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- W3141489250 abstract "Enhanced cardiac generation of peroxynitrite contributes to septic cardiomyopathy. Since matrix metalloproteinases (MMPs) are activated in vitro by perox ynitrite, we hypothezised that MMP s may contribute to cardiac mechanical dysfunction in sepsis. Rat s were injected (i .p.) with either lipopolysacch aride (LPS, 4 mg/kg) or vehicle . MMP inhibitors, either Ro 3 1-9790 (20 mg/kg), doxycycline (4 mg/kg), or vehicle were administered i.p. 30 min after LPS . At 6 h, when the symptoms of endotoxemia peak, heart s were excised and perfused as working hearts with Krebs-Hen seleit buffer at 37°C. Card iac work (cardiac output x peak systol ic pressure product) was measured. Perfusate and ventricle samples were analyzed by gelatin zymography to quantify MMP activity. Cardiac function was significantly depressed in LPS-treated rats compared to control rats (control: 55 ± 4, LPS : 26 ± 6 mmHg *mL*min-) . LPS also caused a loss of 72 kDa MMP-2 activity in the ventricles and the perfu sate . Although MMP -9 activity was not detected in the ventricles, LPS resulted in an increa se in perfu sate 92 kDa MMP -9 activity. The MMP inhibitors significantly impro ved cardiac function of LPS-treated rats (Ro 31-9790: 38 ± 3, doxycycline: 51 ± 3 mmHg *mL*min-'), had no effect on the loss of MMP-2 acti vity, and significantly reduced the MMP-9 activity in the perfusate. These results demonstrate , for the first time, that LPS induced cardiac dysfunction is associated with a loss in ventricular MMP -2 activity and the relea se of MMP-9 from the heart. MMP inhibitors can significantly preserve cardiac mec hanical function during septic shock. (Mol Cell Biochem 251: 61-66, 2003)" @default.
- W3141489250 created "2021-04-13" @default.
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- W3141489250 date "2011-01-01" @default.
- W3141489250 modified "2023-09-26" @default.
- W3141489250 title "Matrix metalloproteinase inhibitors attenuate endotoxemia induced cardiac dysfunction: A potential role for MMP-9" @default.
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