Abstract 254: Ultrasound Improves the Outcomes After Cardiopulmonary Resuscitation by Stimulating the Cholinergic Anti-Inflammatory Pathway

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Peng Sun ◽  
Yuhan Zhang ◽  
Tingting Shu ◽  
Licai Liang ◽  
Weijing Shao ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hippocampal Neurons ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Mechanical Index ◽  
Inflammatory Pathway ◽  
The Us ◽  
Anti Inflammatory ◽  
The Right

Introduction: Recently it was shown that the ultrasound (US) treatment prevented renal ischemia- reperfusion injury (IRI) in mice. In the present study, we investigated the effects of the US treatment against IRI after CPR . Hypothesis: US would improve the outcomes after resuscitation in a rat model of CPR, and the protective effect of US would be dependent on the cholinergic anti-inflammatory pathway (CAP) via α7nAChR. Methods: The animals were randomized into 5 groups (n=8 each): (1) CPR group: the rats underwent 6 mins of untreated ventricular fibrillation (VF) followed by CPR and defibrillation; (2) US group: the treatment was identical to the CPR group except that rats were exposed to US treatment 24h before CPR; (3) MLA group: the treatment was identical to the US group except thatα7nAChR antagonist MLA (4mg/kg) was administered 30 mins prior to US treatment and VF respectively; (4) GTS group: the treatment was identical to the CPR group except that α7nAChR agonist GTS-21(4mg/kg) was injected 30 mins before VF. (5) SHAM group: the rats were exposed to surgical preparation without CPR and US application. One day before CPR, the US treatment was delivered to the left kidney by US pulses (contrast general mode with 9 MHz) with a bursting mechanical index of 0.72. US pulses were 1 second in duration and were applied once every 6 seconds for 2 mins. After the treatment of the left kidney, the right kidney was exposed to US treatment for another 2 mins. Results: Significantly longer duration of survival was observed in US-treated animals. And US treatment also suppressed the TNF-α and IL-6 following resuscitation, and improved neurological function. The expression of α7nAChR were promoted in hippocampal neurons in US group. Moreover, the protective effect of US treatment could be abolished by MLA and imitated by GTS-21. Conclusions: US treatment before IRI improves the outcomes after CPR, and CAP via α7nAChR plays an important role during CPR.

scholarly journals Protective effect of cordycepin on experimental renal ischemia/reperfusion injury in rats

2020 ◽  
Vol 92 (4) ◽  
Author(s):  
Hasan Riza Aydin ◽  
Cagri Akin Sekerci ◽  
Ertugrul Yigit ◽  
Hatice Kucuk ◽  
Huseyin Kocakgol ◽  
...  
Keyword(s):  
Protective Effect ◽  
Rat Model ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Female Rat ◽  
Biochemical Analyses ◽  
The Right

Aim: To date, various molecules have been investigated to reduce the effect of renal ischemia/reperfusion (I/R) injury. However, none have yet led to clinical use. The present study aimed to investigate the protective effect of cordycepin (C) on renal I/R injury in an experimental rat model. Materials and methods: Twenty-four mature Sprague Dawley female rat was randomly divided into three groups: Sham, I/R, I/R+C. All animals underwent abdominal exploration. To induce I/R injury, an atraumatic vascular bulldog clamp was applied to the right renal pedicle for 60 minutes (ischemia) and later clamp was removed to allow reperfusion in all rats, except for the sham group. In the I/R + C group, 10 mg/kg C was administered intraperitoneally, immediately after reperfusion. After 4 hours of reperfusion, the experiment was terminated with right nephrectomy. Histological studies and biochemical analyses were performed on the right nephrectomy specimens. EGTI (endothelial, glomerular, tubulointerstitial) histopathology scoring and semi-quantitative analysis of renal cortical necrosis were used for histological analyses and superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), total oxidant status (TOS) for biochemical analyses. Results: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. The I/R group had higher histopathological scores than the I/R + C group. In the biochemical analysis of the tissues, SOD, MDA, TOS values were found to be statistically different in the I/R group compared to the I/R + C group (p: 0.004, 0.004, 0.001 respectively). Conclusions: Intraperitoneal cordycepin injection following ischemia preserve renal tissue against oxidative stress in a rat model of renal I/R injury.

scholarly journals Effect of sildenafil in renal ischemia/reperfusion injury in rats

2010 ◽  
Vol 25 (6) ◽  
pp. 490-495 ◽  
Author(s):  
Paulo José de Medeiros ◽  
Arthur Villarim Neto ◽  
Francisco Pignataro Lima ◽  
Ítalo Medeiros Azevedo ◽  
Layra Ribeiro de Sousa Leão ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Histopathological Examination ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Renal Ischemia ◽  
Renal Scintigraphy ◽  
Control Group ◽  
Left Renal Artery ◽  
Differential Function ◽  
The Right

PURPOSE: To evaluate the effect of sildenafil, administered prior to renal ischemia/reperfusion (I/R), by scintigraphy and histopathological evaluation in rats. METHODS: Twenty-four rats were divided randomly into two groups. They received 0.1 ml of 99mTechnetium-etilenodicisteine intravenous, and a baseline (initial) renal scintigraphy was performed. The rats underwent 60 minutes of ischemia by left renal artery clamping. The right kidney was not manipulated. The sildenafil group (n=12) received orally 1 mg/kg of sildenafil suspension 60 minutes before ischemia. Treatment with saline 0.9% in the control group (n=12). Half of the rats was assessed after 24 hours and half after seven days I/R, with new renal scintigraphy to study differential function. After euthanasia, kidneys were removed and subjected to histopathological examination. For statistical evaluation, Student t and Mann-Whitney tests were used. RESULTS: In the control group rats, the left kidneys had significant functional deficit, seven days after I/R, whose scintigraphic pattern was consistent with acute tubular necrosis, compared with the initial scintigraphy (p<0.05). Sildenafil treatment resulted in better differential function of the left kidneys 24h after reperfusion, compared with controls. Histopathologically, the left kidney of control rats (24 hours after I/R) showed a higher degree of cellular necrosis when compared with the sildenafil treated rats (p<0.05). CONCLUSION: Sildenafil had a protective effect in rat kidneys subjected to normothermic I/R, demonstrated by scintigraphy and histomorphometry.

scholarly journals Role of Cholinergic Anti-Inflammatory Pathway in Treatment of Intestinal Ischemia-Reperfusion Injury by Electroacupuncture at Zusanli

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Yanxia Geng ◽  
Dong Chen ◽  
Jiang Zhou ◽  
Hua Jiang ◽  
Haidong Zhang
Keyword(s):  
Mrna Expression ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mucosal Damage ◽  
Control Group ◽  
Inflammatory Pathway ◽  
Ischemic Disease ◽  
Group I ◽  
Anti Inflammatory ◽  
Intestinal Ischemia Reperfusion

Electroacupuncture (EA) at Zusanli is a widely used method for the treatment of intestinal ischemic disease. The current study attempts to investigate the possible mechanism from the point of cholinergic anti-inflammatory pathway (CAP) in rats. Thirty rats were divided into five groups: control group, I/R group, EA group (I/R + EA), PNU group (I/R + α7 nAChR agonist), and α-BGT group (I/R + EA + α7 nAChR antagonist). EA and medicine injection were performed immediately after ischemia. After 2 h of reperfusion, blood and intestine samples were collected and intestinal histopathological score, mRNA expression of mucosal α7 nAChR and NF-κBp65, and serum cytokine levels (IL-6, TNF-α) were examined. Compared with the I/R group, the EA group and PNU group could significantly attenuate the mucosal damage, promote α7 nAChR mRNA expression, and reduce levels of NF-κBp65, IL-6, and TNF-α. Compared with the EA group, α7 nAChR mRNA was decreased, while concentrations of NF-κBp65, IL-6, and TNF-α increased in the α-BGT group. EA at Zusanli could inhibit NF-κBp65 and proinflammatory cytokines production after intestinal I/R injury; its mechanism may be related to the cholinergic anti-inflammatory pathway.

Abstract P298: Finerenone Protects Against the Acute and Chronic Consequences of Renal Ischemia/reperfusion Injury

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Jonatan Barrera-Chimal ◽  
Alan Le Mercier ◽  
Soumaya El-Moghrabi ◽  
Peter Kolkhof ◽  
Frederic Jaisser
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Kidney Injury ◽  
Fold Increase ◽  
Renal Ischemia ◽  
Mrna Levels ◽  
Beneficial Effects ◽  
The Right

Introduction: One of the most common causes of acute kidney injury (AKI) is renal ischemia/reperfusion (IR). Mineralocorticoid receptor (MR) antagonism has shown beneficial effects against renal IR consequences. The potential benefit of novel non-steroidal MR antagonists such as finerenone has not been explored. Objective: Evaluate the efficacy of finerenone to prevent the acute and chronic consequences of ischemic AKI. Methods: For the acute study (24 hours), 18 rats were divided in: sham, rats subjected to bilateral renal ischemia of 25 min and rats that received three doses of finerenone at -48 h, -24 h and -1 h before the ischemia. For the chronic study (4 months), 21 rats were divided in: sham, rats with 45 min of bilateral ischemia and rats treated with Finerenone at day -2, -1 and 1h before IR. The left kidney was used for histology and the right kidney for molecular analysis. Results: After 24 h of reperfusion, the untreated IR rats presented a 3-fold increase in plasma creatinine, accompanied by 40% of tubules presenting cell detachment and casts. Kim-1 and NGAL mRNA levels were induced by 30-fold. In contrast, the rats that received finerenone presented normal creatinine and significantly fewer injured tubules (11%) and a less pronounced induction of kim-1 and NGAL (8-fold). After 4 months, the untreated IR rats developed chronic kidney disease (CKD), evidenced by kidney dysfunction, increased proteinuria (121.6 vs. 14.3 mg/24h in sham) and renal vascular resistance (16.8 vs. 11.4 mmHg/mL in sham). Tubular dilation, extensive tubule-interstitial fibrosis and an increase in kidney TGF-β and Collagen-I mRNA levels also characterized CKD. The transition from AKI to CKD was fully prevented by finerenone administration at the time of IR. Conclusion: Altogether, our data shows that finerenone is able to prevent AKI induced by IR as well as the chronic and progressive deterioration of kidney function and structure.

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