Mediation of arachidonic acid metabolite(s) produced by endothelial cytochrome P-450 3A4 in monkey arterial relaxation.

We investigated mechanisms of endothelium-dependent relaxation by acetylcholine resistant to indomethacin and N(G)-nitro-L-arginine and sensitive to cytochrome P-450 (CYP) inhibitors or charybdotoxin + apamin in the monkey lingual artery. Treatment with quinacrine, an inhibitor of phospholipase A2, abolished the relaxation by acetylcholine. However, treatment with alpha-glycyrrhetinic acid, an inhibitor of gap junctions, or catalase, an enzyme which dismutates hydrogen peroxide to form water and oxygen, did not affect the relaxation by acetylcholine. Immunohistochemistry demonstrated the presence of CYP3A4 in endothelial cells of the artery. Anti-CYP3A4 antibody inhibited relaxations by products of arachidonic acid incubated with human liver microsomes rich in CYPs in the endothelium-denuded artery. Purified CYP3A4 produced epoxyeicosatrienoic acids (EETs) from arachidonic acid, and the production was abolished by a selective CYP3A inhibitor, ketoconazole. It may be concluded that endothelium-derived relaxing substance(s) other than nitric oxide and prostanoids in the monkey lingual artery opens charybdotoxin + apamin-sensitive K+ channels in smooth muscle cells, and arachidonic acid metabolite(s) produced by endothelial CYP3A4 is likely to be the major substance.     

Chronic Changes of End-Systolic Pressure-Volume Relationship After Regional Myocardial Infarction

The chronic changes of the end-systolic pressure-volume relationship (ESPVR) after regional myocardial infarction were evaluated in a sheep model. Pressure-volume area (PVA) obtained from the pressure-volume diagram and left ventricular oxygen consumption (LVO₂) were studied. The regional myocardial infarction was created by ligating distal branches of the left coronary artery. ESPVR was obtained using a conductance catheter during transient inferior vena cava occlusion. Measurements were performed at baseline (n = 13), 1 hour (n = 8), 3 months (n = 9), and 6 months (n = 4) after infarction. Ees, the slope of the ESPVR did not change at 1 hour after infarction and remained the same at 3-month and 6-month measurements (baseline 2.26 ± 1.24 mmHg/mL, 1 hour 2.71 ± 1.06, 3 months 3.46 ± 1.51, 6 months 2.45 ± 0.64, NS). Because of the ventricular dilatation, which was demonstrated as an increase in changes of end-systolic volume (Ves) correlating with the time course after infarction (y = -3.21 + 0.128±, r = 0.454, p < 0.05), V₀, the volume intercept of the ESPVR increased at 1 hour after the infarction, and showed a tendency to increase at 3 months and 6 months after the infarction (baseline -18.0 ± 22.5 mL; 1 hour -0.9 ± 11.6; 3 months 5.4 ± 10.9, 6 months 9.2 ± 23.1, baseline vs 3 months p < 0.05, baseline vs 6 months p < 0.05). PVA and LVO₂ were unchanged over time after infarction (PVA: baseline 2097 ± 1526 mmHg/mL per 100 g^-1; 1 hour 1771 ± 699; 3 months 2483 ± 1086; 6 months 1,608 ±1,010, NS), (LVO₂: baseline 40.6 ± 13.1 ± 10–³ mL/100 g^-1 per beat^-1; 1 hour 42.9 ± 9.7; 3 months 35.0 ± 8.6; 6 months 31.2 ± 18.1, NS). Chronic regional infarction in the sheep model did not affect Ees over 6 months, but significantly increased V₀ after the increase in the acute phase. PVA and LVO₂ were not affected by this regional infarction either acutely or over 6 months.     

Vascular complications of vascularized composite tissue transfer: Outcome and salvage techniques

Two hundred fifty-two vascularized composite tissue transfers were performed from 1985 to 1992 at Nara Medical University Hospital. Free tissue transfers were performed in 185 patients and island tissue transfers in 67 patients. Of these, 39 flaps were reexplored because of vascular complications. On initial reexploration, vascular obstruction was found at the site of anastomosis or in the main vascular pedicle in 36 patients and in the perforating vessels to the monitor flap in three patients. Arterial thrombus occurred in 11 patients, venous thrombosis in 12, and both in nine. Twenty-five reexplored flaps were salvaged. Initially, heparin was administered systemically when vascular compromise was suspected intraoperatively or postopera-tively. Recently, we have used a ?continuous local heparinization”? technique to minimize blood loss. This method has been used in 12 patients who underwent reexploration and in nine patients in whom vascular compromise was suspected. Nineteen flaps survived completely, and two flaps failed. © 1993 Wiley-Liss Inc.     

Mesenchymal chondrosarcoma of the rib: Report of a case

Mesenchymal chondrosarcoma is a rare malignant cartilaginous tumor arising within the bone or soft tissue. An 18-year-old woman presented with a tumor on her left fourth rib. We performed a wide resection of the tumor and administered three cycles of postoperative adjuvant chemotherapy. Three years after the operation, the patient is alive without any evidence of either local recurrence or distant metastases. The findings of this case may thus support the usefulness of a radical resection and adjuvant chemotherapy for mesenchymal chondrosarcoma.     

Non-marfan idiopathic medionecrosis (cystic medial necrosis) presenting with multiple visceral artery aneurysms and diffuse connective tissue fragility: Two brothers

Two brothers with multiple visceral artery aneurysms or dilatations and diffuse connective tissue fragility who did not have clinical features of Marfan syndrome are reported. One presented with retroperitoneal hemorrhage during angiography, and idiopathic medionecrosis was proved by resection of the aneurysms. These cases belong to the heterogeneous group of Marfan syndrome. The angiographical features (multiple dilation of visceral arteries) suggests fragility of connective tissue and is predictive of hazards during and after a catheterization and operation.