In this study we investigated gastrointestinal (GI) bleeding and its relationship to arteriovenous malformations (AVMs) in patients with the continuous-flow HeartMate II (HMII) left ventricular assist device (LVAD). The records of 172 patients who received HMII support were reviewed. Patients were considered to have GI bleeding if they had 1 or more of the following symptoms guaiac-positive stool hematemesis melena active bleeding at the time of endoscopy or colonoscopy and blood within the stomach at endoscopy or colonoscopy. The symptom(s) had to be accompanied by a decrease of )1 g/dl in the patient's hemoglobin level. The location of the bleeding was identified as upper GI tract, lower GI tract or both. Post-LVAD implantation anti-coagulation therapy consisted of warfarin, aspirin and dipyridamole. Thirty-two of the 172 patients (19%) had GI bleeding after 63,62 (range 8 to 241) days of HMII support. Ten patients had GI bleeding from an AVM these included 3 patients who had 2 bleeding episodes and 2 patients who had 5 episodes each. Sixteen patients had upper GI, 4 of them gastric AVM;15 patients had lower GI bleeding, 6 of them jejunal AVM. Other patients had different causeds of GI bleeding. Conclusions: Arteriovenous malformations can cause GI bleeding in patients with continuous-flow LVADs.
COBISS.SI-ID: 29616857
Primary hepatocytes are an important in vitro model for studying metabolism in man. Caspase-9 and Bax are regulators of apoptotic pathway. Here we report on the translocation of procaspase-9 and Bax from cytoplasm to nuclei as well as on dispersion of mitochondria after isolation of primary hepatocytes. The observed changes appear similar to those at the beginning of apoptosis, however, the isolated hepatocytes are not apoptotic for the following reasons: (1) cells have a normal morphology and function; (2) the mitochondria are energized; (3) there is no apoptosis unless it is induced by e.g. staurosporine or nodularin. We propose that the observed translocation of procaspase-9 and Bax into the nuclei reduces the ability to trigger apoptosis through the intrinsic apoptotic pathway. The shifts of procaspase-9 and Bax are reversible in the absence of the apoptotic trigger; the spontaneous reversion was confirmed experimentally. To distinguish this process from apoptosis, we call it pre-apoptotic cell stress response. It shares some features with apoptosis, but it is reversible. Knowledge on pre-apoptotic cell stress response is important for assessing the quality of the cells used in cell therapies, in regenerative medicine and of those used for modelling metabolic processes.
COBISS.SI-ID: 26839513
Despite worldwide distribution in the environment, the effects of microcystin- YR have not been studied extensively. The aim of the study was to evaluate whether microcystins- YR, in relatively low doses, have a toxic effect on cardiomyocytes of chronically treated rats. Male adult Wistar rats were treated every second day for 8 months with microcystins- YR. Control groups were treated either with vehicle (ethanol and methanol 4 : 1 v/v) or with physiologic saline. The heart sections of microcystin- YR-treated rats revealed decreased volume density of cardiac muscle tissue due to fibrous proliferation. A few lymphocyte infiltrates were observed. Most of cardiomyocytes were enlarged, with enlarged and often bizarre-shaped nuclei and decreased myofibril volume fraction. The results allow the conclusion that chronic exposure to low doses of microcystin-YR may cause atrophy and fibrosis of the heart muscle.
COBISS.SI-ID: 26577369
A model of ventricular remodeling and reverse remodeling has been developed by creating congestive heart failure (CHF) and then treating it by implanting a left ventricular assist device (LVAD). We induced volume-overload heart failure in experimental animals; 20 weeks later, we implanted an LVAD and assessed recovery 11 weeks thereafter. We examined changes in histologic and hemodynamic data and levels of cellular markers of CHF. After CHF induction, we found increases in LV end-diastolic pressure, LV systolic and diastolic dimensions, wall thickness, left atrial diameter, and atrial natriuretic protein (ANP) and endothelin-1 (ET-1) levels; β-adrenergic receptor (BAR) and dystrophin expression decreased markedly. Biopsies confirmed LV remodeling. After LVAD support, LV systolic and diastolic dimensions, wall thickness, and mass, and ANP and ET-1 levels decreased. Histopathologic and hemodynamic markers improved, and BAR and dystrophin expression normalized. Conclusions. We describe a successful sheep model for ventricular and reverse remodeling.
COBISS.SI-ID: 30523865