Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity* W.Charles Sternbergh, MD, Raymond.

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Presentation transcript:

Heparin prevents postischemic endothelial cell dysfunction by a mechanism independent of its anticoagulant activity* W.Charles Sternbergh, MD, Raymond G. Makhoul, MD, Burt Adelman, MD Journal of Vascular Surgery Volume 17, Issue 2, Pages 318-327 (February 1993) DOI: 10.1016/0741-5214(93)90417-K Copyright © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 1 Time line of experimental protocol. Arrows below time line indicate measurement of flow rates, which were subsequently used to calculate TVR of hindlimb. Phenylephrine was added directly to perfusate, and acetylcholine (0.001, 0.01, 0.1, 1 μg/min) and nitroprusside (0.5, 5.0, 50 μg/min) were delivered by constant infusion into arterial cannula. With exception of 60-minute ischemic interval, nonischemic and ischemia/reperfusion groups were treated identically. See text for details. Journal of Vascular Surgery 1993 17, 318-327DOI: (10.1016/0741-5214(93)90417-K) Copyright © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 2 Changes in endothelial-dependent vasorelaxation in nonischemic (n = 7), nonischemic with heparin 1 U/ml (n = 5), ischemia/reperfusion (n = 12), and ischemia/reperfusion with heparin 0.5 U/ml (n = 6) groups. Asterisk indicates p < 0.05 ischemia/reperfusion versus nonischemic group; double asterisk indicates p < 0.05 ischemia/reperfusion versus all other groups. Data are mean ± SE. Journal of Vascular Surgery 1993 17, 318-327DOI: (10.1016/0741-5214(93)90417-K) Copyright © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 3 Dose-dependent nature of the protective effect of heparin on postischemic endothelial cell function. Five reperfusion groups were treated with O (n = 12), 0.1 (n = 7), 0.25 (n = 6), 0.5 (n = 6), or 1 U/ml heparin (n = 7). After treatment with heparin there was dose-dependent increase percent change in TVR compared with that in nontreated group. Asterisk indicates p < 0.05 versus no heparin. Data are mean ± SE. Journal of Vascular Surgery 1993 17, 318-327DOI: (10.1016/0741-5214(93)90417-K) Copyright © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 4 Changes in endothelial-independent vasorelaxation in nonischemic (n = 7), non-ischemic with heparin 1 U/ml (n = 5), ischemia/reperfusion (n = 12), and ischemia/reperfusion with heparin 0.5 U/ml (n = 6) groups. There were no significant differences between groups at any dose of nitroprusside. Data are mean ± SE. Journal of Vascular Surgery 1993 17, 318-327DOI: (10.1016/0741-5214(93)90417-K) Copyright © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 5 Heparin had no consistent dose-dependent effect on postischemic endothelial-independent vasorelaxation. All groups underwent 60 minutes of ischemia and reperfusion. Asterisk indicates p < 0.05 versus ischemia/reperfusion with 0.1 U/ml heparin group; otherwise there were no significant differences. Data are mean ± SE. Journal of Vascular Surgery 1993 17, 318-327DOI: (10.1016/0741-5214(93)90417-K) Copyright © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions