No abstract available.
Pneumothorax* ; Thorax*

Adrenal Cortex Hormones* ; Prospective Studies* ; Stents*

No abstract available.

No abstract available.

No abstract available.
Heart Septal Defects, Atrial* ; Hemodynamics*

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

No abstract available.
Esophageal Neoplasms*

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

Plaque disruption and subsequent thrombotic occlusion is the primary mechanism by which atherosclerosis leads to acute coronary syndromes and ischemic stroke. Platelets are the key component of arterial thrombus formation in response to sudden fissuring or rupture of the atheromatous plaque. Low dose aspirin (100~300 mg/day) rapidly inhibits platelets through permanent inactivation of the key platelet enzyme, cyclooxygenase (COX). The efficacy and safety of aspirin have been extensively studied in several populations, ranging from healthy individuals to highrisk patients with acute myocardial infarction or ischemic stroke. It is well established that aspirin reduces the risk of serious vascular events (death, myocardial infarction, and stroke) by approximately 25% in patients with established vascular diseases. However, long-term therapy with aspirin approximately doubles the risk of major extracranial bleeding (mostly gastrointestinal bleeding) and also increases the risk of hemorrhagic stroke. In contrast to the clear benefit of aspirin in secondary prevention, its benefits in primary prevention are less clear. A meta-analysis of primary prevention trials in men demonstrated that aspirin reduces the risk of myocardial infarction by approximately 30% but has no effects on the risk of stroke. By contrast, the Women's Health Study showed that aspirin reduces the risk of stroke by 17% but has no effects on the risk of myocardial infarction. The reasons for this discrepancy remain unclear, requiring additional studies. Taken together, aspirin is recommended for primary prevention in healthy individuals with an annual risk of vascular events >1.5%. In conclusion, aspirin is recommended for secondary prevention in all patients, but its risk-benefit ratio should be carefully considered for primary prevention.
Acute Coronary Syndrome ; Aspirin* ; Atherosclerosis ; Blood Platelets ; Hemorrhage ; Humans ; Male ; Myocardial Infarction ; Primary Prevention ; Prostaglandin-Endoperoxide Synthases ; Rupture ; Secondary Prevention ; Stroke ; Thrombosis ; Vascular Diseases ; Women's Health