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ABSTRACT: The aim of this study was to investigate if the preservation of isolated skeletal muscles for 16 h at 4 degrees C could be improved by pre-storage perfusion (PSP). Two rat muscle models were used: the soleus (SOL) and a posterior strip of the cutaneous trunci (CT). The effects of a 10 min PSP (at 25 degrees C) with University of Wisconsin solution (UW) or HTK-Bretschneider solution (HTK) on muscle function were analysed. The perfusion model was validated by the demonstration that the SOL and CT could be perfused with donor blood, UW and HTK at a flow rate of 0.2 ml x min(-1) x g(-1) muscle for 10 min without any immediate adverse effects on muscle weight, function (maximum tetanus tension) and cytoarchitecture (multivariate analysis of variance, P >0.05; n =6). For each muscle type and for each solution, six perfused and six non-perfused muscles were stored for 16 h at 4 degrees C. In the perfused groups, the storage and perfusion solution were matched. For both muscle types, the function (maximum tetanus tension), weight and cytoarchitecture of pre-storage perfused muscles was not preserved any better than that of non-perfused muscles, irrespective of the solution used (multivariate analysis of variance, P >0.05). We conclude that PSP for 10 min with UW and HTK does not improve the preservation of function of rat skeletal muscles during storage for 16 h at 4 degrees C.
Clinical Science 08/2003; 105(1):29-37. · 4.61 Impact Factor
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ABSTRACT: Vasodilation originating within the microcirculation ascends into proximal feed arteries during muscle contraction to attain peak levels of muscle blood flow. Ascending vasodilation (AVD) requires an intact endothelium, as does conducted vasodilation in response to acetylcholine (ACh). Whereas ischemia-reperfusion (I-R) can affect endothelial cell function, the effect of I-R on AVD is unknown. The authors tested the hypothesis that I-R (1h-1h) would impair AVD.
Using the retractor muscle of anesthetized hamsters, contractions were evoked using field stimulation (200 ms at 40 Hz every 2 s for 1 min) and ACh was delivered using microiontophoresis (1 microm tip, 500-4000 ms pulse at 800 nA). Feed artery responses were monitored 500-1500 microm upstream.
Neither resting (51 +/- 4 microm) nor maximal diameter (81 +/- 5 microm; 10 microm sodium nitroprusside) following I-R (n = 8) were different from time-matched controls (n = 10). With peak active tension of 23 +/- 4 mN x mm(-2), control AVD was 26 +/- 2 microm. Following I-R, active tension fell by 48% (p < .05) and AVD by 57% (p < .05). Stimulation at 70 Hz restored active tension but AVD remained depressed by nearly half (p < .05), as did local and conducted responses to ACh. Nevertheless, control responses to 500 ms ACh were restored by increasing stimulus duration to 4000 ms.
Ischemia-reperfusion impairs the initiation of feed artery dilation with muscle contraction and with ACh while conduction along the vessel wall is preserved. Respective components of endothelial cell signaling events may differ in their susceptibility to I-R.
Microcirculation 12(7):551-61. · 2.57 Impact Factor
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ABSTRACT: IntroductionCold hypoxia is a common factor in cold tissue preservation and mammalian hibernation. The purpose of this study was to determine the effects of cold preservation on the function of the retractor (RET) muscle of the hamster in the non-hibernating state and compare these with previously published data (van der Heijden et al., 2000) [52] on the rat cutaneus trunci (CT) muscle.Materials and methodsAfter cold storage (16 h at 4 °C), muscles were stimulated electrically to measure maximum tetanus tension (P0) and histologically analyzed. The protective effects of addition of the antioxidants trolox and deferiprone and the calcium release inhibitor BDM to the storage fluid were determined.ResultsAfter storage, the twitch threshold current was increased (from 60 to 500 μA) and P0 was decreased to 27% of control. RET morphology remained unaffected. RET muscle function was protected by trolox and deferiprone (P0, resp., 43% and 59% of control). Addition of BDM had no effect on the RET.Conclusions
The observed effects of cold preservation and of trolox and deferiprone on the RET were comparable to those on CT muscle function, as reported in a previously published study (van der Heijden et al., 2000) [52]. Both hamster RET and rat CT muscles show considerable functional damage due to actions of reactive oxygen species. In contrast to the CT, in the RET cold preservation-induced functional injury could not be prevented by BDM and was not accompanied by morphological damage such as necrosis and edema. This suggests that the RET myocytes possess a specific adaptation to withstand the Ca2+ overload induced by cold ischemia.
Cryobiology 59(3):308-316. · 2.06 Impact Factor
