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Biomedical subjects

K Hirata

Publications and source records attributed to K Hirata.

At least 181 records · Page 10Linked to original sources
PubMed2000

Gastric amyloidosis with massive bleeding requiring emergency surgery.

We report a 66-year-old woman who had massive bleeding from a gastric ulcer complicating primary systemic amyloidosis, in whom emergency surgery proved lifesaving. Physical examination revealed anemia and macroglossia. Gastroscopy was performed, and an extensive, irregular, hemorrhagic ulcer was found in the gastric body. Biopsy resulted in a diagnosis of amyloidosis. On the 11th hospital day the patient went into shock as a result of a massive hemorrhage. Emergency surgery was performed, but the extent of the submucosal lesion in the stomach could not be identified, and total gastrectomy was unavoidable. Histological examination of the surgical specimen and biopsy tissue collected from other organs revealed amyloid deposition extending from the submucosa to the muscularis propria of the stomach. There was also deposition of large amounts of amyloid around the small blood vessels in the liver and under the mucosa of the small intestine. The amyloid was AA-antibody-negative and resistant to treatment with K2MO4, and a diagnosis of AL-type systemic amyloidosis was made. The patient's general condition recovered after the operation, but on the 103rd hospital day, she experienced sudden onset of arrhythmia and died. Patients with amyloidosis in whom gastrointestinal surgery is performed are rare; only 41 cases, including our own, have been reported in the Japanese literature since 1972.

Aged↗
PubMed2000

A chylous cyst of the mesentery: report of a case.

A case is presented of an adult chylous cyst of the mesentery that was preoperatively diagnosed to be a pancreatic cystadenoma. A 66-year-old asymptomatic male was followed up for 15 months under the diagnosis of a benign pancreatic cyst. On October 1997, computed tomography showed a 45 x 40 mm cystic mass in the upper abdomen which came in contact with the pancreas. Endoscopic ultrasonography revealed a multilocular mass with a 7 x 4 mm elevated lesion. Endoscopic retrograde cholangiopancreatography and magnetic resonance cholangiopancreatography revealed the cystic mass to be unrelated to the pancreatic duct. The preoperative diagnosis was a pancreatic cystadenoma or cystadenocarcinoma. A laparotomy showed a 50 x 40 mm cystic mass containing chylous fluid, that arose from the mesentery of the upper part of the jejunum. The pathological diagnosis was a chylous cyst of the mesentery. The preoperative diagnosis in this case was very difficult because the chylous cyst appeared to be attached to the pancreas and this phenomenon is considered to be extremely rare.

Aged↗
PubMed2000

Changes in hepatic venous oxygen saturation in hepatic warm ischemia/reperfusion injury in pigs.

To clarify the changes that occur in hepatic venous oxygen saturation (ShVO2) during hepatic ischemia/reperfusion (I/R) injury, we examined the relationship between ShVO2, hepatic tissue blood flow (HTBF), and portal vein pressure (PVP) in a warm I/R model using pig livers. Female pigs weighing 18-23 kg were subjected to warm I/R under extracorporeal circulation between the superior mesentric vein and the left jugular vein to avoid portal congestion. The warm ischemic times were 120 min (n = 4), 180 min (n = 14), and 240 min (n = 4). ShVO2, HTBF, and PVP were measured after reperfusion. The survival rates of the pigs 3 days after reperfusion were 100% in the 120-min group, 57% in the 180-min group, and 25% in the 240-min group. In the 180-min group, the ShVO2 was lower in the pigs that died than in those that survived. There was a significant correlation between ShVO2 and both PVP and HTBF after reperfusion. Histological examination revealed findings of severe I/R injury in pigs with a low ShVO2, and mild I/R injury in pigs with a stable ShVO2. These observations suggest that the changes in ShVO2 could reflect the degree of hepatic I/R injury, especially that related to microcirculatory disturbances occurring at the sinusoid levels.

Animals↗
PubMed2000

T102C polymorphism of the serotonin (5-HT) 2A receptor gene in patients with non-fatal acute myocardial infarction.

Serotonin (5-HT), released from activated platelets, has been implicated in the pathogenesis of acute myocardial infarction (AMI). 5-HT induces platelet aggregation and vascular contraction through 5-HT2A receptor activation at sites of coronary atherosclerosis, leading to thrombus formation. Recently, a 5-HT2A receptor gene T102C polymorphism has been reported to be associated with clinical response to 5-HT2A receptor antagonist in patients with schizophrenia, suggesting this polymorphism of the gene affects the 5-HT2A receptor function. To investigate the relationship between the T102C polymorphism and AMI, we conducted a case-control study of 255 non-fatal AMI patients and 255 control subjects. Among the patients, the prevalence of TT genotype was significantly higher than in controls (32.5 vs. 24.3%; P<0.05). In male patients (n=216), the prevalence was much higher than in control subjects (33.8 vs. 24. 1%, P<0.03). In multiple logistic regression models, odds ratio of TT genotype was 1.45 (95% CI 0.96-2.20) in all and 1.61 (95% CI 1. 03-2.53) (P<0.05) in males. The association of T102C polymorphism of the 5-HT2A receptor gene with non-fatal AMI was statistically significant and independent of other risk factors in males. The TT genotype of the 5-HT2A receptor gene may enhance susceptibility to AMI. Our observations suggest that the T102C polymorphism of the 5-HT2A receptor gene can serve as a new genetic marker for AMI.

Aged↗
PubMed2000

Inhibition of endothelium-dependent arterial relaxation by oxidized phosphatidylcholine.

Formation of oxidized phosphatidylcholine (ox-PC), oxidatively fragmented phosphatidylcholine (PC) containing a short-chain and/or polar oxidative residue at the sn-2 position, in the process of LDL oxidation as well as its existence in atherosclerotic lesions has been demonstrated. To clarify the pathophysiological role of ox-PC in the vascular reactivity, we investigated the effects of various ox-PCs on the isometric tensions in rabbit thoracic aortas. Ox-PCs, which were produced upon oxidation of sn-2 polyunsaturated fatty acid (PUFA)-containing PCs, dose-dependently inhibited endothelium-dependent relaxation (EDR) evoked by acetylcholine or substance P. On the other hand, neither native PUFA-containing PCs nor an oxidative product of monounsaturated fatty acid-containing PC showed an inhibitory effect. None of ox-PCs affected endothelium-independent relaxation to nitroglycerin. The PC-headgroup fraction, but not the oxidized fatty acids fraction, was responsible for the inhibition of EDR by ox-PC. EDR was reduced by 2-(5-oxovaleroyl)-PC, one of the secondary oxidative products of PCs that contains a short chain aldehydic residue at the sn-2 position, but not by PC hydroperoxide, the primary oxidative product. Although the possibility could not be completely ruled out that lysophosphatidylcholine rather than ox-PC may be responsible for inhibitory effects on EDR, these results suggest a novel vascular activity of ox-PCs generated from sn-2 PUFA-containing PCs which may be implicated in the pathophysiology of vascular tone.

Acetylcholine↗
PubMed2000

Computer-assisted infrared thermographic study of axon reflex induced by intradermal melittin.

The aim of the present study was to investigate whether melittin, the principal toxin of the honeybee (Apis mellifera) venom, can be used as an algogenic agent in the study of pain in humans. Five micrograms of melittin in 0.5 ml of saline was intradermally injected into the volar aspect of the forearm. Resultant pain was scored by a visual analogue scale (VAS), and skin temperature change was analyzed by means of a computer-assisted infrared thermography. Intradermal melittin temporarily produced severe pain, followed by a sustained increase in skin temperature. The skin temperature increase peaked in about 10 min and outlasted 1 h. Topical application of 10% lidocaine gel did not significantly suppress the melittin-induced pain, but markedly suppressed both the increase in the peak temperature and the area of temperature increase. In conclusion, 5 microg of melittin is sufficient to produce pain in humans and 10% lidocaine gel differentially decreases the melittin-induced axon reflex without any significant analgesic effect.

Administration, Topical↗