Insulin-induced improvement of postischemic recovery is abolished by inhibition of protein kinase C in rat heart Ulrich Fischer-Rasokat, BS, Torsten.

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Insulin-induced improvement of postischemic recovery is abolished by inhibition of protein kinase C in rat heart Ulrich Fischer-Rasokat, BS, Torsten Doenst, MD The Journal of Thoracic and Cardiovascular Surgery Volume 126, Issue 6, Pages 1806-1812 (December 2003) DOI: 10.1016/S0022-5223(03)01229-7

Figure 1 Experimental protocols for hearts perfused under normoxic conditions (A) or subjected to 15 minutes of total, global, normothermic ischemia (B). All hearts were perfused at physiological workload with Krebs-Henseleit buffer containing glucose (5 mmol/L) and oleate (0.4 mmol/L) as substrates and were freeze-clamped at the end of experiments. Chelerythrine (5 μmol/L) or insulin (1 mU/mL) or both were present in the perfusate for the indicated time periods. The Journal of Thoracic and Cardiovascular Surgery 2003 126, 1806-1812DOI: (10.1016/S0022-5223(03)01229-7)

Figure 2 Postischemic recovery of contractile function in percent of preischemic power of hearts subjected to the ischemic protocols (see Figure 1, n = 4 to 6 per group). Insulin (Ins, 1 mU/mL) was added at the beginning of reperfusion. Chelerythrine (Chel, 5 μmol/L) was added either at the beginning of the experiment (I-Chel(0)) or at the beginning of reperfusion (I-Chel(35)). See text for details. Values are mean ± SEM. *P < .05 compared with control. The Journal of Thoracic and Cardiovascular Surgery 2003 126, 1806-1812DOI: (10.1016/S0022-5223(03)01229-7)