No abstract available.
Pneumothorax* ; Thorax*

Adrenal Cortex Hormones* ; Prospective Studies* ; Stents*

No abstract available.

No abstract available.

BACKGROUND: The purpose of this study was to investigate the mechanism of endothelium-dependent and independent responses to endothelins (ETs) in porcine coronary artery. METHODS: The vascular rings of left anterior descending artery or left circumflex artery from 7 pigs were suspended in conventional organ chambers for the measurement of isometric force. To evaluate relaxation responses, vascular rings with endothelium were exposed to ET-1 and ET-3. To evaluate contraction responses, vascular rings with and without endothelium were exposed to ET-1 and ET-3 in the presence or absence of BQ 123 (ET(A) receptor antagonist) or TAK-044 (ET(A) and ET(B) receptor antagonist). RESULTS: Transient relaxation responses of vascular rings occurred after exposure of ET-1 and ET-3. These transient responses disappeared after preincubation with N-nitro-L arginine. There was an increased contractions of vascular rings according to increasing concentration of ET-1 and ET-3. The initial responses were enhanced in vascular rings without endothelium in ET-1 and ET-3. In vascular rings with endothelium, the contraction responses were more reduced in vascular rings with preincubation of BQ 123 than in vascular rings without BQ 123 in ET-1. In vascular rings without endothelium, the contraction responses were more reduced in vascular rings with preincubation of TAK-044 than in vascular rings without TAK-044 in ET-1. CONCLUSION: ET(B) receptor on the endothelium might mediate the transient vasodilator responses to ET-1 and ET-3 through release of nitric oxide in porcine coronary artery. ET(A) and ET(B) receptor on vascular smooth muscle cells might mediate vasoconstrictor responses to ETs.
Arginine ; Arteries ; Coronary Vessels* ; Endothelins* ; Endothelium ; Muscle, Smooth, Vascular ; Nitric Oxide ; Receptors, Endothelin ; Relaxation ; Swine

The long QT syndrome is believed to result from abnormalities of cardiac sympathetic innervation and of myocardial repolarization. The therapeutic modalities for patients with ventricular arrhythmias due to the long QT syndrome include beta blocker, cardiac sympathetic denervation, pacemaker and ICD implantation. Recently, we underwent transvenous ICD implantation in a patient with this syndrome who had recurrent syncopal episodes due to rapid polymorphic ventricular tachycardia and strong family history of sudden death.
Arrhythmias, Cardiac ; Death, Sudden ; Humans ; Long QT Syndrome* ; Sympathectomy ; Syncope ; Tachycardia, Ventricular

The long QT syndrome is believed to result from abnormalities of cardiac sympathetic innervation and of myocardial repolarization. The therapeutic modalities for patients with ventricular arrhythmias due to the long QT syndrome include beta blocker, cardiac sympathetic denervation, pacemaker and ICD implantation. Recently, we underwent transvenous ICD implantation in a patient with this syndrome who had recurrent syncopal episodes due to rapid polymorphic ventricular tachycardia and strong family history of sudden death.
Arrhythmias, Cardiac ; Death, Sudden ; Humans ; Long QT Syndrome* ; Sympathectomy ; Syncope ; Tachycardia, Ventricular

No abstract available.
Esophageal Neoplasms*

No abstract available.
Adult* ; Esophageal Atresia* ; Fistula* ; Humans