Short chain fatty acid rectal irrigation for left-sided ulcerative colitis: a randomised, placebo controlled trial.

Background: Short chain fatty acid (SCFA) deficiency is associated with colitis in animals and humans, and the mucosal metabolism of these compounds is decreased in ulcerative colitis.

Aims: To assess the efficacy of topical SCFA treatment in ulcerative colitis.

Patients And Methods: 103 patients with distal ulcerative colitis were entered into a six week, double-blind, placebo controlled trial of rectal SCFA twice daily; patients who were unchanged on placebo were offered SCFA in an open-label extension trial.

Ca2+ handling and myofibrillar Ca2+ sensitivity in ferret cardiac myocytes with pressure-overload hypertrophy.

Experiments were performed in aequorin-loaded left ventricular myocytes isolated from hypertrophied hearts and age-matched controls. Five to six months after postvalvular aortic banding, left ventricular hypertrophy was present, as indicated by a 97% (P < 0.001) increase in the left ventricular weight-to-body weight ratio and a 24% (P < 0.

Time course of postnatal changes in rat heart action potential and in transient outward current is different.

The rat ventricular action potential shortens after birth. The contribution of increases in the transient outward current (Ito) to postnatal action potential shortening was assessed by measuring Ito in isolated cells and by determining the effect of 2 mM 4-aminopyridine (4-AP) on the action potentials of papillary muscles. 4-AP had no effect on 1-day action potential duration at 25% repolarization (APD25), and 1-day cells had little Ito.

Endothelin-1 enhances cross-bridge function of ferret myocardium: role of second messengers.

To investigate postreceptor pathways of endothelin and the site of action responsible for enhancing myocardial contractility, studies were performed on ferret papillary muscles loaded with the Ca2+ indicator aequorin. Endothelin-1 (ET) and the alpha 1-adrenoceptor agonist, phenylephrine (PE) produced similar dose-dependent increases in tension development and peak intracellular Ca2+ concentration ([Ca2+]i); moreover, pretreatment with PE eliminated effects of ET, suggesting similar postreceptor pathways. Because alpha 1-adrenoceptor activation is thought to cause the hydrolysis of phosphatidylinositol and generate D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and 1,2-diacylglycerol (DAG), the protein kinase C (PKC) activator 4 beta-phorbol 12-myristate 13-acetate (PMA) was used to determine whether activation of PKC was responsible for the myocardial actions of ET.