scholarly journals Skeletal muscle ischemia and reperfusion in rats increase lipid peroxidation in rats

2004 ◽  
Vol 19 (5) ◽  
pp. 578-581 ◽  
Author(s):  
Carlos Eli Piccinato ◽  
Armando De Domenico Jr ◽  
Alceu Afonso Jordão Jr ◽  
Helio Vannucchi

PURPOSE: To determine the effects of 30 minutes of ischemia followed by 30 minutes of reperfusion in skeletal muscle of rats receiving three different diets (supplemented, normal and vitamin E deficient) on lipoperoxidation (LP). METHODS: LP measured by TBARS levels, and plasma and hepatic concentrations of vitamin E measured by HPLC. RESULTS: The deficient group presented higher lipoperoxidation levels in muscle compared to the control and supplemented groups. CONCLUSION: Supplementation with vitamin E decrease the free radicals production in ischemia/reperfusion in skeletal muscle of rats.

1989 ◽  
Vol 24 (sup162) ◽  
pp. 55-58 ◽  
Author(s):  
S. Ueda ◽  
T. Yoshikawa ◽  
S. Takahashi ◽  
H. Ichikawa ◽  
M. Yasuda ◽  
...  

1992 ◽  
Vol 23 (6) ◽  
pp. 627-634 ◽  
Author(s):  
Lucia Formigli ◽  
Lola Domenici Lombardo ◽  
Chiara Adembri ◽  
Sandra Brunelleschi ◽  
Enrico Ferrari ◽  
...  

Author(s):  
Sandra Loerakker ◽  
Emmy Manders ◽  
Gustav J. Strijkers ◽  
Frank P. T. Baaijens ◽  
Dan L. Bader ◽  
...  

Sustained mechanical loading of soft tissues covering bony prominences, as experienced by bedridden and wheelchair-bound individuals, may cause skeletal muscle damage. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Damage pathways leading to DTI can involve ischemia, ischemia/reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2h loading period [1,2]. However, ischemia and reperfusion may play a more important role in the damage process during prolonged loading periods.


1997 ◽  
Vol 273 (4) ◽  
pp. C1130-C1135 ◽  
Author(s):  
Devendra R. Deshmukh ◽  
Oleg Mirochnitchenko ◽  
Vikram S. Ghole ◽  
Doreen Agnese ◽  
Pritesh C. Shah ◽  
...  

Superoxide dismutase (SOD) scavenges oxygen radicals that are implicated in the pathogenesis of intestinal ischemia-reperfusion injury. The effect of intestinal ischemia and reperfusion was investigated in transgenic mice overexpressing human Cu-Zn SOD. Ischemia was induced by occluding the superior mesenteric artery. Myeloperoxidase activity was determined as an index of neutrophil infiltration, and malondialdehyde levels were measured as an indicator of lipid peroxidation. Forty-five minutes of intestinal ischemia followed by 4 h of reperfusion caused an increase in intestinal levels of malondialdehyde in both nontransgenic and transgenic mice, but the concentration of malondialdehyde was significantly greater in nontransgenic mice. Intestinal ischemia-reperfusion also caused an increase in intestinal and pulmonary myeloperoxidase activity in nontransgenic and transgenic mice, but the transgenic mice had significantly lower levels of myeloperoxidase activity than nontransgenic mice. Transgenic mice had higher levels of intestinal SOD activity than nontransgenic mice. There were no significant differences in the catalase or glutathione peroxidase activities. In conclusion, our study demonstrates that the overexpression of SOD protects tissues from neutrophil infiltration and lipid peroxidation during intestinal ischemia-reperfusion.


1996 ◽  
Vol 270 (4) ◽  
pp. H1407-H1413 ◽  
Author(s):  
S. K. Liauw ◽  
B. B. Rubin ◽  
T. F. Lindsay ◽  
A. D. Romaschin ◽  
P. M. Walker

Sequential ischemia/reperfusion in a paired canine gracilis muscle model resulted in significant muscle salvage. In this model, one randomly chosen gracilis muscle was subjected to 5 h of ischemia followed by 48 h of in vivo reperfusion. The contralateral (second) muscle was then made ischemic and reperfused using the same protocol. Muscle necrosis was determined at the end of 48 h of reperfusion. A mean 60% reduction in muscle necrosis was observed in the second group of muscles. Analysis of tissue adenine nucleotides indicated that significant sparing of ATP utilization occurred in the second muscle group during ischemia. Preliminary analysis of tissue heat shock proteins (HSP) showed that the second group of muscles had a different pattern of HSP expression before the onset of ischemia. The results suggest that reduced ATP utilization and altered HSP expression in the second muscle play a role in the tissue salvage observed in this sequential muscle ischemia model.


1990 ◽  
Vol 68 (1) ◽  
pp. 387-392 ◽  
Author(s):  
W. L. Sexton ◽  
R. J. Korthuis ◽  
M. H. Laughlin

The purpose of this study was to determine the suitability of the maximally vasodilated (papaverine) isolated rat hindquarters preparation to study the effects of ischemia and reperfusion on the microvasculature of skeletal muscle. The osmotic reflection coefficient for plasma proteins (sigma) and total vascular resistance (RT, mmHg.ml-1.min.100 g-1) were determined before ischemic periods of 30, 60, 120, 180, and 240 min in intact (with skin) and 30, 60, and 120 min in skinned hindquarters and again after 60 min of reperfusion. In both intact and skinned hindquarters, reductions in sigma and increases in RT were observed during reperfusion and were correlated with the ischemic period duration. After 120 min of ischemia in intact and skinned hindquarters, sigma was reduced from preischemia values of 0.92 +/- 0.02 and 0.89 +/- 0.02 to 0.61 +/- 0.03 and 0.57 +/- 0.03, respectively, whereas RT was increased from preischemia levels of 8.9 +/- 0.3 and 8.1 +/- 0.1 to 28.4 +/- 2.9 and 74.2 +/- 16.8, respectively. The increases in RT were associated with proportional increases in skeletal muscle vascular resistance. Thus, in isolated rat hindquarters, increasing the duration of ischemia results in progressive increases in the permeability to plasma proteins (decreased sigma) and RT, which are associated primarily with skeletal muscle.


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