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)

The short-term hemodynamic effects of molsidomine (4 mg sublingually) were evaluated in 13 patients with congestive heart failure following acute myocardial infarction. Right heart catheterization was performed by means of a Swan-Ganz thermodilution catheter. Hemodynamic measurements were made 30, 60, 120, and 180 minutes after the administration of the drug. Molsidomine significantly reduced systolic blood pressure from 121.5 +/- 3.3 (mean +/- SEM) to 111.1 +/- 2.9 mm Hg (p less than 0.001) after 60 minutes, mean right atrial pressure from 6.1 +/- 1 to 2.6 +/- 0.6 mm Hg (p less than 0.0001), mean pulmonary arterial pressure from 29.8 +/- 1.9 to 20.1 +/- 1.3 mm Hg (p less than 0.0001), and left ventricular filling pressure from 20.3 +/- 0.6 to 12.2 +/- 0.7 mm Hg (p less than 0.0001). No significant change occurred in heart rate, diastolic and mean blood pressure, cardiac index, stroke volume index, left ventricular stroke work index, systemic vascular resistance, and pulmonary vascular resistance. No side effects were seen after the administration of molsidomine.
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PMID:Hemodynamic effects of molsidomine in patients with heart failure following acute myocardial infarction. 383 10

Molsidomine is a derivative of the sydnonimines and is a long-acting vasodilator that may be effective in the treatment of chronic stable angina pectoris. To evaluate the therapeutic efficacy and drug tolerance, eight men with stable angina pectoris performed a symptom-limited maximal exercise test on a computer-assisted treadmill. After ingesting either placebo or molsidomine administered in single blind fashion 90 min before the exercise test on the first day of treatment, molsidomine decreased the average systolic blood pressure response from 154 +/- 3 (SEM) to 135 +/- 4 mmHg (p less than 0.01). However it did not significantly change the average heart rate response (117 +/- 7 to 124 +/- 8 beats/min) and the rate-pressure product (18.1 +/- 1.2 X 10(3) to 16.8 +/- 1.1 X 10(3]. The average time up to the onset of ischemia at which significant ST-segment deviation (0.1 mV) first appeared was increased from 9.0 +/- 1.7 to 12.8 +/- 1.2 min (p less than 0.001) after molsidomine. At peak exercise after molsidomine, the mean value of ST-segment deviation in V5 or aVF was decreased (p less than 0.001). This result was obtained even though the average exercise duration was increased from 11.4 +/- 1.7 to 13.6 +/- 1.2 min (p less than 0.001). The treadmill score according to Hollenberg was also improved from -47 +/- 24 to 1 +/- 14 after molsidomine administration. After six weeks of continued therapy with molsidomine the favorable effect on exercise tolerance was significantly decreased in terms of exercise duration, the time up to the onset of ischemia, and the treadmill score.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of molsidomine on exercise tolerance in patients with exertional angina pectoris. 668 83

In vascular smooth muscle cells, NO stimulates the synthesis of cGMP by soluble guanylate cyclase (sGC), a heterodimer composed of alpha(1) and beta(1) subunits. NO/cGMP signal transduction affects multiple cell functions that contribute to neointima formation after vascular injury. Balloon-induced vascular injury was found to decrease sGC subunit expression and enzyme activity in rat carotid arteries. The effect of restoring sGC enzyme activity on neointima formation was investigated using recombinant adenoviruses specifying sGC alpha(1) and beta(1) subunits (Adalpha1 and Adbeta1). Coinfection of cultured rat aortic smooth muscle cells with Adalpha1 and Adbeta1 increased NO-stimulated intracellular cGMP levels 60-fold and decreased DNA synthesis and migration by 16% and 48%, respectively. Immunoreactivity for alpha(1) and beta(1) subunits colocalized in carotid arteries infected with Adalpha1 and Adbeta1. Molsidomine-stimulated carotid tissue cGMP levels were greater after coinfection with Adalpha1 and Adbeta1 than after infection with a control virus, AdRR5 (0.53+/-0.09 pmol/mg protein, mean+/-SEM, versus 0.23+/-0.09, P<0.05). Mean intima/media ratio, 2 weeks after balloon injury and twice-daily administration of 5 mg/kg molsidomine, was less in rats coinfected with Adalpha1 and Adss1 than in rats infected with AdRR5 or in uninfected rats (0.36+/-0.11 versus 0. 81+/-0.13 and 0.75+/-0.25, respectively, P<0.05). Thus, Adalpha1 and Adbeta1 gene transfer to balloon-injured rat carotid arteries increases NO responsiveness and attenuates neointima formation via a direct antiproliferative and antimigratory effect on vascular smooth muscle cells.
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PMID:Soluble guanylate cyclase alpha(1) and beta(1) gene transfer increases NO responsiveness and reduces neointima formation after balloon injury in rats via antiproliferative and antimigratory effects. 1113 81