Brain Death Further Promotes Ischemic Reperfusion Injury of the Rabbit Myocardium

Background. Little is known about preload-dependent cardiac function after brain death (BD) and subsequent graft preservation.

Methods. A validated model of BD in rabbits was developed and myocardial performance was studied after BD induction and 1 hour of subsequent global hypothermic ischemia using a validated rabbit model and an isolated work-performing heart preparation.

Results. Significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed 2 hours after BD. After global hypothermic ischemia, significant decreases in stroke work, left ventricular contractility, and left ventricular relaxation were observed in the BD group compared with controls. Cardiac output and coronary flow were also significantly decreased in BD hearts compared with controls. Creatine kinase release was increased by 32.5% in BD hearts compared with controls.

Conclusions. In a rabbit model, BD combined with global hypothermic ischemia causes a significant decrease in left ventricular function compared with global hypothermic ischemia. This dysfunction may be attributed to a significant decrease in coronary flows in BD hearts.     

Studies on the effects of Pluchea indica less root extract on gastroduodenal ulcer models in rats and guineapigs

The methanolic fraction of P. indica root extract was found to possess significant antiulcer activity in different experimental animal models. In preventive antiulcer tests, significant protective actions in acetylsalicylic acid, serotonin and indomethacin-induced gastric lesions were observed in experimental rats. The extract also afforded significant protection to chemically-induced duodenal lesion in guineapigs. Significant enhancement of healing process in acetic acid-induced chronic gastric lesions were also observed in the extract-treated animals.     

All-cause and cardiovascular mortality in diabetic subjects increases significantly with reduced estimated glomerular filtration rate (eGFR): 10 years' data from the South Tees Diabetes Mortality study.

AIMS: To investigate the association between estimated glomerular filtration rate (eGFR) and total and cardiovascular mortality in a population-based cohort of diabetic subjects. METHODS: A longitudinal study using a population-based district diabetes register comprising 3288 subjects in South Tees, UK. The eGFR was calculated using the Modification of Diet in Renal Disease (MDRD) study equation. Patients were stratified by baseline eGFR into five stages as per the National Kidney Foundation guidelines: Stage 1, eGFR > 90; Stage 2, eGFR 60-89; Stage 3, eGFR 30-59; Stage 4, eGFR 15-29; and Stage 5, eGFR < 15 ml/min per 1.73 m(2). Main outcome was all-cause and cardiovascular mortality between 1 January 1994 and 31 July 2004. RESULTS: At baseline, mean age (58.4 years) differed between groups. Persons with lower eGFR were older (P < 0.001). Thirty-six percent (n = 1193, males 56%) had died by 10 years (cardiovascular cause in 60%). Median follow-up was 10.5 years amounting to 28 342 person years. Stages 4 and 5 (eGFR 相似文献   

Early abdominal complications of intestinal surgery: the radiologist's role in management

Abdominal complications of intestinal surgery are an important cause of postoperative morbidity and mortality. We define early complications as those occurring within the first 30 days after surgery. The radiological contribution towards prompt and accurate diagnosis of common complications is discussed and the radiologist's role in non-operative management is outlined.     

Ultrastructural localization of lectin receptors on cerebral endothelium

Summary Oligosaccharide residues on the endothelial luminal plasma membrane of rat cerebral cortical vessels were localized using biotinylated lectins. In addition, the effect of pretreatment of brain slices with neuraminidase prior to the binding of cationized ferritin (CF) and certain lectins was studied.Conjugates of biotinylated lectins and avidin-d horseradish peroxidase reaction product were evenly distributed on the endothelium of arterioles, capillaries, and venules. Lectin binding sites were observed on the plasma membrane of pinocytotic vesicles open onto the vascular lumen and at the luminal end of the interendothelial space only. The following sugar residues were localized: -d-mannosyl, -d-glucosyl, -N-acetylglucosaminyl, sialyl,d-galactosyl, -l-fucosyl, and -N-acetyl-d-galactosaminyl.Following pretreatment of brain slices with neuraminidase -d-gal-(1–3)-d-galN-acetyl groups were demonstrated on endothelium. In this respect, cerebral endothelium differs from noncerebral endothelium which is reported to have peanut agglutinin binding sites without neuraminidase pretreatment.Anionic groups on cerebral endothelium were demonstrated at the same locations as the lectin binding sites. Following neuraminidase pretreatment there was reduction, but not absence, of CF binding supporting the observation that surface charge is not wholly due to sialyl groups.The role of monosaccharide residues in states of altered cerebrovascular permeability remains to be determined.Supported by Ontario Heart Foundation grant no. 2-6     

Anti-inflammatory activity of Indian black tea (Sikkim variety).

In this study, the anti-inflammatory (in reference to the cardinal signs of inflammation) and other related pharmacological activities of the hot water extract of black tea (Camellia sinensis, Sikkim variety) were evaluated along with certain standard drugs. The extract showed significant inhibitory activity against carrageenin, histamine, serotonin and prostaglandin-induced pedal inflammation. The extract inhibited exudative inflammation. The tea extract also inhibited cotton pellet-induced granuloma formation and adjuvant-induced polyarthritis. Black tea extract showed significant inhibition against glucose oxidase-mediated inflammation. The present observations establish the efficacy of this particular variety of black tea, both in the exudative and proliferative forms and as well in the chronic phase of inflammation.