Protective effects of human urinary trypsin inhibitor against trypsin-induced relaxation in rat aorta
Autor: | Manabu Yamamoto, Shizuya Saika, Yoshio Hatano, Kohji Ogawa, Takuji Ooka |
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Rok vydání: | 1996 |
Předmět: |
Male
medicine.medical_specialty Vascular smooth muscle Endothelium Trypsin inhibitor Vasodilation Tachyphylaxis Critical Care and Intensive Care Medicine Muscle Smooth Vascular Nitric oxide chemistry.chemical_compound Internal medicine medicine.artery medicine Animals Humans Trypsin Rats Wistar Aorta business.industry URINARY TRYPSIN INHIBITOR Rats Endocrinology medicine.anatomical_structure Anesthesiology and Pain Medicine Biochemistry chemistry Biophysics Microscopy Electron Scanning Relaxation (physics) Endothelium Vascular business Trypsin Inhibitors medicine.drug |
Zdroj: | Critical care medicine. 24(11) |
ISSN: | 0090-3493 |
Popis: | OBJECTIVES To investigate the vasodilatory responses induced by trypsin, and to determine the antitrypsin effects of human urinary trypsin inhibitor on blood vessels. DESIGN Prospective, randomized, controlled study, with repeated measurements. SETTING University research laboratory. INTERVENTIONS The isometric tension of the aortic rings isolated from male Wistar rats was recorded. The vasodilatory responses to varying amounts of trypsin (0.01 to 10 U/mL) were examined under pretreatment with human urinary trypsin inhibitor (1 to 10 U/mL), chicken-egg-white trypsin inhibitor (0.1 to 10 mg/mL), N infinity-nitro-L-arginine (3 x 10(-5) M), and denudation of the endothelium. In addition, with the scanning electron microscopy, the endothelium of aorta was examined under treatment with trypsin alone (10 U/mL), and with trypsin plus human urinary trypsin inhibitor (10 U/mL each).4 MEASUREMENTS AND MAIN RESULTS The addition of trypsin produced dose-dependent relaxation in aortic rings with an intact endothelium, which was abolished by denudation and treatment with N infinity-Nitro-L-arginine. Pretreatment with human urinary trypsin inhibitor and with chicken-egg-white trypsin inhibitor caused dose-dependent inhibition against trypsin-induced vasorelaxation. On the repeated trials of the response to trypsin, the responses gradually developed tachyphylaxis in control aortic rings, whereas no tachyphylaxis developed in rings pretreated with human urinary trypsin inhibitor (10 U/mL). Scanning electron microscopy demonstrated endothelial disruption in aorta exposed to trypsin alone, whereas the endothelium was intact in strips treated with trypsin plus human urinary trypsin inhibitor. CONCLUSIONS The data indicate that relaxation induced by trypsin is attributable to nitric oxide released from the endothelium, and that human urinary trypsin inhibitor protects vessels against trypsin-induced endothelial injury. It appears that the clinical antishock effect of human urinary trypsin inhibitor is ascribable in part to its antitrypsin activity on the endothelium of vascular smooth muscle. |
Databáze: | OpenAIRE |
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