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2. Nonuniform behavior of intravenous anesthetics on postischemic adhesion of neutrophils in the guinea pig heart. Szekely A; Heindl B; Zahler S; Conzen PF; Becker BF Anesth Analg; 2000 Jun; 90(6):1293-300. PubMed ID: 10825310 [TBL] [Abstract][Full Text] [Related]
3. Soluble complement receptor type 1 inhibits the complement pathway and prevents contractile failure in the postischemic heart. Evidence that complement activation is required for neutrophil-mediated reperfusion injury. Shandelya SM; Kuppusamy P; Herskowitz A; Weisfeldt ML; Zweier JL Circulation; 1993 Dec; 88(6):2812-26. PubMed ID: 8252695 [TBL] [Abstract][Full Text] [Related]
4. Postischemic dysfunction of the heart induced by small numbers of neutrophils via formation of hypochlorous acid. Raschke P; Becker BF; Leipert B; Schwartz LM; Zahler S; Gerlach E Basic Res Cardiol; 1993; 88(4):321-39. PubMed ID: 8240225 [TBL] [Abstract][Full Text] [Related]
6. Preischaemic as well as postischaemic application of a calcium antagonist affords cardioprotection in the isolated guinea pig heart. Massoudy P; Becker BF; Seligmann C; Gerlach E Cardiovasc Res; 1995 Apr; 29(4):577-82. PubMed ID: 7796453 [TBL] [Abstract][Full Text] [Related]
7. Bradykinin accounts for improved postischemic function and decreased glutathione release of guinea pig heart treated with the angiotensin-converting enzyme inhibitor ramiprilat. Massoudy P; Becker BF; Gerlach E J Cardiovasc Pharmacol; 1994 Apr; 23(4):632-9. PubMed ID: 7516015 [TBL] [Abstract][Full Text] [Related]