancy toxemia]. 178 Jun 12

Bisoprolol, (+/-)1-(4-[(2-isopropoxyethoxy)-methyl]-phenoxy)-3-isopropyl-amino -2- propanol-hemifumarate, is a new, highly selective beta 1-adrenoceptor blocking agent without intrinsic sympathomimetic activity and low to moderate local anaesthetic activity. As demonstrated in binding experiments, and in classical pharmacological studies using rats, guinea pigs, cats, and dogs, bisoprolol markedly differentiated between beta 1-adrenoceptors of the heart, or the renal juxtaglomerular apparatus, and the beta 2-subtype in arterial blood vessels, bronchi, liver, or skeletal muscle. Up to concentrations nearly 100-fold higher than the therapeutic plasma levels in humans, bisoprolol did not affect the functional refractory period of the heart, and was devoid of a direct suppressive effect on myocardial contractility and of calcium antagonistic properties in heart and vascular muscle. The pattern of haemodynamic effects of bisoprolol was typical of beta-blockers and included decreases in blood pressure (BP), heart rate (HR), and cardiac output, concomitant with an increase in calculated total peripheral resistance. In contrast to other beta-blockers, bisoprolol increased renal blood flow in anaesthetized dogs. Bisoprolol lowered BP in hypertensive dogs and rats, attenuated the development of spontaneous hypertension in rats, decreased plasma renin activity and protected the heart from the sequelae of transient ischemia. It did not block presynaptic beta-adrenoceptors in blood vessels. Serum lipids and the serum lipoprotein profile remained unaltered after bisoprolol. Bisoprolol was devoid of affinity for autonomic receptors other than beta-adrenoceptors or for autacoid receptors. This is probably one of the reasons why bisoprolol did not affect the function of the central nervous, respiratory, and gastrointestinal systems in an obvious way. The high beta 1-selectivity of bisoprolol is linked with extremely favourable pharmacokinetic properties. These include nearly complete enteral absorption and virtual absence of liver first-pass metabolism, both resulting in high bioavailability, long plasma half-life, pharmacokinetics that are linear over a wide dose range and independent of age, food intake and hydroxylator status, low plasma protein binding, and a 1:1 ratio of hepatic metabolization to renal elimination of the unaltered substance. This sum of favourable pharmacological and pharmacokinetic properties characterize bisoprolol as an optimized beta-blocker.
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PMID:High beta 1-selectivity and favourable pharmacokinetics as the outstanding properties of bisoprolol. 243 93

In a group of 288 patients with acute inferior (diaphragmatic) myocardial infarction, second and third degree atrioventricular (AV) block was diagnosed in 37 (14%). Three of the 37 died. The AV block in the 34 survivors could be differentiated into two distinct types, namely, early and late AV block. In 15 patients, second and third degree AV block developed within 6 hours of the first signs of infarction. In these 15 patients, all signs of AV block disappeared within 24 hours after infarction. Second and third degree AV block appeared suddenly in the vast majority, and first degree AV block could be detected in only a few patients and for a very short time before normalization of conduction. Atropine either abolished AV block completely or caused a marked acceleration of ventricular escape rhythm. In 14 patients, second and third degree AV block developed later than 6 hours (in 12 later than 24 hours) after infarction. It was heralded and followed by relatively long periods of first degree AV block in all cases (except in two patients who were admitted 72 hours after infarction). The total duration of AV block was longer than 40 hours in all of these patients, and the ventricular rate was relatively high. In no patient was abolishment of AV block achieved by atropine, and ventricular acceleration was relatively slight in all. In five patients, early and late AV block could be recognized consecutively. The two types of AV block seem to have different causes. Increased vagal tone is probably operative in the first type, and metabolic changes due to ischemia in the second. Response to atropine and sympathomimetic drugs is much better, and cardiac pacing only rarely indicated, in patients with early than in those with late AV block.
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PMID:Early and late atrioventricular block in acute inferior myocardial infarction. 673 51

The essential goal of medical treatment following myocardial infarction with left ventricular dysfunction must be the prevention of secondary cardiac failure. The existence of left ventricular dysfunction, in particular when it is not accompanied by clinical cardiac failure, is a virtually formal indication for beta-blocker treatment after an infarction. Beta-blockers with intrinsic sympathomimetic activity (ISA) are possibly better tolerated in this context. However, experience shows that cardiologists and general practitioners often remain reluctant to prescribe beta-blockers whenever left ventricular function is impaired. Converting enzyme inhibitors decrease the risk of onset of secondary cardiac failure, reduce sudden deaths by ventricular arrhythmias, reduce recurrences of myocardial infarction or unstable coronary insufficiency, and more generally reduce overall and cardiovascular mortality. This is a class effect. While there is no urgency to prescribe them during the acute phase, it is generally considered that it is extremely useful to give them fairly quickly, i.e. during the first 72 hours. At the end of the hospital phase, around two weeks, it is desirable, whenever possible, to prescribe a dose of the order of 75 mg/day of captopril or 2.5 mg/day of ramipril. The administration of aspirin can be considered virtually routine. Oral anticoagulants are desirable in the presence of a large akinetic pocket, a frequent starting point of thrombosis and/or systemic emboli, or in the presence of atrial fibrillation. Digitalis/diuretic treatment does not appear to be indicated at this stage. Other types of anti-ischemic treatment are not theoretically indicated as a matter of principle at this stage in the absence of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[What is the appropriate treatment for myocardial infarction with left ventricular dysfunction?]. 786 55

The effect of bunitrolol, a beta-adrenergic blocking agent having intrinsic sympathomimetic activity, on ischemic myocardial metabolism was examined in anesthetized dog hearts. Ischemia was induced by ligating the left anterior descending coronary artery for 3 or 30 min. Bunitrolol (0.3 or 1.0 mg/kg of body weight) was injected intravenously 5 min before the onset of ischemia. Ischemia reduced myocardial high-energy phosphate levels and changed the levels of glycolytic intermediates. Bunitrolol at a dose of 0.3 mg/kg significantly decreased heart rate, whereas the drug at a dose of 1.0 mg/kg did not. This result suggests that intrinsic sympathomimetic activity is observed only at a high dose of bunitrolol. Pretreatment with bunitrolol at 0.3 but not 1.0 mg/kg attenuated the myocardial metabolic changes caused by 3 min of ischemia. After 30 min of ischemia, a beneficial effect of bunitrolol on the ischemic myocardium was not observed. These results suggest that bunitrolol may lessen the ischemic influence on the myocardium in the early stage of ischemia and that intrinsic sympathomimetic action may not have a beneficial effect on the ischemic myocardium.
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PMID:Effects of bunitrolol on ischemic myocardial energy metabolism in dogs. 809 74

Arbutamine (Gensia, Inc., San Diego, CA) is a newly-developed sympathomimetic agent specifically designed for cardiovascular stress testing. It has been successfully used for the detection of coronary artery disease in conjunction with electrocardiography, echocardiographic and radionuclide techniques. Arbutamine increases heart rate and contractility, thus provoking ischaemia in a manner analogous to that of physical exercise. Ischaemia becomes manifest by reproduction of typical angina, diagnostic electrocardiographic changes, the development of a wall motion abnormality on two-dimensional echocardiography or of a perfusion defect on thallium scintigraphy. Thus far in clinical trials it has shown an acceptable side-effect profile and a level of diagnostic accuracy for the detection of patients with coronary disease equivalent to or exceeding that seen with physical exercise.
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PMID:Clinical and diagnostic utility of arbutamine for cardiovascular stress testing during echocardiographic monitoring. 886 20


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