Health care systems  Control values of the F340/F380 ratio and muscle tension were determined approximately 5 min after 60 mM KCl application in each strip . The cumulative addition of Nattokinase levobupivacaine induced concentration-dependent increases in both   and muscle tension . Fig. 2 shows that levobupivacaine and K+ induced concentration-dependent increases in   and tension. The levobupivacaine-induced increase in   was smaller than that induced by KCl . There was a positive correlation between   and the development of tension in the presence of KCl and levobupivacaine . However, the slope of the  -tension curve for levobupivacaine was higher than that for KCl .

GF 109203X (10 5 M), Y-27632 (10 6 M), genistein (5×10 5 M), SP600125 (10 5 M), PD penlac 98059 (3×10 5 M), and SB 203580 (3× 10 5 M) did not significantly affect baseline tension. Pretreatment with GF 109203X (3×10 6 and 10 5 M) and Y-27632 (3×10 7 and 10 6 M) attenuated levobupivacaine-induced contraction in a concentration-dependent manner (Pb0.05 versus no drug 3A and B). Pretreatment with 10 6 M Y-27632 and 10 5M GF 108203X greatly attenuated levobupivacaine-induced maximal contraction (maximal contraction; no drug: 59±6% versus 10 5 M GF 109203X: 17±3%, no drug: 61±2% versus 10 6 M Y27632: 14±1%; Pb0.001 versus no drug 3A and B). Pretreatmentwith 5×10 5Mgenistein attenuated levobupivacaine-induced contraction (Pb0.01 versus no drug 3C). Pretreatment with SP600125 (10 6 to 10 5 M) attenuated levobupivacaine-induced contraction in a concentration-dependent manner (Pb0.001 versus no drug 4A). However, pretreatment with only 3×10 5 M PD 98059 or SB 203580 attenuated Dihydroartemisinin 71939-50-9 levobupivacaineinduced contraction (Pb0.05 versus no drug 4B and C).activity, whereas PKC only phosphorylates 17-kDa PKC-potentiated inhibitory protein of type 1 protein phosphatase, leading to MLCP inhibition (Hirano, 2007).

GF 109203X and Y-27632 attenuated levobupivacaine-induced contraction in a concentration-dependent manner, suggesting that levobupivacaine-induced contraction involves the activation of PKC- and Rho-kinase-mediated pathways. Both direct phosphorylation ofMLC20 and inhibition ofMLCP, which are induced by PKC and purchase SNX-5422 Rho-kinase, may explain the greater inhibitory effect of Y-27632 and GF 109203X on the levobupivacaine-induced contraction than that of other protein kinase inhibitors. In addition, tyrosine kinase phosphorylation and PKC activation appear to be involved in the regulation of myofilament Ca2+ sensitivity through the activation of MAPK (Hughes andWijetunge, 1998; Khalil et al., 1995). Genistein attenuated levobupivacaine-induced contraction, suggesting that levobupivacaineinduced contraction involves a tyrosine kinase-mediated pathway.Much evidence suggests that vasopressors produce vasoconstriction via stimulation of the ERK-dependent MAPK pathway (Dessy et al., 1998; Touyz et al., 1999;Watts et al., 2001).

SP600125 (10 6 to 10 5 M) attenuated levobupivacaine-induced contraction; conversely, only 3×10 5M SB 203580 and PD 98059 attenuated levobupivacaine-induced contraction in the current study. Taken together, these results suggest that levobupivacaine-induced contractions are mediated mainly by the activation of a JNK-mediated pathway and in part by .