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Interaction between paracrine tumor necrosis factor-alpha and paracrine angiotensin II during myocardial ischemia

^a Department of Thoracic and Cardiovascular Surgery, Tel Aviv Medical Center, Tel Aviv, Israel
^b Felsenstein Medical Research Center, Petah Tikva, Israel
^c Department of Nephrology, Tel Aviv Medical Center, Tel Aviv, Israel

View larger version (44K): [in a new window]   Figure 1 Effects of captopril and losartan on myocardial TNF-alpha mRNA expression in ischemic hearts. A, Representative PCR analysis of RNA samples (in duplicate). B, Relative optical density of TNF-alpha PCR signal. Data were normalized to relative GAPD PCR signal. Samples withdrawn at the beginning of perfusion (n = 5) (baseline) and after 90 min of normal, nonischemic perfusion (n = 4) (90' Perf) served as the control groups. In hearts undergoing global cardioplegic ischemia (n = 5), TNF-alpha mRNA expressions increased (*p < 0.03) (60' ischemia). A significant decrease in TNF-alpha mRNA expression is observed in hearts receiving either captopril (360 µmol/liter, n = 5) (Capt) or losartan (182.2 µmol/liter, n = 5) (Los) in cardioplegic solution, before ischemia. Band intensities were significantly lower than those of the ischemic group (p < 0.01 and 0.02, respectively).

View larger version (31K): [in a new window]   Figure 2 Effect of TNF-alpha depletion on myocardial TNF-alpha mRNA expression in the ischemic rat heart. A, Representative PCR analysis of RNA samples (in duplicate). B, Relative optical densities of TNF-alpha PCR signal. Data were normalized to relative GAPD PCR signal. 90' Perf = 90 min of normal nonischemic perfusion, serving as control group (n = 4); 60' Isch = hearts undergoing 1 h of global cardioplegic ischemia (n = 5); Anti TNF = hearts receiving monoclonal anti–TNF-alpha antibodies in the cardioplegia (n = 5) just before ischemia, showing significantly lower TNF-alpha mRNA expression than detected in untreated ischemic hearts (*p < 0.03).

View larger version (14K): [in a new window]   Figure 3 Effect of losartan on Ang-II-induced TNF-alpha production in rat cardiac myocyte culture. No TNF was measured in the supernatant of untreated cultures, serving as the control group (n = 5). Incubation with 10 and 50 nmol/liter of Ang-II caused significant, dose-dependent TNF-alpha release from myocytes. Preincubation with 350 or 700 µmol/liter of losartan (n = 5 in each group) decreased or abolished the observed Ang-II-induced TNF-alpha release.