Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental and clinical studies suggest that somatostatin, a regulatory peptide widely distributed in human tissues may have electrophysiologic effects. We studied a group of 14 patients who underwent a complete electrophysiologic study for different rhythm disturbances. Somatostatin significantly increased the spontaneous cycle length, the atrial and atrioventricular nodal effective refractory periods, and the Wenckebach cycle length. The AH and HV intervals during sinus rhythm remained unchanged. The effectiveness of somatostatin to interrupt paroxysmal supraventricular tachycardias was assessed in 18 patients. Termination was obtained in 15 (82.5%). Our results show that somatostatin has a significant electrophysiologic effect on the human heart, and confirm its clinical effectiveness in some arrhythmias.
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PMID:Electrophysiologic effects of somatostatin in man. 287 49

Somatostatin (S), a naturally occurring peptide, was first discovered more than 20 years ago. This peptide was later found in many tissues, including human cardiac tissue. High concentration of S was found in the sinus and atrioventricular (AV) nodes. Negative chronotropic activity of S and depressive effects of this substance on AF junction have also been described. The purpose of the present study was to determine the effect of S on the cardiac conduction system in man during antegrade and retrograde conduction. The study group consisted of 12 pts (5 women and 7 men, mean age 43 years). They were subjected to invasive electrophysiologic testing because of sudden unexplained heart palpitations. After measuring all electrophysiologic variables in the control state, each patient was given S (preparation Stilamin, Serono) intravenously with a syringe pump at a dose of 8.5 micrograms/min, for about 30 min. All the electrophysiologic measurements were repeated in the same order, beginning from the 6th min after the start of S injection. S prolonged mean sinus cycle length by 13%, sinoatrial, intraatrial and AV nodal conduction times by 15, 9 and 10%, respectively. Effective refractory periods of the atrium, AV node and right ventricle were prolonged by 7, 8 and 8%, respectively (all p values less than 0.01). Antegrade AV nodal Wenckebach cycle length, as well as retrograde, increased significantly (by 9 and 10% respectively). There were no significant changes of the mean HV interval, corrected QT interval, ventriculoatrial conduction time and corrected sinus node recovery time during S infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of somatostatin on the conduction system of the heart]. 810 33

The effects of met-enkephalin, leu-enkephalin, D-Ala2-metenkephalin, and somatostatin on Wenckebach arrhythmia and atrioventricular dissociation was investigated in experiments on anesthesized cats. Arrhythmias were induced by stimulation of the vagus with short repetitive bursts of pulses. Enkephalins evoked a protective effect in both arrhythmias whereas somatostatin had no antiarrhythmic properties. The protective effect of enkephalins persisted after blockage of mu-opiate receptors with naloxone (0.2 mg/kg), but in high doses (2 mg/kg), which blocked both mu- and delta-opiate receptors, antiarrhythmic effects was abolished. It is concluded that the protective effect of enkephalins against vagally induced arrhythmias may be due to the stimulation of delta-opiate receptors located on the presynaptic vagal endings. As a results, stimulation-evoked acetylcholine release is diminished, which prevent the arrhythmogenic effect of the vagus nerve.
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PMID:[Peptide correction of arrhythmias induced by stimulation of the vagal sympathetic trunk in cats]. 931 11