No abstract available.
Animals ; Arteries* ; Rats*

A case of Coats' disease, apparently as the first report in Korea, is presented. The patient was 17 years old Korean female and hospitalized Woo-Suk University hospital on May 23, 1969. Although cyclodialysis had been performed to the patient her intraocular pressure remained as the same as before the treatment, and thus enucleation Was done finally.
Adolescent ; Female ; Humans ; Intraocular Pressure ; Korea

In this study the effects of two unrelated vasodilators, nifedipine and nitroprusside, on the pressor responsiveness to the 1-adrenoceptor full agonist cirazoline and partial agonist Sgd 101/75 in pithed rats were examined. The experiments were performed on the vasoconstriction which was mediated by newly synthetized 1-adrenoceptors after removal of existing 1-adrenoceptors by phenoxybenzamine treatment(5mg/kg, i. p.). The t1/2 for recovery of the maximum response and ED50 of cirazoline were 23.1 +/- 5.5 and 26.9 +/- 7.4 hours, respectively, while that for recovery of the maximum response of Sgd 101/75 was 59.2 +/- 18.9 hours. The relationship between the pressor response and the fractional receptor occupancy for cirazoline showed a rectangular hyperbola. This occupancy-response curve markedly shifted to the right one day after phenoxybenzamine and subsequently returned to the control, indicative of a large receptor reserve. However, for Sgd 101/75 the occupancy-response curve exerted less of a hyperbola and shifited little after phenoxybenzamine. While the maximum response to cirazoline in the control rats was resistant to inhibition by the calcium entry blocker nifedipine, this resistance was significantly reduced one and 3 days after phenoxybenzamine, just as the maximum response to Sgd 101/75 was sensitive to nifedipine in the control rats. Likewise, when nitroprusside was used instead, the results were similar for the cirazoline and Sgd 101/75 effects. In summary, it seems unlikely that the resistance to the calcium entry blocker of the full agonist effect can be wholly ascribed either to the receptor reserves or to the differential calcium utilization itself. Alternatively, it is suggested that the differential resistance to calcium antagonists can result from the magnitude of the variables involved in the activation of 1-adrenoceptor coupling processes depending on the full or partial agonist.
Animal ; Blood Pressure/*drug effects ; Clonidine/*analogs and derivatives/antagonists and inhibitors/pharmacology ; Comparative Study ; Ferricyanides/*pharmacology ; Imidazoles/antagonists and inhibitors/*pharmacology ; Male ; Nifedipine/*pharmacology ; Nitroprusside/*pharmacology ; Rats ; Rats, Inbred Strains ; Vasoconstriction/*drug effects

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.
Extremities* ; Sarcoma*

BACKGROUND AND OBJECTIVES: Many studies have shown that coronary artery bypass graft (CABG) surgery prolongs the life of patients with left main coronary artery disease (LMCD). Recently, percutaneous coronary intervention (PCI) has been applied to treat LMCD, with good clinical results. However, a significant portion of patients decline any revascularization therapy, so receive medical treatment only. The aim of this study was to evaluate the long term clinical outcome in these patients with LMCD, according to the treatment strategies. SUBJECTS AND MEHTODS: The clinical outcomes of 281 consecutive patients, with significant LMCD, between January 1997 and December 2000, were evaluated. The patients were divided into three groups, according to their initial treatment strategies;1) CABG, 2) PCI and 3) medical treatment. The mean follow-up duration was 37.4+/-14.9 months. RESULTS: The 1- and 3-year survival rates in the CABG group (97.4+/-1.5% and 95.6+/-1.9%) were significantly higher than those of the medical group (89.8+/-3.9% and 76.1+/-5.9%;p=0.03). The survival rates in the PCI group (one year and 3-year survival rate, 98.1+/-1.3% and 93.8+/-2.5%) were similar to those of the CABG group (p=0.93). The incidence of 3-year MACE in the medical group (40.7%) was higher than those of the CABG (10.5%, p<0.001) and PCI groups (20.4%, p=0.007). There was no significant difference between the CABG and PCI groups (p=0.06). CONCLUSION: In patients with LMCD, a CABG remains the standard therapy for prolonging survival and lowering the incidence of MACE. PCI offers similar survival benefits in selected patients. Medical treatment is associated with a significantly higher mortality and MACE. Active revascularization therapy should be the treatment of choice for the patients with LMCD.
Angioplasty ; Coronary Artery Bypass ; Coronary Artery Disease ; Coronary Disease* ; Follow-Up Studies* ; Humans ; Incidence ; Mortality ; Percutaneous Coronary Intervention ; Survival Rate ; Transplants

No abstract available.
Mitral Valve* ; Quinidine*

Apoptosis is a distinct mode of cell death that is responsible for deletion of cells in normal tissues. Apoptotic cell death plays an important role in the proliferation and turnover of cells in various tumors. Apoptosis occurs spontaneously in malignant tumors, often markedly retarding their growth, and increased in tumors responding to irradiation, cytotoxic chemotherapy, heating and hormone ablation. Flowcytometric analysis of the cellular DNA content appears to be a useful clinical prognostic indicator in colorectal cancer. The relationship of apoptotic index(AI) and proliferative indices have being investigated. We analyzed the tumor DNA content and AI in 84 patients who underwent resection for colorectal cancer between January 1989 and December 1994 in order to evaluate the prognostic significance of apoptosis, DNA ploidy and index using in situ apoptosis detection method and flowcytometry. The mean value of AI was 32.4, and median value 21. In the cellular DNA, forty-two percent of the tumors were diploidy, fifty-eight percent aneuploidy. The mean value of DNA index(DI) was 1.38, G0/G1 72%, S phase fraction 21.7%, G2/M 6.3%, and proliferative fraction 28%. There was no significant difference between AI and tumor invasion, LN metastasis, DNA ploidy, DI.(p>0.05) There was no significance between overall survival and AI, DNA ploidy, DI. But patients who had tumors with low DNA index had a significantly longer disease free survival than high DNA index.(p<0.05) As a result, this study shows that AI is a less useful as prognostic factor and DNA index is a more important prognostic factor in patients undergoing surgery for colorectal cancer.
Aneuploidy ; Apoptosis ; Cell Death ; Colorectal Neoplasms* ; Diploidy ; Disease-Free Survival ; DNA* ; Drug Therapy ; Heating ; Hot Temperature ; Humans ; Neoplasm Metastasis ; Ploidies ; S Phase

The study aims to identify the mechanism (s) underlying the altered vasodilatory responses of the pial artery of spontaneously hypertensive rats (SHR) under a hypothesis that calcitonin gene-related peptide (CGRP) exerts a modulator role in the autoregulation of cerebral blood flow (CBF). The animals were divided into four groups: 1) Sprague-Dawley rats (SDR), 2) Wistar rats (WR), 3) SHR with high blood pressure (BP gtoreq 150 mmHg), and 4) SHR with normotensive BP (ltoreq 150 mmHg). The lower limit of CBF autoregulation in SHR shifted to a higher BP (82.8 +/- 9.3 mmHg, P < 0.05) than that in SDR (58.9 +/- 5.7 mmHg). In SHR, whether the BP levels were high or normotensive, the vasodilator responses to a stepwise hypotension were significantly attenuated unlike with SDR and WR. When artificial cerebrospinal fluid (CSF) containing capsaicin (3 X 10-7 M) was suffused over the cortical surface, a transient increase in pial arterial diameter was observed in the SHR with high or normotensive BP. In contrast, SDR and WR showed a large increase in diameter, and the increase was sustained for over 10 minutes. In line with these results, the basal releases of CGRP-like immunoreactivity (CGRP-LI) in the isolated pial arteries from SHR with high and normotensive BP were 12.5 +/- 1.4 and 9.8 +/- 2.8 fmole/mm2/60 min (P < 0.05), while those from SDR and WR were 25.5 +/- 3.1 and 24.6 +/- 3.1 fmole/mm2/60 min, respectively. The isolated basilar arteries showed similar results to those of the pial arteries in SHR. Thus, it is summarized that, in the SHR, the reduced autoregulatory vasodilator responses to stepwise hypotension and capsaicin may be, in part, ascribed to the decreased release of CGRP from the perivascular sensory nerve fibers of the pial arteries, and that altered vasomotor activity in SHR may not be related with the hypertensive tone.
Animals ; Arteries* ; Basilar Artery ; Calcitonin Gene-Related Peptide ; Capsaicin ; Cerebrospinal Fluid ; Homeostasis ; Hypertension ; Hypotension ; Nerve Fibers ; Rats, Inbred SHR* ; Rats, Sprague-Dawley ; Rats, Wistar

OBJECTIVES: Septic shock is characterized by the circulatory failure including vasodilation, hyporeactivity to vasoconstrictor agents and organ ischemia in association with multiple organ failure and increased platelet aggregation and blood coagulation. In the present study, we investigated the preventive effects of N-nitro-L-arginine methyl ester (L-NAME, 30mg/kg, i.p.), a non-selective nitric oxide synthase (NOS) inhibitor, S-methylisothiourea sulfate (SMT, 5mg/kg, i.p.) and pentoxifylline (PTX,10mg/kg, i.p.) on the multiple organ dysfunction in a rat model of circulatory shock induced by bacterial endotoxin (E. coli lipopolysaccharide: LPS) and discussed the mechanism underlying the development of multiple organ failure. METHODS: The effect of each other N-nitro-L-arginine methyl ester(L-NAME, 30 mg/kg, i.p.), a non-selective nitric oxide synthase(NOS) inhibitor, S-methyli-sothiourea sulfate(SMT, 5mg/kg, i.p.) and pentoxifylline (PTX, 10mg/kg, i.p.) were comparatively evaluated following inducing circulatory shock by means of infusion of bacterial endotoxin to the rat model. RESULTS: 1) The systemic mean arterial blood pressure decreased by 48.7mmHg and vascular hyporeactivity to noradrenaline injection(1 g/kg, i.v.) upon intravenous administration of LPS. 2) Endotoxemia for 6hours resulted in little change in the numbers of white blood cells and neutrophils but a significant reduction in the numbers of platelets. The variables were not affected by the inhibitors. 3) Endotoxemia for 6hours caused a significant increase in serum nitric oxide level (P<0.01) which was inhibited by SMT, but not by L-NAME and PTX. 4) Upon injection of LPS, serum creatinine(0.65+/-0.08mg/dl) and urea(28.7+/-5.9mg/dl) were significantly elevated to 0.92+/-0.12 (P<0.05) and 54.3+/-2.1mg/dl (P< 0.01). These elevated levels were significantly attenuated by PTX but not by L-NAME and SMT. 5) Endotoxemia for 6 hours resulted in a significant increases in serum ALT(988.8+/-28.2 IU/L, P<0.01) and AST levels(1470.5+/-396.5 IU/L, P<0.01) from basal levels of ALT(67.8+/- 11.7IU/L) and AST(170.3+/-14.8IU/L). These increased activities were significantly attenuated by PTX, but not by L-NAME and SMT. The level of LDH(1279.8+/-156.2IU/L) was significantly increased by LPS treatment to 2932.0+/-519.9IU/L (P<0.05), which was inhibited by PTX. 6) Upon LPS treatment, the myeloperoxidase activity in the lung homogenate was significantly increased by LPS treatment (P<0.05), whereas that in the liver showed less change. The increased activity was reduced by PTX (P<0.05), but not by L-NAME and SMT. 7) The level of serum malondialdehyde, an index of lipid peroxidation by oxygen free radicals, was little influenced by LPS. CONCLUSION: Based on these results, it is summarized that PTX characteristically inhibited the development of multiple ogran dysfunction in a murine model of endotoxemia. Thus, it is concluded that the formation of TNF and increased activity of neutrophils may importantly contribute to the development of LPS-induced endotoxemia.
Administration, Intravenous ; Animals ; Arterial Pressure ; Blood Coagulation ; Endotoxemia ; Free Radicals ; Ischemia ; Leukocytes ; Lipid Peroxidation ; Liver ; Lung ; Malondialdehyde ; Models, Animal ; Multiple Organ Failure ; Neutrophils ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitric Oxide Synthase ; Norepinephrine ; Oxygen ; Pentoxifylline* ; Peroxidase ; Platelet Aggregation ; Rats* ; Shock ; Shock, Septic ; Vasoconstrictor Agents ; Vasodilation