Experimental study on the hemostatic effect of cyanoacrylate intended for catheter securement.

Purpose:: The use of cyanoacrylate for intravenous catheter securement is of interest to clinicians and patients, because of the superior adhesive strength and hemostatic effect of cyanoacrylate compared to current securement devices. The purpose of this study is to use novel in vitro and in vivo testing methods to analyze the hemostatic effect of a catheter securement cyanoacrylate (cyanoacrylate).

Methods:: An unprecedented in vitro method was performed to determine the effects of a cyanoacrylate on a customized modified activated clotting time assay and blood flow inhibition assay by exposing blood or plasma to either one or three drops of cyanoacrylate.

Toxicological and toxicokinetic analysis of angiotensin (1-7) in two species.

The objectives of this study were to determine the potential systemic and local toxicity, as well as evaluate the toxicokinetic (TK) profile of angiotensin (1-7) [A(1-7)] when administered daily via subcutaneous injection for 28 days to Sprague-Dawley rats and Beagle dogs. A(1-7) is a member of the renin-angiotensin system and has undergone clinical evaluation for the treatment of chemotherapy-induced myelosuppression. In this present study, A(1-7) was given at 10 mg/(kg day) for 28 days to rats and canines.

Reactive nitrogen species in acetaminophen-induced mitochondrial damage and toxicity in mouse hepatocytes.

Acetaminophen (APAP) toxicity in primary mouse hepatocytes occurs in two phases. The initial phase (0-2 h) occurs with metabolism to N-acetyl-p-benzoquinoneimine which depletes glutathione, and covalently binds to proteins, but little toxicity is observed. Subsequent washing of hepatocytes to remove APAP and reincubating in media alone (2-5 h) results in toxicity.

Mechanisms of chloroform-induced hepatotoxicity: oxidative stress and mitochondrial permeability transition in freshly isolated mouse hepatocytes.

The role of mitochondrial permeability transition (MPT) and oxidative stress in chloroform toxicity was determined in freshly isolated female B6C3F1 mouse hepatocytes. Incubation of chloroform (12 mM) with hepatocytes resulted in cell death (alanine aminotransferase release and propidium iodide fluorescence). Chloroform had volatilized from the incubation and glutathione was depleted by 1 h; however, toxicity was not significantly different between control and chloroform-incubated cells.

Induction of the nuclear factor HIF-1alpha in acetaminophen toxicity: evidence for oxidative stress.

Hypoxia inducible factor (HIF) controls the transcription of genes involved in angiogenesis, erythropoiesis, glycolysis, and cell survival. HIF-1alpha levels are a critical determinant of HIF activity. The induction of HIF-1alpha was examined in the livers of mice treated with a toxic dose of APAP (300 mg/kg i.