We investigated the effect of interleukin-6 (IL-6) expression on sarco/endoplasmic reticulum Ca 2+ -ATPase (SERCA), atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) mRNA levels in cultured rat neonatal ventricular myocytes. IL-6 plays a key role in regulating cardiac hypertrophy and the development of heart failure, and SERCA, ANP and BNP are all cardiac hormones with regulatory properties. Compared with baseline measurements, treatment with 50 U/ml IL-6 significantly decreased SERCA gene expression, but significantly increased ANP and BNP gene expression in the cardiac myocytes. These results suggest that the clinical overproduction of IL-6 in response to infection, autoimmune disease and cancer might be responsible for cardiac hypertrophy. Cardiac hypertrophy may result from the imbalance of both natriuretic peptides and SERCA transciption levels, caused by elevated IL-6 expression.
Several studies have implicated endocannabinoids in various forms of shock. However, the role of endocannabinoids in hepatic ischemia-reperfusion injury remains unclear. The purpose of this study was to evaluate the changes of two endocannabinoidsin hepatic ischemia-reperfusion injury: anandamide (ANA) and 2-arachidonoylglycerol (2-AG). Male Sprague-Dawley rats were divided into 2 groups: the short (15 min) ischemic group and the long (60 min)ischemic group in the segmental (70%) hepatic tissue. Blood levels of aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), ANA, and 2-AG were examined. Serum lev-els of AST, ALT, and LDH were significantly higher in the long-ischemia group than in the short-ischemia group. Plasma levels of 2-AG showed similar augmentation prior to and after reperfusion in both the short- and long-ischemia groups, although plasma 2-AG lev-els tended to be higher in the long-ischemia group than in the short-ischemia group. Plasma levels of ANA were augmented in the early phase of reperfusion in the short-ischemia group and did not differ significantly from the normal level with time after reperfusion in the long-ischemia group. These results suggest that the endocannabinoid 2-AG increases in hepatic ischemia-reperfusion injury of rats, rather than ANA.
BackgroundSpontaneous isolated dissection of the superior mesenteric artery (SMA) can lead to bowel ischemia, aneurysm rupture, or even death. Studies have suggested that mechanical or hemodynamic stress on the vascular wall of the SMA may be a contributor, but its pathogenesis is unclear.Case presentationA 57-year-old Japanese man with a history of untreated hypertension and hyperuricemia was admitted to our hospital with the sudden onset of severe epigastric pain. Laboratory findings showed elevated white blood cell count and C-reactive protein, and contrast-enhanced computed tomography (CT) of the abdomen demonstrated arterial dissection with luminal stenosis and aneurysm formation at the distal portion of the SMA after the branching of the jejunal artery, and intravenous nicardipine was administered. The patient’s epigastric pain resolved spontaneously but recurred on day 6 of his hospital stay. Contrast-enhanced abdominal CT revealed an enlarged aneurysm with wall thinning. Because of the risk of aneurysm rupture, the decision was made to perform aneurysmectomy and bowel resection on day 6. Histologic examinations revealed two separate dissecting lesions: one latent and the other resulting in aneurysm formation. Both lesions showed characteristics of segmental arterial mediolysis (SAM) with lack of arterial media, absence of internal and external elastic laminae and intimal proliferation.ConclusionsHistologic findings in the present case suggest that mechanical or hemodynamic stress on the vascular wall and SAM-related vascular vulnerability may concomitantly contribute to the onset of isolated SMA dissection.
This study investigated the effect of a spontaneous nitric oxide (NO) donor, FK409 (FK), in a rat model of segmental hepatic ischemia. Rats were allocated to four experimental groups. Two of the groups underwent segmental hepatic ischemia of 60 min duration and received FK (0.4 mg/kg, iv) or vehicle alone before inducing ischemia and again 5 min before reperfusion. Sham-FK and sham groups were treated identically, but did not have vascular occlusion. Serum aspartate transaminase (AST), alanine transaminase (ALT), and lactate dehydrogenase (LDH) were measured, and the livers were examined for histological evidence of injury, polymorphonuclear neutrophil (PMN) infiltration, and immunohistochemical expression of inducible NO synthase (iNOS) before and 6 h after reperfusion. AST, ALT, and LDH levels were significantly (p < .05) reduced 6 h after reperfusion in the FK-treated group compared with the vehicle-treated control group. FK treatment also reduced the degree of hepatic damage apparent on histopathology and reduced PMN infiltration and iNOS expression. Thus, FK treatment is protective against hepatic ischemia reperfusion injury and attenuates neutrophil infiltration and iNOS expression.
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