1990年 · 第103卷第04期

Phrenic nerve transfer was performed in 164 patients with root avulsion of the brachial plexus. The methods of operation consisted of phrenic nerve transfer to and anastomosis with the musculocutaneous nerve, the phrenic nerve bridging to the musculocutaneous nerve, phrenic nerve anastomosis with or bridging to the median nerve, and phrenic nerve anastomosis with other nerves. Follow-up of 65 patients for more than 2 years showed an effective rate of 84.6%. The result indicated that this operation has no deleterious effects on respiration, and the surgical effects are related to severity of injury, duration, mode of operation and patient's age.

Seventy-one patients with 80 lower limbs clinically suspected of deep venous thrombosis (DVT) were investigated by both Doppler ultrasound and venography. Sixty-seven lower limbs demonstrated by venography to have DVT, in 5 the thrombus was confined to the calf, and all were detected by the Doppler ultrasound. In 62 limbs thrombus extended into the popliteal and more proximal veins, the Doppler ultrasound detected 61 of them, a sensitivity of 98%. Venography showed a deep venous system without any evidence of thrombosis in 13, the Doppler findings were normal in all of the 13 lower limbs, a specificity of 100%. We found that the examination of the popliteal vein with patient in a semi-lateral prone position was important in detecting the presence of thrombosis in popliteal and more proximal vein.

From 1963 through 1988, a total of 194 hysterographies were performed for 111 patients. Three types of abnormalities were observed on the hysterogram: filling defect, intramural invasion of the uterine wall by the contrast medium; and intravasation of the contrast medium into the pelvic veins. The pathology and clinical significance of three types of abnormalities were studied. The results showed that hysterography demonstrated better images than pelvic arteriography and B-scan for the diagnosis of choriocarcinoma and invasive mole, especially when combined with B-scan/or pelvic arteriography, a greater accuracy was achieved.

This study was designed to investigate effects of cellular injury mediated by oxygen-derived free radicals on the intestine, heart, liver, kidney and lung tissues during superior mesenteric artery occlusion shock in rats. The animals were divided into four groups: control (Group 1, n=6), one hour occlusion (Group 2, n=8), one hour after releasing the clamp (Group 3, n=8), and two hours after releasing the clamp (Group 4, n=8). Compared to control values, the contents of malondialdehyde (MDA) in each tissue in Group 2 had 110 significant changes (P greater than 0.05); in Group 3, MDA in the intestine and heart tissues significantly elevated by 62% (P less than 0.05) and 56% (P less than 0.05); in Group 4, MDA in the intestine, heart, liver, and lung tissues increased by 121% (P less than 0.01), 65% (P less than 0.05), 32% (P less than 0.05), and 31% (P less than 0.05), respectively. Plasma lactic acid, β-glucuronidase and acid phosphatase increased significantly (P less than 0.01). The results showed that oxygen-derived free radical could cause lipid peroxidation damage not only in the intestine tissue, but also in the heart, liver, and lung tissues, suggesting that oxygen-derived free radicals might play an important role in cellular injury during superior mesenteric artery occlusion shock.

The mechanism of cellular processes responsible for proteinuria induced by adriamycin (ADR) remains unclear. In this study, we examined whether oxygen radicals contribute to the development of proteinuria in ADR-induced nephrosis. The peak concentration of malondialdehyde (MDA) of kidney was found on 8th day after ADR treatment in rats. ADR-treated rats received either superoxide dismutase (SOD, scavenger of O2-, catalase (CAT, scavenger of H2O2) or dimethyl sulfoxide (DMSO, scavenger of ·OH). The SOD, CAT or DMSO treated groups had a significant suppression of urinary protein excretion, serum and renal MDA compared to ADR control group. There were also less severe renal morphologic changes in the former three groups vs the ADR controls. These data provide indirect evidence that oxygen radicals generated by ADR are important mediators of ADR-induced proteinuria.

The surface structure of four different articular cartilages of the femoral head was studied with scanning electron microscope in 12 cases of hip joint osteoarthritis. These articular cartilages were mink white, yellow, dusky red and hyperplastic and thickened. The osteoarthritic articular cartilage surface was uneven with puckerings of various height, width and orientation. The puckerings were covered with fibril network. The fibrils were exposed collagen fibrils and of different diameters. Wider fiber bundles without orientation were found on the fibril network. On the surface of the hyperplastic articular cartilage observed were many deep and oval spaces left behind after breakdown of the lacunae of cells in the clusters of articular chondrocytes. In the spaces, remnants of articular chondrocytes were seen.

The effects of direct sheath closure, partial sheath excision, and interposing sheath grafting at different repair stages were evaluated in the chicken model. Primary repair was done after sheath incision and tendon transection, and delayed primary repair was done 4 days after sheath and tendon injuries. The sheath grafting was accomplished by interposing a patch of sheath between the longitudinal incision of the plantar sheath. Six weeks later, biomechanical tests for measuring gliding excursions of the repaired tendons, morphological examinations of the extent of adhesions, and histological observations of the closed sheath or the grafted sheath were carried out. At the primary repair stage, the sheath interposing graft achieved more significant gliding excursion than the groups of direct sheath closure (P less than 0.01) and partial sheath excision (P less than 0.001), and no difference was found between the latter two groups (P greater than 0.05). At the delayed primary repair stage, the sheath interposing graft group was better than the partial excision graft group (P less than 0.05), and the partial excision group was better than the direct closure group (P less than 0.001). The sheath graft and sheath closure at the primary repair stage prevented adhesion formation, but the directly closed sheath did not keep intact after the delayed primary repair and extensive adhesion occurred. In this paper, the importance of volume of the repaired sheath tunnel and possible reasons for results of the delayed primary sheath closure were discussed and the management of flexor tendon sheath for different injuries at different repair stages was suggested.

The patients suffering from Coxsackie B viral myocarditis with depressed natural killer (NK) activity were treated with Astragulas membranaceus (AM) intramuscularly for 3-4 months. After the treatment, the NK activity was increased significantly from 11.5±11.9% before therapy to 44.9±15.0%. Another 6 patients of Coxsackie B viral myocarditis with depressed NK activity were treated with conventional therapy. The NK activity remained unchanged in 12.9±6%. The general condition and symptoms improved in all patients with AM therapy, while the titers of neutralizing antibody remained at the same level. Two days after AM treatment, the mean titers of α- and γ-interferon (IFN) markedly increased in comparison with those before therapy and 3 weeks after AM therapy in 16 patients with Coxsackie B viral myocarditis, with left ventricular ejection fraction (LVEF) less than 65% and/or weak ventricular wall motion assayed by radionuclide angiocardiography. Whereas, in 12 patients treated with conventional therapy, there was no statistical difference among the results before and 2 days and 3 weeks after treatment. The results indicate that AM could partly regulate the lost of control of cellular immunity in patients with viral myocarditis.

RIA method was used in this study to determine immunoreactive β-endorphin (ir-β-EP) in gastric mucosa of patients with benign and malignant gastric diseases. The results showed that the content of ir-β-EP in gastric mucosa in the peptic ulcer group was the highest (68±9.5 pg/mg wet weight tissue, P less than 0.01), while its content in gastric carcinoma was closely related to the degree of differentiation of the tumor, that is, in poorly differentiated carcinoma it was lower than that in well differentiated carcinoma (P less than 0.02), and was also lower than that in gastritis (P less than 0.05). At the same time, we found that β-endorphin can markedly augment the 3H-TdR incorporation of lymphocytes (P less than 0.01). This effect was not blocked by naloxone.

Platelet aggregation, platelet cAMP levels and thromboxane B2 (TXB2) synthesis had been investigated in 40 diabetics (20 with microangiopathy and 20 without) and 24 normal controls. The washed platelets, but not platelet rich plasma (PRP), from the diabetics show greater sensitivity to aggregation in response to thrombin, collagen and arachidonic acid than controls (P less than 0.05). Platelets from the diabetics contain the significantly decreased cAMP levels (P less than 0.01) and synthesize the significantly greater amount of TXB2 (P less than 0.01) when induced by thrombin or collagen. Conversion of exogenously added arachidonic acid to TXB2 remained unchanged (P greater than 0.05). cAMP levels in platelets from the diabetics exhibited a significant negative linear correlation with thrombin- and collagen-induced TXB2 synthesis. There was no significant difference in platelet aggregation, platelet cAMP levels and platelet TXB2 synthesis between the diabetics with and without microangiopathy. It was suggested that in the diabetic platelets: The observed increase in platelet thromboxane A2 (TXA2) synthesis should be due to the increased activity of arachidonic acid-metabolizing system, most likely at phospholipase site; the elevated platelet TXA2 levels should inhibit platelet membrane-associated adenylate cyclase which lowered the cAMP levels in platelets; and this alternation should be the mechanism of platelet hyperaggregability, which might contribute in some way to diabetic microangiopathy.