Although active oxygen species play important roles in the pathogenesis of various diseases, the molecular mechanism for oxygen toxicity in vascular diseases remains to be elucidated. Since endothelium-derived relaxing factor (EDRF) is inactivated by superoxide radicals in vitro, oxidative stress in and around vascular endothelial cells may affect the circulatory status of animals. To study the role of superoxide radicals and related enzymes, such as superoxide dismutase (SOD), in vascular diseases, we have developed a fusion protein (HB-SOD) consisting of human Cu/Zn-type SOD and a C-terminal basic peptide with high affinity for heparan sulfate on endothelial cells. When injected intravenously, BB-SOD bound to vascular endothelial cells, underwent transcellular transport, and localized within vascular walls by a heparininhibitable mechanism. The blood pressure of spontaneously hypertensive rats (SHR) but not normal animals was decreased significantly by HB-SOD. Heparin inhibited the depressor effect of HB-SOD. In contrast, native SOD had no effect on blood pressure of either SHR or normal rats. Neither H202-inactivated HB-SOD nor the C-terminal heparin-binding peptide showed such a depressor effect, suggesting that the catalytic function of HB-SOD is responsible for its depressor action. To know the source of superoxide radicals, we determined xanthine oxidase activity in the aorta and uric acid levels in the plasma. Although no appreciable difference in xanthine oxidase activity was found between the two animal groups, uric acid levels were significantly higher in SHR than in normal rats. Oxypurinol, a potent inhibitor of xanthine oxidase, also decreased the blood pressure of SHR but not of normal rats. These rmdings indicate that superoxide radicals in and around vascular endothelial cells play critical roles in the pathogenesis of hypertension of SHR.Reactive oxygen species play critical roles in the pathogenesis of various diseases, such as cardiovascular injury associated with circulatory disturbance (1, 2). Many factors, such as endothelin and endothelium-derived relaxing factor (EDRF), affect the circulatory status of animals by modulating vascular resistance. Nitric oxide (NO) and NOgenerated compounds account for the biological actions of EDRF (3, 4). EDRF is synthesized predominantly in vascular endothelial cells and is transferred to smooth muscle cells, where it facilitates cGMP generation leading to vasodilatation. Superoxide radicals can inactivate NO and, hence, EDRF-dependent relaxation of aortic rings and endotheliumdenuded aortas was enhanced by Cu/Zn-type superoxide dismutpse (SOD) (5, 6). Based on such in vitro experiments, superoxide radicals have been postulated to affect vascular resistai e by inactivating EDRF. Since intravenously injected eu/Zn-SOD lacks tissue-specific localization and disappears rapidly from the circulation, predom'iantly due to The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marjceq "ad...
Detailed dissections were performed on 83 pelvic halves from 45 cadavers in order to obtain more accurate data on the composition of the lateral ligament of the rectum and the rectosacral fascia. The middle rectal artery was observed in only 18 out of 81 spcimens (22.2%). The lateral ligament of the rectum was divided into lateral and medial portions, according to the positional relationship to the pelvic plexus. The lateral part consisted of a superoanterior and an inferoposterior subdivision. The main component of the former was the middle rectal artery, while the pelvic splanchnic nerves were contained in the latter. Both compoents can be considered to contribute to the formation of the medial part, although the middle rectal vessels were not always present. The medial part consisted of the rectal branches from the pelvic plexus and their connective tissue. The rectosacral fascia was formed by dense connective tissue between the posterior wall of the rectum and the third and fourth sacral vertebrae. The main components of the fascia were branches of the lateral and median sacral vessels and the sacral splanchnic nerves which arose directly from the sacral sympathetic ganglia.
For an accurate assessment of jaw movement, it is crucial to understand the comprehensive formation of the masticatory muscles with special reference to the relationship to the disc of the temporomandibular joint. Detailed dissection was performed on 26 head halves of 14 Japanese cadavers in order to obtain precise anatomical information of the positional relationships between the masticatory muscles and the branches of the mandibular nerve. After complete removal of the bony elements, the midmedial muscle bundle in all specimens and the discotemporal muscle bundle in 6 specimens, derivatives of the temporalis, which insert into the disc were observed. On the anterior area of the articular capsule and the disc of the temporomandibular joint, the upper head of the lateral pterygoid, the midmedial muscle bundle of temporalis and the discotemporal bundle of temporalis were attached mediolaterally, and in 3 specimens the posterosuperior margin of the zygomaticomandibularis was attached to the anterolateral area of the disc. It is suggested that these muscles and muscle bundles contribute to various mandibular movements. Although various patterns of the positional relationships between the muscles and muscle bundles and the their innervating nerves are observed in the present study, relative positional relationships of the muscles and muscle bundles and of nerves of the mandibular nerve are consistent. A possible scheme of the developmental formation of the masticatory muscles based on the findings of the positional relationships between the muscles and the nerves is presented.
The objective of this study is to describe a technique for preserving the autonomic nerve systematically, including the hypogastric nerves, pelvic splanchnic nerves, and pelvic plexus and its vesical branches, based on anatomic considerations for the autonomic nerves innervating the urinary bladder, in radical hysterectomies and to assess postsurgical bladder function. A nerve-sparing radical hysterectomy was carried out on 27 consecutive patients with uterine cervical cancer treated between 2000 and 2002. The FIGO stages of the disease consisted of 10 stage Ib1, 6 stage Ib2, 3 stage IIa, and 8 stage IIb. The nerve-sparing procedure was successfully completed in 22 of the 27 patients (81.5%) in the study. At 1 year after the operation, bladder symptoms were significantly improved in the nerve-sparing group compared to the non-nerve-sparing group. Urinary incontinence and abnormal (diminished) bladder sensation were observed in three of the five patients (two patients had both symptoms), for whom the nerve-sparing procedure could not be performed, but none of the 22 patients for whom the nerve-sparing procedure was performed had incontinence, and only two patients had abnormal (increased) bladder sensation (P= 0.0034 for incontinence and P= 0.030 for abnormal bladder sensation). The patients' survival was not adversely affected by the nerve-sparing procedure. Although it is still preliminary, the surgical technique described in this report is thought to be effective for preserving bladder function, and thus, the quality of life could be improved for patients with cervical cancer who are treated with a radical hysterectomy. For further evaluation of the efficacy of nerve-sparing radical hysterectomy, a prospective randomized trial needs to be performed.
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