The protective effects of sevoflurane post-conditioning against myocardial ischemia/reperfusion (I/R) injury (MIRI) have been previously reported. However, the mechanisms responsible for these protective effects remain elusive. In this study, in order to investigate the molecular mechanisms responsible for the protective effects of sevoflurane post-conditioning on isolated rat hearts subjected to MIRI, Sprague-Dawley rat hearts were randomly divided into the following 6 groups: i) the sham-operated control; ii) 2.5% sevoflurane; iii) ischemia/reperfusion (I/R); iv) 2.5% sevoflurane post-conditioning plus I/R; v) 2.5% sevoflurane post-conditioning + NG-nitro-L-arginine methyl ester (L-NAME) plus I/R; and vi) L-NAME plus I/R. The infarct size was measured using 2,3,5-triphenyl tetrazolium chloride (TTC) staining. Additionally, the myocardial nitric oxide (NO), NO synthase (NOS) and nicotinamide adenine dinucleotide (NAD+) levels were determined. Autophagosomes and apoptosomes in the myocardium were detected by transmission electron microscopy. The levels of Bcl-2, cleaved caspase-3, Beclin-1, microtubule-associated protein light chain 3 (LC3)-I/II, Na+/H+ exchanger 1 (NHE1) and phosphorylated NHE1 protein were measured by western blot analysis. NHE1 mRNA levels were measured by reverse transcription-quantitative polymerase chain reaction. Compared with the I/R group, 15 min of exposure to 2.5% sevoflurane during early reperfusion significantly decreased the myocardial infarct size, the autophagic vacuole numbers, the NHE1 mRNA and protein expression of cleaved caspase-3, Beclin-1 and LC3-I/II. Post-conditioning with 2.5% sevoflurane also increased the NO and NOS levels and Bcl-2 protein expression (P<0.05 or P<0.01). Notably, the cardioprotective effects of sevoflurane were partly abolished by the NOS inhibitor, L-NAME. The findings of the present study suggest that sevoflurane post-conditioning protects the myocardium against I/R injury and reduces the myocardial infarct size. The underlying protective mechanisms are associated with the inhibition of mitochondrial permeability transition pore opening, and with the attenuation of cardiomyoctye apoptosis and excessive autophagy. These effects are mediated through an increase in NOS and a decrease in phopshorylated NHE1 levels.
The purpose of the present study was to investigate the effects of the Chinese medical herb Astragali Radix on myocardial injury in vivo and its possible mechanisms. Myocardial injury in rats was induced by the subcutaneous injection of a high dose of isoproterenol for 10 days, and the therapeutic effects of Astragali Radix were observed. Cardiac hemodynamics, heart coefficient and marker enzymes in serum showed that Astragali Radix prevented isoproterenol-induced myocardial damage. Astragali Radix also improved the antioxidant status by decreasing the lipid peroxidative product malondialdehyde and increasing the activity of the antioxidant enzyme superoxide dismutase. The observed depressions in sarcoplasmic reticulum Ca2+-ATPase mRNA and protein expression as well as Ser(16)-phosphorylated phospholamban protein expression in isoproterenol-treated rats were attenuated by Astragali Radix treatment. Moreover, treatment with Astragali Radix showed higher myocardial cAMP content compared with the isoproterenol-alone group. These results suggest that the antioxidant property and partial prevention of changes in protein and gene expression of cardiac sarcoplasmic reticulum Ca2+ regulatory proteins which may be mediated through the cAMP pathway could help to explain the beneficial effects of Astragali Radix on myocardial injury in vivo.
Background Ulnar head fractures are increasingly higher with the growing proportion of the elderly people. Failure to achieve a stable anatomic reduction of ulna head fracture may lead to a distal radioulnar joint (DRUJ) dysfunction and nonunion of the distal radius. Due to the lack of the postoperative reporting outcomes and the biomechanical studies, it has not been well established about the optimal management of the comminuted distal ulna head fracture. Hence, the purpose of this study is to use finite element analysis to explain the advantages and disadvantages of ulnar-side locking plate fixation compared with dorsal-side locking plate fixation and its screw arrangement in the treatment of ulnar head fractures. Methods FE models of the ulnar head fracture and the models of ulnar-side locking plate and dorsal-side plate with two or three distal screws was constructed. In order to simulate forces acting on the ulnar and the osteosynthesis material during daily-life activity in subjects who underwent reconstructive surgery, we applied three loading conditions to each model, viz. 20 N axial compression, 50 N axial compression, 1 N∙m torsion moment, 1 N∙m lateral bending moments, and 1 N∙m extension bending moments. Under these conditions, values of the von Mises stress (VMS) distribution of the implant, peak VMS, the relative displacement of the head and shaft fragments between the fracture ends and the displacement and its direction of the models were investigated. Results The stress values of ulnar-side plates were lower than those of dorsal-side plates. And the ulnar-plate fixation system also has smaller maximum displacement and relative displacement. When adding a screw in the middle hole of the ulnar head, the values of model displacement and the peak stress in fixation system are lower, but it may evidently concentrate the stress on the middle screw. Conclusions In conclusion, our study indicated that ulnar-side locking plates resulted in a lower stress distribution in the plate and better stability than dorsal-side locking plates for ulnar head fracture fixation. Adding an additional screw to the ulnar head could increase the stability of the fixation system and provide an anti-torsion function. This study requires clinical confirmation of its practicality in the treatment of ulnar head fractures. This study requires clinical confirmation as to its practicality in the treatment of ulnar head fracture.
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