Novel predictors for immediate puncture site bleed during endoscopic glue injection for gastric varices without using lipiodol.

Endoscopic obturation of gastric varices using tissue adhesive glues like cyanoacrylate is an accepted modality for the treatment of gastric varices. This study was undertaken to determine whether it was possible to predict immediate puncture site bleed on withdrawal of needle catheter during endoscopic glue injection without lipiodol. We prospectively analyzed 100 consecutive patients with cirrhosis who underwent glue injection. Glue injection was successful in all the patients. Immediate puncture site bleed was observed in only four cases and all of them correlated with negative catheter pull sign and positive red catheter sign. Catheter pull sign and red catheter sign were excellent predictors of immediate puncture site bleed during endoscopic glue injection and should be routinely tested.

Pathophysiology of modulation of local glucocorticoid levels by 11beta-hydroxysteroid dehydrogenases.

11beta-Hydroxysteroid dehydrogenases (11beta HSDs) are enzymes that catalyse the interconversion of active glucocorticoids (cortisol and corticosterone) into their inactive 11-keto products (cortisone and 11-deoxycorticosterone). Two isozymes have been identified: 11beta HSD type 1 is a predominant reductase, reactivating glucocorticoids from inert metabolites, whereas 11beta HSD type 2 is a potent dehydrogenase, inactivating glucocorticoids. They play a major role in the modulation of local cortisol levels and hence access of active steroid to corticosteroid receptors. This review focuses on the clinical importance of 11beta HSDs. We describe recent research that has not only advanced our understanding of the physiological role of these enzymes, but also their role in common diseases, including primary obesity and essential hypertension. These data provide encouragement that novel therapies will arise from a fuller understanding of the 11beta HSD system.

Endothelium-derived hyperpolarizing factor and potassium use different mechanisms to induce relaxation of human subcutaneous resistance arteries.

This investigation examined the hypothesis that release of K(+) accounts for EDHF activity by comparing relaxant responses produced by ACh and KCl in human subcutaneous resistance arteries. Resistance arteries (internal diameter 244+/-12 microm, n=48) from human subcutaneous fat biopsies were suspended in a wire myograph. Cumulative concentration-response curves were obtained for ACh (10(-9) - 3x10(-5) M) and KCl (2.5 - 25 mM) following contraction with noradrenaline (NA; 0.1 - 3 microM). ACh (E(max) 99.07+/-9.61%; -LogIC(50) 7.03+/-0.22; n=9) and KCl (E(max) 74.14+/-5.61%; -LogIC(50) 2.12+/-0.07; n=10)-induced relaxations were attenuated (P<0.0001) by removal of the endothelium (E(max) 8.21+/-5.39% and 11.56+/-8.49%, respectively; n=6 - 7). Indomethacin (10 microM) did not alter ACh-induced relaxation whereas L-NOARG (100 microM) reduced this response (E(max) 61.7+/-3.4%, P<0.0001; n=6). The combination of ChTx (50 nM) and apamin (30 nM) attenuated the L-NOARG-insensitive component of ACh-induced relaxation (E(max): 15.2+/-10.5%, P<0.002, n=6) although these arteries retained the ability to relax in response to 100 microM SIN-1 (E(max) 127.6+/-13.0%, n=3). Exposure to BaCl(2) (30 microM) and Ouabain (1 mM) did not attenuate the L-NOARG resistant component of ACh-mediated relaxation (E(max), 76.09+/-8.92, P=0.16; n=5). KCl-mediated relaxation was unaffected by L-NOARG+indomethacin (E(max); 68.1+/-5.6%, P=0.33; n=5) or the combination of L-NOARG/indomethacin/ChTx/apamin (E(max); 86.61+/-14.02%, P=0.35; n=6). In contrast, the combination of L-NOARG, indomethacin, ouabain and BaCl(2) abolished this response (E(max), 5.67+/-2.59%, P<0.0001, n=6). The characteristics of KCl-mediated relaxation differed from those of the nitric oxide/prostaglandin-independent component of the response to ACh, and were endothelium-dependent, indicating that K(+) does not act as an EDHF in human subcutaneous resistance arteries.