Differential analgesic effect of tenoxicam on post-cesarean uterine cramping pain between primiparous and multiparous women.

BACKGROUND AND PURPOSE: Uterine cramping pain is related to prostaglandins, which are mediated by cyclooxygenase. However, it is unknown whether the analgesic effects of the non-selective cyclooxygenase inhibitor tenoxicam are different between primiparous and multiparous women. This placebo-controlled, double-blind study compared the analgesic effect of tenoxicam on post-cesarean uterine cramping pain in primiparous and multiparous women. METHODS: Forty primiparous women and 40 multiparous women who were scheduled for elective cesarean delivery were allocated into the following 4 groups: saline-primipara (SP) group, tenoxicam-primipara (TP) group, saline-multipara (SM) group, and tenoxicam-multipara (TM) group. Saline or 20 mg tenoxicam was intravenously injected immediately after clamping of the umbilical cord. All patients received patient-controlled analgesia for postoperative pain control. Resting wound pain, uterine cramping pain, morphine consumption, and morphine-related side effects were evaluated at 4 and 24 hours after surgery. RESULTS: At 24 hours after surgery, tenoxicam-related relief of uterine cramping pain was 2.1 in primiparous women (visual analog scale: SP 5.6 (4.4-6.8) minus TP 3.5 (2.2-4.9); p < 0.01). The tenoxicam-related morphine-sparing effect was 14 mg (45%) in primiparous women (SP 31.4 mg (23.9-38.8) minus TP 17.4 mg (11.6-23.2); p < 0.01). The tenoxicam-related relief of uterine cramping pain and tenoxicam-related morphine-sparing effect were not significant in multiparous women. CONCLUSIONS: This study revealed that the analgesic effect of tenoxicam on post-cesarean uterine cramping pain is greater in primiparous women than in multiparous women. Further studies are required to determine whether a higher dosage of tenoxicam is beneficial to reduce uterine cramping pain in multiparous women.     

Adenosine''s role in the genesis of bradyarrhythmias induced by acute myocardial hypoxia.

A close or even causal relation between myocardial adenosine and bradyarrhythmias during acute myocardial hypoxia was testified in guinea pig, rabbit and dog mainly by using specific competitive antagonist and synchronous quantitative analysis of 3 variables: intensity of myocardial hypoxia, degree of endogenous adenosine increment and severity of bradyarrhythmias. Results disclosed: A) striking resemblance of the bradyarrhythmias with hypoxic origin to those caused by exogenous adenosine, B) same locality of A-V conduction block induced by both myocardial hypoxia and exogenous adenosine, C) precise parallelism among the above-listed 3 variables with very high correlativity (r = 0.99, P < 0.01), D) frequent accompaniment of reversal of hypoxic bradyarrhythmias through resupply of 21% O2 with normalization of preexisted increase in myocardial adenosine, E) satisfactory blockade of hypoxic bradyarrhythmias by adenosine's specific antagonist--aminophylline and their augmentation by adenosine's uptake inhibitor--dipyridamole, F) close similarity of the characteristic curve representing relation among the above 3 variables to that among intensity of myocardial hypoxia, degree of endogenous adenosine increment and amount of coronary blood flow in which adenosine's role as a mediator has been well documented and G) reproducible persistence of bradyarrhythmias during myocardial hypoxia irrespective of preliminary vagotomy and atropinization, denoting independence of the occurrence of such dysarrhythmias upon vagal drive, suggestive of a mechanism other than vagotonia. We advocated that hypoxia-induced bradyarrhythmias was caused by increment in endogenous adenosine.

     

INVASIVE MUCORMYCOSIS WITH GASTRIC INVOLVEMENT IN A PATIENT WITH SEVERE ATHEROMATOUS VASCULAR DISEASE

Gastric mucormycosis involvement is a rare condition that usually occurs in inmunocompromised patients and frequently has a fatal outcome. We report the case of a 73‐year‐old woman admitted to the intensive care unit with severe bleeding after an acute pulmonary disease. Upper endoscopy disclosed wide and deep necrotic ulcers in the body and fundus of the stomach and greenish exudates with the antrum and the duodenum undamaged. Autopsy revealed an invasive mucormycosis and a severe atheromatosis. Several predisposing factors for mucormycosis infection have been reported until now. We postulate that ischemic gastritis could be a predisposing factor for colonization of zygomycete.     

自信，男人成长的催化剂

人的成长要经历不同的阶段，每个阶段的跨越，都是在“高压”、“高温”、“催化剂”的作用下，经过所有的物质、精神、社会的转换而完成。自信——则是男人成长的最好催化剂。[编者按]     

Effect of tacrolimus and partial hepatectomy on transthyretin metabolism in rats

Liver transplantation, which serves as treatment of familial amyloidotic polyneuropathy (FAP), and domino liver transplantation, which utilizes resected livers from patients with FAP for treatment of liver diseases, may induce changes in transthyretin (TTR), a pathogenic FAP-related protein. To evaluate this possibility, we performed a 70% hepatectomy or administered tacrolimus to Dark Agouti (DA) rats for 7 days and then measured changes in liver TTR mRNA levels and changes in serum TTR concentrations. After hepatectomy, TTR mRNA levels decreased by 77%; at day 3, they returned to preoperative levels. Except for slightly elevated serum TTR concentrations 12 h after operation, serum TTR levels remained unchanged. Thus, partial hepatectomy did not influence serum TTR concentrations. After tacrolimus administration, TTR mRNA declined by 56% 12 h after the experiment started; however, after day 3, a rebound phenomenon occurred until day 7. Tacrolimus may facilitate serum TTR degradation, although production of TTR in the liver also increased. This finding -- that TTR, the source of FAP-inducing amyloid, did not increase after transplantation -- may help post-transplantation treatment of patients who have FAP and other liver diseases.     

Anti-ulcer activity and mode of action of the polysaccharide fraction from the leaves of Panax ginseng.

The effects of a weakly acidic polysaccharide fraction, GL-4, from the leaves of Panax ginseng C. A. Meyer on various experimental gastric ulcer models in mice and rats have been studied. Oral administration of GL-4 at doses of 50 to 200 mg/kg inhibited the formation of the gastric lesions induced by necrotizing agents such as HCl/ethanol and ethanol in a dose-dependent manner. This protective effect was observed not only upon oral but also upon subcutaneous administration of GL-4 (50-100 mg/kg). GL-4 also inhibited the formation of gastric ulcers which were induced by water immersion stress, indomethacin, or pylorus-ligation. The contents of prostaglandin E2 in the gastric juice from rats were not influenced by oral administration of GL-4. The protective action of GL-4 against HCl/ethanol-induced gastric lesions was not abolished by pretreatment with indomethacin. When GL-4 (100 mg/kg, p.o.) was administered into pylorus-ligated rats, both gastric acidity and pepsin activity in the gastric juice decreased significantly.     

Microencapsulated pancreatic islets: a pathologic study.

Dog pancreatic islets isolated by an enzymatic digestion method were encapsulated in an alginate-poly L-lysine-alginate membrane. These microencapsulated pancreatic islets were cultured in vitro to study their ability of insulin secretion. Portions of these in vitro-cultured microencapsulated pancreatic islets were taken out for a viability dye exclusion study as well as for pathologic studies to correlate them with insulin secretion ability. We found that there was a strong correlation between them. Good insulin-secreting microcapsules showed well-preserved cell membranes and beta-cell granules. An in vitro culture for one to two days in RPMI-1640 made the islets more stable, the cellular surface became smoother and the beta-granules were in better shape. The microencapsulated pancreatic islets were also injected into the peritoneum of streptozotocin-induced diabetic CDF1 mice. Blood glucose levels dropped and stayed low for up to 60 days. But, when non-encapsulated dog pancreatic islets were used, the blood glucose levels remained low for only about 14 days. A small portion of the injected microcapsules were washed out at specific times for pathologic study. Up to 28 days after injection, only a few of the injected microcapsules showed pericapsular cellular infiltrate. However, after 56 days, most of the microcapsules showed dense pericapsular cellular infiltrate. Immunohistochemical analysis of these infiltrates showed that the majority of cells were fibroblasts and macrophages. Most of the cells located in the inner portion of the infiltrate were fibroblasts, while the macrophages were located mainly on the outer portion. Both scanning and transmission electron microscopy showed that the surface of the microcapsule outer wall was much smoother than the inner wall. The size of the microcapsules was approximately 0.6-0.8 mm and the thickness of the wall measured around 10 nm. The smaller the microcapsule is, the less chance there is of rupture with release of the xenographic islets. Once the wall of the transplanted microcapsules was ruptured, the inner surface showed more increased inflammatory cell and fibroblast infiltration than the outer surface.