No abstract available.
Estrogens*

No abstract available.
Blood Pressure*

No abstract available.

No abstract available.

No abstract available.
Geriatrics*

No abstract available.
Disasters*

No Abstract Available.
Fatigue Syndrome, Chronic* ; Fatigue* ; Prevalence*

BACKGROUND: Many studies reported that endothelium-dependent vasodilator response is impaired in patients with congestive heart failure. But the opposite results also were reported. The aim of this study was to determine the presence of endothelial dysfunction and its characteristics. METHODS AND MATERIALS: Forearm blood flow was measured in 12 patients with congestvie heart failure (7 males and 5 females, mean age 53+/-11 years old) and 10 normal control subjects (5 males and 5 females, mean age 41+/-10 years old) using strain-gauge plethysmography. The endothelium-dependent vasodilators were acetylcholine (7.5, 15, and 30 microgram/min), which uses a pertussis toxin-sensitive signal transduction pathway, and bradykinin (100, 200, and 400 ng/min), which uses a pertussis toxin-insensitive signal transduction pathway to activate nitric oxide production. Sodium nitroprusside (0.8, 1.6, and 3.2 microgram/min) was used as an endothelium-independent vasodilator. All drugs were infused into the brachial artery with random order. RESULTS: The basal forearm blood flow was similar between both groups. The maximum flow in response to acetylcholine, bradykinin, and sodium nitroprusside was also similar in two groups. CONCLUSIONS: Patients with congestive heart failure showed normal endothelium-dependent vasodilator responses to both acetylcholine and to bradykinin. This finding indicates that the endothelial vasodilator function is normal in the patients with heart failure.
Acetylcholine ; Brachial Artery ; Bradykinin ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Estrogens, Conjugated (USP)* ; Female ; Forearm ; Heart Failure* ; Humans ; Male ; Nitric Oxide ; Nitroprusside ; Plethysmography ; Signal Transduction ; Vasodilation* ; Whooping Cough

Survival after acute myocardial infarction (AMI) is related to the number of diseased vessel, ejection fraction, extent of residual ischemic tissue, presence of ventricular arrhythmia. Because a variety of revascularization modalities are tried in recent years, the natural course after AMI seems to become difficult ot assess. From the experience of 129 cases of coronary angiography in AMI from Jan 1984 to Apr 1987, the factors related to invasive modality were analysed to evaluate the effect on the survival after AMI. The following results are obtained. 1) Single vessel disease and insignificant lesion were present in 60%, and multivessel disease comprised 40% in all group. 2) Patients were followed for a mean of 16.3 months and 2 cases(1.6%) expired suddenly and reinfarction developed in 6 cases(4.7%). 3) After exclusion of 4 cases taken CABG operation, the event free survival of all patients was 0.98, 0.90, 0.78, 0.78, 0.78 in double vessel disease, 0.94, 0.87, 0.87, 0.77, 0.51 in triple vessel disease. The survival was better in single vessel disease compared to multivessel disease (p<0.05), but no difference was present between double and triple vessel disease. 5) Event free survival in group with left ventricular end diastolic pressure(LVEDP) >16mm Hg was better than that of a group with LVEDP <16mm Hg. But no difference was present between group with ejection fraction <40% and group with ejection fraction >40%. From the above results, it can be concluded that the event free survival after mainly uncomplicated AMI in Koreans depends on the number of diseased vessel and LVEDP.
Arrhythmias, Cardiac ; Coronary Angiography ; Disease-Free Survival* ; Humans ; Myocardial Infarction*

BACKGROUND: Proliferation of vascular smooth muscle cells(VSMC) is a critical event in the development of atherosclerosis. Endothelin-1(ET-1), a vasoconstrictor peptide produced by endothelial cells and VSMC, might play a role in vascular remodeling. To investigate the proposed 'mitogenic' potential of ET-1, we examined the effects of ET-1 on the proliferation if cultured porcine aortic VSMC and on the potential synergism with platelet-derived growth factor(PDGF). MATERIALS AND METHODS: VSMC were obtained from porcine aorta and cultured in Dulbecco's modified Eagle medium supplmented with 10% fetal bovine serum(FBS). VSMC grown subconfluently in 12-well plate were stimulated by ET-1, PDGF, and ET-1 & PDGF and DNA synthesis was determined as the uptake of 3H-thymidine into cell cultures. We also examined the effects of BQ123, a selective ETA receptor antagonist, and NG-methyl-L-arginine(NMLA), a nitric oxide synthase (NOS) inhibitor. RESULTS: ET-1 elicited a 2.5-fold increase of cultured VSMC DNA synthesis, comparing with basal medium, and PDGF elicited a 4.8-fold increase, whereas ET-1 and PDGF elicited a 8.8-fold increase, showing synergistic effect. Proliferative activity of ET-1 on VSMC was blocked(39%) by BQ123, however, the synergistic effect of ET-1 and PDGF was not blocked by BQ123. The synergistic effect of ET-1 and PDGF was increased when co-stimulated with NMLA. CONCLUSION: ET-1 is a co-mitogen for VSMC from porcine aorta, whose proliferative activity requires serum or other growth factors such as PDGF for its maximal activity. The proliferative activity of ET-1 is considered to be transduced partly by selective activation of the ETA receptor, however, the synergistic effect of of ET-1 and PDGF is to be stimulated by non-ETA receptor.
Aorta ; Atherosclerosis ; Cell Culture Techniques ; Cell Proliferation* ; DNA ; Eagles ; Endothelial Cells ; Endothelin-1* ; Intercellular Signaling Peptides and Proteins ; Muscle, Smooth, Vascular* ; Nitric Oxide Synthase