No abstract available.
Chloroform*

Pelvic Bones* ; Sex Differentiation*

BACKGROUND: Although hypoxic pulmonary vasoconstriction (HPC) and hypoxic coronary vasodilatation (HCD) have been recognized by many researchers, the precise mechanism remains unknown. As isolated arteries will constrict or relax in vitro in response to hypoxia, the oxygen sensor/transduction mechanism must reside in the arterial smooth muscle, the endothelium, or both. Unfortunately, much of the current evidence is conflicting, especially concerning to the dependency of HPC and HCD on the endothelium and the role of the K+ channel. Therefore, this experiment was attempted to clarify the dependency of HPC and HCD on the endothelium and the role of the K+ channel on HPC and HCD. METHODS: HPC was investigated in isolated main pulmonary arteries precontracted with norepinephrine (NE). HCD was investigated in isolated left circumflex coronary artery precontracted with prostaglandin F2 alpha. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit solution. Hypoxia was induced by gassing the chamber with 95% N2 +5% CO2, which was maintained for 15 - 25 min. RESULTS: 1)Hypoxia elicited a vasoconstriction in NE-precontracted pulmonary arteries with endothelium, but a vasodilatation in PGF 2 alpha-precontracted coronary arteries with and without endothelium. There was no difference between the amplitude of the HPC and HCD induced by two consecutive hypoxic challenges and the effect of normoxic and hyperoxic control Krebs-Henseleit solution on subsequent response to hypoxia. 2)Inhibition of NO synthesis by the treatment with Nw-nitro-L-arginine reduced HPC in pulmonary arteries, but inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HPC and HCD, respectively. 3)Blockades of the TEA-sensitive K+ channel abolished HPC and HCD. 4)Apamin, a small conductance Ca2+/-activated K+ (KCa) channel blocker, and iberiotoxin, a large conductance KCa channel blocker, had no effect on the HCD. 5)Glibenclamide, an ATP-sensitive K+ (KATP) channel blocker, reduced HCD. 6)Cromakalim, an K(ATP) channel opener, relaxed the coronary artery precontracted with prostaglandin F2 alpha. The degree of relaxation by cromakalim was similar to that by hypoxia and glibenclamide reduced both hypoxia- and cromakalim-induced vasodilations. 7)Verapamil, a Ca2+ entry blocker, caffeine, a Ca2+ emptying drug; and ryanodine, an inhibitor of Ca2+ release from SR, reduced HPC, respectively. CONCLUSION: HPC is dependent on the endothelium and is considered to be induced by inhibition of the mechanisms of NO-dependent vasodilation while HCD is independent of the endothelium and is considered to be induced by activation of the K(ATP) channel.
Anoxia ; Arteries ; Caffeine ; Coronary Vessels ; Cromakalim ; Dinoprost ; Endothelium ; Glyburide ; Indomethacin ; Muscle, Smooth ; Norepinephrine ; Oxygen ; Prostaglandin-Endoperoxide Synthases ; Prostaglandins F ; Pulmonary Artery ; Relaxation ; Ryanodine ; Vasoconstriction* ; Vasodilation*

A 24-year-old man presented with a 1.5 × 0.5 cm-sized erythematous nodule with central crust on the forehead since 5 years ago. There was no history of trauma or previous skin disorders. Histopathologic examination showed a typical picture of osteoma cutis. In addition, transepidermal elimination of bony material was observed: red linear plate-like calcified lamella structures had extruded to the skin surface through the perforated epidermis. The perforating type of osteoma cutis was discussed.
Epidermis ; Forehead ; Humans ; Osteoma* ; Skin ; Young Adult

The present study was intended to examine the effect of sodium vanadate on contractility of vascular smooth muscle. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various conditions. The results were summarized as follows; 1) Sodium vanadate induced contraction of vascular smooth muscle in a dose-dependent fashion. 2) The contractile effects were not blocked by treatments with adrenergic blocking agent(phentolamine) and indomethacin, indicating the direct action of the drug on vascular smooth muscle. 3) In the presence of ouabain, Na(+)-K(+)-ATPase inhibitor, sodium vanadate still increased the contractility of vascular smooth muscle. 4) Treatment with 4.4'-diisothiocyanostilbene-2.2'-disulfonic acid(DIDS) blocked completely the contractile effects of sodium vanadate. 5) In the presence of verapamil, lanthanum and ryanodine, the contractility of the vascular smooth muscle by sodium vanadate was decreased. From the above results. it was suggested that sodium vanadate acts directly on vascular smooth muscle and causes contraction. It was probably due to inhibition of Ca(++)-ATPase in plasma membrane as well as increasing the release of Ca(++) from sarcoplasmic reticulum and Ca(++) influx across the plasma membrane, but not inhibition of Na(+)-K(+)-ATPase.
Aorta, Thoracic ; Cell Membrane ; Endothelial Cells ; Indomethacin ; Lanthanum ; Muscle, Smooth, Vascular* ; Ouabain ; Ryanodine ; Sarcoplasmic Reticulum ; Sodium* ; Vanadates* ; Verapamil

No abstract available.
Calcium* ; Erythrocytes* ; Sodium* ; Spherocytes

No abstract available.
Leukemia*

No abstract available.
Macrophages, Peritoneal* ; Nitric Oxide ; Nitric Oxide Synthase* ; Shock* ; Tumor Necrosis Factor-alpha

A 45-year-old woman presented with a generalized fixed drug eruption due to mefenamic acid, characterized by recurring erythematous patches with central bullae on the same sites of the whole body and leaving hyperpigmentation after each attack. Patch testing of a quiescent lesion with 50% mefenamic acid in vaselin revealed an eczematous reaction after 48 hours. The disease course was mild compared to the severe clinical manifestation. We here-in report a case of generalized fixed drug eruption due to mefenamic acid which is considered a rare occurrence.
Drug Eruptions* ; Female ; Humans ; Hyperpigmentation ; Mefenamic Acid* ; Middle Aged ; Patch Tests

A case of situs inversus totalis was observed in the cadaver of a 35 year old Korean female and the anatomical structures were investigated. The fact that she had received intestinal resection due to tuberculosis of intestines was confirmed. The results are summarized as follows : 1. All thoracic and abdominal viscera were completely transposed and in the left lower quadrant of abdomen, it was observed that the distal portion of the small intestine, cecum, appendix and part of the ascending colon had been resected. 2. Classic mirror-image dextrocardia with patent foramen ovale (large diameter, 7mm), sinusitis in the left maxillary sinus, bilateral thoracic duct, variation of the opennig site of the common bile duct and the main pancreatic duct, and maldvelopment of the left adrenal gland were observed together with the sinus inversus totalis.
Abdomen ; Adrenal Glands ; Appendix ; Cadaver ; Cecum ; Colon, Ascending ; Common Bile Duct ; Dextrocardia ; Female ; Foramen Ovale, Patent ; Humans ; Intestine, Small ; Intestines ; Maxillary Sinus ; Pancreatic Ducts ; Sinusitis ; Situs Inversus* ; Thoracic Duct ; Tuberculosis ; Viscera