Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nineteen patients, aged 58-80 years, with severe isolated aortic valve stenosis, severely reduced ejection fraction and clinical heart failure underwent aortic valve replacement between January 1970 and April 1977. Ten had concomitant coronary artery disease (all underwent additional coronary bypass surgery), 17 had angina pectoris and four had syncope. Aortic valve area index was 0.32 +/- 0.03 cm2/m2 (mean +/- SEM); left ventricular (LV) end-diastolic volume index was 117 +/- 9 ml/m2 and LV ejection fraction was 0.37 +/- 0.02. There were four operative deaths and one late death. The follow-up time ranged from six to 74 months (38 +/- 6 months). Actuarially determined three-year survival is 74 +/- 10%; the expected five-year survival is the same. One patient had a serious cerebrovascular accident. Of the remaining survivors, seven were initially Functional Class IV and six Class III; currently, six are Class I and seven Class II (New York Heart Association classifications). The cardiothoracic ratio has decreased from 0.54 +/- 0.03 to 0.49 +/- 0.03. Repeat hemodynamic evaluation has been performed in 10 patients, 22 +/- 6 months after surgery. In these 10 patients, the aortic valve gradient decreased from 55 +/- 7 11 +/- 1.3 mm Hg; LV end-diastolic pressure from 22 +/- 2.4 to 9 +/- 1.9 mm Hg; LV end-diastolic volume index from 119 +/- 16 ml/m2 to 107 +/- 11 ml/m2. LV ejection fraction has increased dramatically from 0.34 +/- 0.03 to 0.63 +/- 0.05 and mean velocity of circumferential fiber shortening from 0.57 +/- 0.08 to 1.3 +/- 0.18 circ/sec. The encouraging long-term survival, improved functional class and the marked improvement in left ventricular function that occurred in our patients indicate that all patients with severe aortic stenosis in clinical heart failure should be offered aortic valve replacement.
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PMID:Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement. 66 73

The hormonal response of the anterior pituitary to various epileptic and nonepileptic events in children was studied. Postictal serum prolactin and cortisol levels were measured in 17 children with epilepsy, 23 with febrile seizures, and 10 with syncope or breath-holding spells. The levels were compared with those of 30 children with nonspecific fever, and 23 afebrile children served as control subjects. Significantly higher (P less than .01) prolactin levels (26.5 +/- 3.3 ng/mL, mean +/- SEM) were found in the epileptic group, compared with levels in children with febrile seizures (13.2 +/- 1.0 ng/mL), fever (11.2 +/- 0.9 ng/mL), syncope (7.3 +/- 0.9 ng/mL), and the control group (7.9 +/- 0.6 ng/mL). In contrast, serum cortisol levels were nonspecifically elevated in the epileptics and patients with febrile seizures or fever only. These findings suggest that elevated prolactin levels may be found after epileptic seizures and much less after febrile seizures, but not after breath-holding spells or syncopal events. Cortisol secretion appears to be nonselectively triggered by all stressful events, such as epileptic and febrile seizures, and fever. Elevated prolactin levels (greater than 15 ng/mL) associated with seizures may help in differentiating epileptic from febrile seizures or syncope.
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PMID:Prolactin and cortisol levels in various paroxysmal disorders in childhood. 188 27

Forty-seven consecutive patients aged 1-38 years underwent operation for hypertrophic obstructive cardiomyopathy (HOCM) between 1972 and 1986. Isolated myectomy-myotomy was performed in 43 patients, three patients underwent myectomy and concomitant aortic valve repair, and one patient underwent concomitant mitral valve replacement. The peak systolic pressure gradient from the left ventricle to the aorta decreased from 70 +/- 33 mm Hg (mean +/- SEM) preoperatively to 10 +/- 15 mm Hg immediately after repair (p less than 0.001). Moderate or severe mitral insufficiency was identified in 16 patients preoperatively and was corrected by myectomy alone in 15. There was no operative mortality; two late deaths occurred during follow-up (median, 5 years; maximum, 16 years) for estimated 5- and 10-year survivals of 97 +/- 2% and 88 +/- 10%, respectively. Reoperation was required for aortic valve replacement (n = 2), remyectomy (n = 2), and permanent pacemaker implantation (n = 3). Preoperative symptoms were relieved in 24 of 29 (83%) patients with dyspnea, in 18 of 19 (95%) with angina, and in six of 10 (60%) with syncope. These results support myectomy-myotomy for symptomatic children and young adults with HOCM. Also, it appears that late survival after myectomy-myotomy in these young patients may be improved over that observed in historical controls treated with medications alone; operation should be considered for asymptomatic children and adults less than 40 years of age with large (greater than 80 mm Hg) left ventricular outflow gradients.
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PMID:Results of operation for hypertrophic obstructive cardiomyopathy in children and adults less than 40 years of age. 276 26

Microneurographic recordings of muscle nerve sympathetic activity, which is governed by baroreceptors and involved in blood pressure regulation, were made in the peroneal nerve in 16 healthy volunteers during physiological bladder distension. When the urge to urinate was pronounced, sympathetic outflow increased from a baseline level of 16.3 +/- 1.7 to 23.2 +/- 1.9 bursts/min (mean +/- SEM, p less than 0.01). There was a concomitant significant rise in both systolic and diastolic blood pressure, from 125 +/- 2/74 +/- 2 to 140 +/- 4/84 +/- 3 mm Hg. After micturition, sympathetic activity and blood pressure returned toward initial values. It is concluded that 1) increased sympathetic outflow contributed to the rise in blood pressure, 2) there is a vesicovascular response mediated by sympathetic vasoconstrictor neurons in humans corresponding to mechanisms observed in animals, and 3) the described functional relation between bladder distension and sympathetic vasoconstrictor activity probably plays a role in clinical conditions such as autonomic dysreflexia in humans with cervical spinal cord lesions and nocturnal micturition syncope.
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PMID:Sympathetic activity and blood pressure increases with bladder distension in humans. 280 12

Fifty consecutive Chinese patients with primary hyperaldosteronism were studied. All were considered to have an adrenal cortical adenoma, this being proven by surgery in 46 cases. In contrast to other reports, periodic paralysis was a presenting feature in 42 per cent of patients. Other notable symptoms were palpitations (30 per cent) and syncope (12 per cent). Vascular complications were present in 20 per cent of cases. Mean serum potassium level at presentation was 2.1 +/- 0.1 (mean +/- SEM) and sodium 145.0 +/- 0.1 mmol/l. Serum potassium was significantly lower and plasma aldosterone higher in patients with periodic paralysis. Adrenal venography in order to localise the tumour was unreliable and was misleading in two cases. Adrenal venous sampling for steroid analysis was much more helpful, despite the difficulty of obtaining right adrenal venous blood. The side of the adenoma could be predicted in 97 per cent of cases from measurements of left adrenal venous and vena caval aldosterone levels. The use of high resolution CT gave 100 per cent accuracy in all 18 patients who underwent surgery, the smallest detected tumour being 0.8 cm in diameter. Surgery corrected hypokalaemia in all cases, and 37 of the 46 patients required no further antihypertensive treatment.
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PMID:Fifty cases of primary hyperaldosteronism in Hong Kong Chinese with a high frequency of periodic paralysis. Evaluation of techniques for tumour localisation. 365 46

To determine the relative participation of skin and muscle capacitance beds of the forearm in venomotor reflexes, epinephrine iontophoresis was combined with forearm plethysmography so that the volume of muscle veins could be estimated simultaneously with the volume of cutaneous veins, at a constant venous pressure. With this technique not only are the cutaneous veins markedly constricted but they also are prevented from filling since skin blood flow is abolished. In 10 normal subjects, the venous volume in the elevated control forearm at a congesting pressure of 30 mm Hg (VV[30]) was 3.16 +/-0.30 SEM cc/100 cc, while in the iontophoresed arm it was 2.54 +/-0.31 cc/100 cc. Thus the forearm cutaneous VV[30] was 1.62 cc/100 cc. With a deep breath, ice to the forehead, and leg exercise, and cutaneous VV[30] decreased 19.8% (P < 0.01), 36.6% (P < 0.01), and 32.6% (P < 0.02), respectively, whereas the muscle VV[30] was not altered significantly. Similar results were observed using the isolated forearm technique and a deep muscle vein. The infusion of epinephrine intra-arterially did not decrease reflex venomotor reactivity until cutaneous blood flow was completely suppressed, indicating that the inability of the veins to react in the iontophoresed arm was not the result of epinephrine diffusion into the muscle bed. Thus, these results indicate that, in the forearm, only cutaneous veins participate in venomotor reflexes. Further, since the forearm is principally composed of skeletal muscle and the hand skin, an explanation is provided for the observation that veins of the forearm, studied as a whole, appear less reactive to stimuli than veins of the hand. An explanation also is provided for fainting which occurs during motionless standing despite intense venoconstriction, thereby emphasizing the importance of the skeletal muscle pump in the legs in preventing postural syncope.
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PMID:Comparison of the reflex reactivity of skin and muscle veins in the human forearm. 582 92

1. The aim of this study was to determine the effects of caffeine on haemodynamic and neurohumoral responses to meal ingestion in elderly patients with a history of symptomatic postprandial hypotension. 2. Postprandial hypotension is a common disorder of blood pressure regulation in the elderly, associated with falls and syncope. The pathophysiological mechanism is thought to be related to impaired vascular compensation for splanchnic blood pooling after a meal. Since caffeine inhibits vasodilatory adenosine receptors in the splanchnic circulation, we postulated that caffeine would reduce splanchnic blood pooling and prevent the development of postprandial hypotension. 3. We conducted a randomized, double-blind, placebo-controlled, cross-over study in nine elderly patients [age 76 +/- 9 (SD) years] with histories of symptomatic postprandial hypotension. Standardized 1674kJ liquid meals with 250 mg of caffeine or placebo were given on two occasions, at least 1 week apart. Blood pressure, heart rate, forearm vascular resistance (by venous occlusion plethysmography), and plasma caffeine and catecholamine levels were measured. Cardiac and splanchnic blood volume were determined by radionuclide scans. 4. By 30 min after both caffeine and placebo meal studies, supine mean arterial blood pressure fell significantly (P = 0.006) by 31 +/- 7 and 19 +/- 6 mmHg, respectively (mean +/- SEM, between group difference was not significant). Heart rate, cardiac output and splanchnic blood volume increased significantly, but to a similar extent, after caffeine and placebo. Forearm vascular resistance was unchanged after both meals. 5. Oral caffeine given with a meal does not reduce splanchnic blood pooling nor prevent postprandial hypotension in symptomatic elderly patients.
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PMID:Haemodynamic and neurohumoral effects of caffeine in elderly patients with symptomatic postprandial hypotension: a double-blind, randomized, placebo-controlled study. 792 73

Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine conditions for this dramatic syndrome are poorly understood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reactions, with sudden hypotension, nausea, and dizziness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15 mmHg (delta = -0.06 +/- (SEM) 0.04 pmol min-1 100mL-1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (delta = 0.31 +/- 0.13 pmol min-1 100mL-1). Plasma levels of beta-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinhibition, and release of endogenous opioids can precede vasodepressor syncope.
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PMID:Neurohumoral antecedents of vasodepressor reactions. 855 62

The neurohumoral events associated with neurocardiogenic syncope remain unclear. The simultaneous assessment of changes in endothelium-dependent and independent hormones and in autonomic balance in patients with tilt-induced syncope has been incompletely studied. Forty-six healthy subjects aged between 21 and 83 years (mean +/- SEM 47 +/- 3) underwent a 30-minute head-up tilt test at 60 degrees. Fourteen subjects (10 females and 4 male subjects) exhibited syncope at 16 +/- 2 minutes into the tilt. Hemodynamics were recorded every 5 minutes and blood samples for the measure of catecholamines, endothelin-1 (ET-1), and angiotensin-II (AT-II), were drawn at baseline, and 5, 10, 15, and 30 minutes into the tilt and immediately before syncope. Heart rate variability was analyzed by 5-minute segments during the test. Both catecholamines and ET-1 levels increased consistently in response to head-up tilt in subjects able to tolerate the test. Epinephrine increased to a greater extent before syncope. In contrast, ET-1 failed to increase at any time during the tilt and just before syncope. AT-II increased at 30 minutes into the tilt only in the control group. Finally, power in high-frequency bands decreased less in the group with syncope. Thus, compared with subjects able to tolerate a head-up tilt test, patients with syncope exhibit a greater increase in adrenomedullary activation, no significant increase in ET-1 levels, and a blunting in the decrease of vagal tone before syncope. The lack of increase in ET-1 during tilt may play a role in the inability to support orthostatic stress.
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PMID:Impaired endothelin-1 release in tilt-induced syncope. 948 37

Eptastigmine is a new acetylcholinesterase (AChE) inhibitor currently under development for the symptomatic treatment of Alzheimer disease. This study was conducted to establish the maximum tolerated dose and the pharmacodynamics of eptastigmine in nine healthy elderly volunteers. Subjects received single oral doses of 8 mg, 20 mg, 32 mg, and 40 mg eptastigmine and placebo according to a double-blind, randomized, rising-dose, five-way crossover design. Adverse events, blood pressure, heart rate, body temperature, forced expiratory volume, salivary flow, and pupilar activity were closely monitored during treatment. Pharmacodynamic activity of eptastigmine was evaluated with an assay of AChE activity in red blood cells. Eptastigmine doses of 8 mg, 20 mg, and 32 mg were well tolerated. Two of four subjects receiving the 40-mg dose developed profound AChE inhibition (58-59%) and reported severe adverse events (nausea, vomiting, syncope, and bradycardia), precluding further administration in the remaining subjects. Eptastigmine administration produced a weak effect on supine heart rate, body temperature, and pupil diameter. There were no effects on blood pressure, forced expiratory volume, salivary flow, and near point of focus. Acetylcholinesterase activity was inhibited in a dose-related fashion according to a sigmoidal (logistic) function. The mean (+/- SEM) maximum inhibition of AChE activity (Imax) was 14.5+/-3.3%, 20.4+/-2.3%, 28.7+/-2.9%, 45.2+/-1.3% and 53.6+/-2.9% after placebo, 8 mg, 20 mg, 32 mg, and 40 mg of eptastigmine, respectively. The theoretical maximum response (Emax) was 72.9%, and the dose that produced half of the maximum response (ED50) was 29.5 mg. At 24 hours, residual AChE inhibition ranged from 9% to 15%, with a half-life of recovery of the enzyme of approximately 10 hours. The maximum tolerated dose of eptastigmine after single-dose oral administration in healthy elderly subjects is 32 mg. Single oral doses of eptastigmine produce sustained, dose-related inhibition of AChE activity. Adverse events are related to the degree of AChE inhibition.
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PMID:Maximum tolerated dose and pharmacodynamics of eptastigmine in elderly healthy volunteers. 970 45


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