Until the advent of Liver transplantation, it was widely believed that Hepatic Encephalopathy (HE) was usually reversible. The exceptions were the so called "Acquired Hepatocerebral Degeneration cases" which were considered irreversible. Paradoxically, it seems, with liver transplantation, we have seen cases that contradict these rules. Whether the "residual effects" of HE, degenerative brain injury or independent neurological insults are causing post transplant neurological deficits is not easy to discern. As more emphasis is being put on maintaining brain 'status' after liver transplantation, we are finding confirmation of the largely reversible nature of HE. But, enough important exceptions to this rule are occurring to make further research on this topic mandatory.

Low dose TNFα improved myocardial function and decreased resultant cellular injury while high dose TNFα decreased myocardial function and increased myocardial injury following ischemia and reperfusion.

Only ISO improved the recovery of the ischemic myocardium during reperfusion. The effects of PRP were global in nature and involved compensatory hypercontractile state in nonischemic regions of the myocardium. Implication. PRP and ISO protect the heart against an ischemic injury, but only ISO preserves the function of the myocardium at the ischemic region. The survival rate of the PRP-treated group versus the ISO-treated group supports the claim that PRP has smaller contribution to recovery from myocardial ischemia.

Introduction: Myocardial ischemia may coincide and interact with sepsis and inflammation. Our objective was to examine the effects of bacterial endotoxin on myocardial functions and cell injury during acute ischemia. Methods: Rabbits were pretreated with incremental doses of E. Coli lipopolysaccharide (LPS) or normal saline. Myocardial ischemia was induced by 50-minute occlusion of left anterior descending artery. S-TNFaR was additionally used to block the effects LPS. Results: Ventricular contractility as it was measured by dp/dt during systole decreased from 2445± 1298 to 1422 ± 944 mm Hg/s, P = .019. Isovolumetric relaxation time as an index of diastolic function was prolonged from 50±18 ms to 102± 64 ms following ischemia. Pretreatment with low concentrations of LPS (<1 μg) had no effect on dp/dt, while at higher concentrations it suppressed both contractility and prolonged IVRT. Cell injury as measured by cardiac troponin I level increased to 15.1± 3.2 ng/dL following ischemia and continued to rise with higher doses of LPS. While blocking TNFa did not improve the myocardial contractility after ischemia, it eliminated additional deleterious effects of LPS. Conclusion: Lower doses of LPS had no deleterious effect on myocardial function, whereas higher doses of this endotoxin cause cardiac dysfunction and increased extent of injury.