Fig 1.
Effects of procainamide on (A) creatine kinase (CK) and (B) lactate dehydrogenase (LDH) in LPS-induced rhabdomyolysis rats.
Depicted are the changes during the experimental period in different groups of animals that received vehicle at time 0 (Control, n = 6), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 6), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 8), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 8). All data are expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats.
Fig 2.
Effects of procainamide on (A) potassium and (B) calcium levels in the arterial blood of LPS-induced rhabdomyolysis rats.
Depicted are the changes during the experimental period in different groups of animals that received vehicle at time 0 (Control, n = 5), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 5), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 6), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 6). The values of all groups are normalized at 0 h as zero. All data are obtained using the same rats in Fig 1 and expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats.
Fig 3.
Effects of procainamide on creatinine in LPS-induced rhabdomyolysis rats.
Depicted are the changes during the experimental period in different groups of animals that received vehicle at time 0 (Control, n = 6), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 6), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 8), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 8). All data are expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats.
Fig 4.
Effects of procainamide on superoxide levels in kidneys obtained from LPS-induced rhabdomyolysis rats.
Depicted are changes at the end of experiments (at 6 h) in different groups of animals that received vehicle at time 0 (Control, n = 6), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 6), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 6), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 6). All data are obtained using the same rats in Fig 1 and expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats.
Fig 5.
Effects of procainamide on (A) HCO3- and (B) base excess (BE) levels in the arterial blood of LPS-induced rhabdomyolysis rats.
Depicted are the changes during the experimental period in different groups of animals that received vehicle at time 0 (Control, n = 5), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 5), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 6), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 6). The values of all groups are normalized at 0 h as zero. All data are obtained using the same rats in Fig 1 and expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats.
Table 1.
Effects of procainamide on hemodynamic parameters and blood glucose in LPS-induced rhabdomyolysis rats.
Fig 6.
(A) Representative histopathologic features and (B) polymorphonuclear neutrophil (PMN) infiltration index of kidney tissue sections obtained from LPS-induced rhabdomyolysis rats.
Depicted are changes in PMN infiltration index at the end of experiment (at 6 h) in different groups of animals that received vehicle at time 0 (Control, n = 3), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 3), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 3), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 3). All data are obtained using the same rats in Fig 1 and expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats. Arrows represent neutrophil infiltration. Original magnification x 400.
Table 2.
Effects of procainamide on plasma IL-6 levels in LPS-induced rhabdomyolysis rats.
Fig 7.
Effects of procainamide on the expressions of (A) DNMT1, (B) DNMT3A, and (C) DNMT3B in the lung of LPS-induced rhabdomyolysis rats.
Depicted are changes in lung DNMT1, DNMT3A, and DNMT3B expressions at the end of experiment (at 6 h) in different groups of rats that received vehicle at time 0 (Control, n = 3), received vehicle at time 0 and then received procainamide at 1 h (Control + Pro, n = 3), received LPS at time 0 (LPS-induced rhabdomyolysis, n = 3), and received LPS at time 0 and then received procainamide at 1 h (LPS-induced rhabdomyolysis + Pro, n = 3). All data are obtained using the same rats in Fig 1 and expressed as mean ± SEM. *P < 0.05, all versus Control rats; #P < 0.05, with versus without procainamide in LPS-induced rhabdomyolysis rats.
Table 3.
Effects of DNMT inhibitor hydralazine on LPS-induced rhabdomyolysis rats.