Circulating Neutrophil CD18 Receptor Expression and Ischemic Flap Neutrophil Infiltration in a Guinea Pig Model

2000 ◽  
Vol 122 (3) ◽  
pp. 374-377
Author(s):  
Robert Dolan ◽  
Kevan Hartshorn ◽  
Daniel Mcavoy

This article demonstrates a correlation between circulating neutrophil CD18 expression, neutrophil infiltration, and varying periods of ischemia induced in guinea pig island skin flaps. Fifty adult female Hartley guinea pigs were equally separated into a control group, a sham group, and ischemic groups of 2, 4, and 10 hours. All, except those in the control group, had single guinea pig island flank skin flaps raised. Systemic neutrophil surface receptor (CD18) expression was analyzed with monoclonal antibodies, and flap skin biopsy specimens were analyzed for neutrophil infiltration. The results show that neutrophil counts and receptor detection increase as flap ischemia increases. However, a trend toward declining receptor expression was observed in the 10-hour ischemic group. In conclusion, systemic neutrophil adhesion receptor upregulation is correlated with cutaneous flap neutrophil infiltration and ischemia-reperfusion injury in a guinea pig model. A trend toward declining receptor expression with advanced ischemia was observed.

2000 ◽  
Vol 122 (3) ◽  
pp. 374-376
Author(s):  
Robert Dolan ◽  
Kevan Hartshorn ◽  
Daniel Mcavoy

This article demonstrates a correlation between circulating neutrophil CD18 expression, neutrophil infiltration, and varying periods of ischemia induced in guinea pig island skin flaps. Fifty adult female Hartley guinea pigs were equally separated into a control group, a sham group, and ischemic groups of 2, 4, and 10 hours. All, except those in the control group, had single guinea pig island flank skin flaps raised. Systemic neutrophil surface receptor (CD18) expression was analyzed with monoclonal antibodies, and flap skin biopsy specimens were analyzed for neutrophil infiltration. The results show that neutrophil counts and receptor detection increase as flap ischemia increases. However, a trend toward declining receptor expression was observed in the 10-hour ischemic group. In conclusion, systemic neutrophil adhesion receptor upregulation is correlated with cutaneous flap neutrophil infiltration and ischemia-reperfusion injury in a guinea pig model. A trend toward declining receptor expression with advanced ischemia was observed.


2004 ◽  
Vol 498 (1-3) ◽  
pp. 287-294 ◽  
Author(s):  
Osamu Mukaiyama ◽  
Kiyoshi Morimoto ◽  
Emi Nosaka ◽  
Sakiko Takahashi ◽  
Makoto Yamashita

Author(s):  
Inmaculada Masa ◽  
César Casado-Sánchez ◽  
Vicente Crespo-Lora ◽  
Alberto Ballestín

Abstract Background Ischemia-reperfusion (I/R) injury is a serious condition that can affect the success rate of microsurgical reconstructions of ischemic amputated limbs and complex tissue defects requiring free tissue transfers. The purpose of this study was to evaluate the effects of ischemic preconditioning (IPC) and C1 esterase inhibitor (C1-Inh) intravenous administration following I/R injury in a rat skin flap model. Methods Superficial caudal epigastric skin flaps (3 cm × 7 cm) were performed on 50 Wistar rats that were randomly divided into five groups. Ischemia was not induced in the control group. All other flaps underwent 8 hours of ischemia prior to revascularization: I/R control group (8-hour ischemia), IPC group (preconditioning protocol + 8-hour ischemia), C1-Inh group (8-hour ischemia + C1-Inh), and IPC + C1-Inh group (preconditioning protocol + 8-hour ischemia + C1-Inh). Survival areas were macroscopically assessed after 1 week of surgery, and histopathological and biochemical evaluations were also measured. Results There were no significant differences in flap survival between the treatment groups that were suffering 8 hours of ischemia and the control group. A significant increase in neovascularization and lower edema formation were observed in the IPC group compared with that in the I/R group. Biochemical parameters did not show any significant differences. Conclusion Intravenous administration of C1-Inh did not significantly modulate I/R-related damage in this experimental model, but further research is needed. On the other hand, IPC reduces tissue damage and improves neovascularization, confirming its potential protective effects in skin flaps following I/R injury.


2018 ◽  
Vol 26 (1) ◽  
pp. 31-38 ◽  
Author(s):  
Wenna Zhou ◽  
Jian Ouyang ◽  
HongLun Wang ◽  
XiaoYan Wang

Background:Gentiana siphonantha Maxim. is a traditional medicine for the treatment of rheumarthritis, icterepatitis, pain and hypertension; it is rich in gentiopicroside with anti-inflammatory, antibacterial, and free radical-scavenging activities. This study was to evaluate the antidermatophyte activity of G. siphonantha on a guinea pig model in vitro and in vivo. Material andMethods: The antidermatophyte activities of 10 plants were tested by the broth microdilution method. Fractions and an extract of G. siphonantha were tested against Trichophyton mentagrophytes by the disc diffusion method. The morphological changes of T. mentagrophytes were observed. Component analysis of the n-butanol (n-BuOH) fraction was made by HPLC. Finally, the antifungal activity in an in vivo guinea pig model of dermatophytosis was examined. Results:G. siphonantha had strong antidermatophyte activity with MIC50 values of 32-64 μg/mL. The n-BuOH fraction of G. siphonantha showed the most potent activity compared to the other fractions. After being exposed to the n-BuOH fraction at 80 and 160 μg/mL, the hyphae were distorted and collapsed. Gentiopicroside is the main active ingredient in the n-BuOH fraction of G. siphonantha. The lesion scores of the guinea pig model of dermatophytosis significantly declined in the 10% and 30% extract and positive control groups in comparison with the untreated control group. Periodic acid-Schiff and hematoxylin/eosin staining displayed similar results. Conclusion: The n-BuOH fraction of G. siphonantha demonstrated antidermatophyte efficacy in experimental dermatophytosis.


2011 ◽  
Vol 19 (2) ◽  
pp. 125 ◽  
Author(s):  
Edin De Bri ◽  
Wei Lei

Matrix metalloproteinases (MMPs) are mediators in connective tissue destruction in a variety of pathologic processes. Recently discovered chemically modified tetracyclines have been found to be effective inhibitors of MMP mediated connective tissue degradation in both rheumatoid arthritis (RA) and osteoarthritis (OA). The Hartley guinea pig model has been described with a high incidence of spontaneous OA-like changes in the knee joint. Therefore we have studied the effect of two tetracyclines, doxycycline (Dox) and chemically modified tetracycline-7 (CMT-7) which have both previously been shown as potent MMP inhibitors. We found that prophylactic orally given CMT-7 decreases OA changes in the knee joints both in vitro and in vivo in the guinea pig OA model. OA changes were most severe in the central compartment of the medial condyle in the control group. Cartilage fibrillation and destruction, in addition to subchondral bone sclerosis and cyst formation were all less in the CMT-7 treated group compared with controls. Collagen, hyaluronan and proteoglycan content in cartilage was higher in the CMT-7 treated group compared with controls. In contrast, OA changes were not decreased in the Dox group. These results show that tetracyclines, but not all tetracyclines, can reduce the severity of OA in the guinea pig model of spontaneous OA.


2020 ◽  
Vol 09 (01) ◽  
Author(s):  
Novoselova EA ◽  
Alimbarova LM ◽  
Monakhova NS ◽  
Lepioshkin AY ◽  
Ekins S ◽  
...  

2020 ◽  
Vol 23 (3) ◽  
pp. 214-224 ◽  
Author(s):  
Esra Cakir ◽  
Ufuk Cakir ◽  
Cuneyt Tayman ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.


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