THE CARBON MONOXIDE DONOR, TOPIRAMATE, AND BLOCKERS OF AQUAPORINE RECEPTORS DECREASE MYOCARDIAL ISCHEMIA-REPERFUSION INJIRY

نویسندگان

چکیده

We investigated the metabolism of mouse isolated heart under influence tricarbonyldichlorothenium (II)- dimer (CORM-2 and 2,3-4,5-bis-O-isopropylidene-βD-fructopyranose sulfamate (topiramate) as potential blockers aquaporine channel (AQP3) cardiac myocytes. The results were compared with those obtained from group receiving anti-AQP3 monoclonal antibodies. A decrease in coronary flow was found during period preceding ischemia (topiramate did not cause this effect). However, at end reperfusion, CORM-2 responsible for its stabilization. This compound affect glucose intake increased it only reperfusion), decreased Ca2+ deposition muscle (AQP3-IgG antibodies topiramate had similar effect), creatinine release, AST (especially reperfusion). action amplitude R waveform before reperfusion. At reperfusion R-wave decreased. effect caused an increase beginning Administration CORM-2, resulted prolongation interval ischemia. same time, these drugs reduced development ischemic damage. indicate that released CO has effects to signs calcium blocking.

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Effects of carbon monoxide on myocardial ischemia.

The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with...

متن کامل

Donor pretreatment with carbon monoxide prevents ischemia/reperfusion injury following heart transplantation in rats

Because inhaled carbon monoxide (CO) provides potent anti-inflammatory and antioxidant effects against ischemia reperfusion injury, we hypothesized that treatment of organ donors with inhaled CO would decrease graft injury after heart transplantation. Hearts were heterotopically transplanted into syngeneic Lewis rats after 8 hours of cold preservation in University of Wisconsin solution. Donor ...

متن کامل

Carbon monoxide increases inducible NOS expression that mediates CO-induced myocardial damage during ischemia-reperfusion.

We investigated the role of inducible nitric oxide (NO) synthase (iNOS) on ischemic myocardial damage in rats exposed to daily low nontoxic levels of carbon monoxide (CO). CO is a ubiquitous environmental pollutant that impacts on mortality and morbidity from cardiovascular diseases. We have previously shown that CO exposure aggravates myocardial ischemia-reperfusion (I/R) injury partly because...

متن کامل

Toll-Like Receptors and Myocardial Ischemia/Reperfusion, Inflammation, and Injury

Cardiac ischemia/reperfusion (I/R) injury occurs in several important clinical contexts including percutaneous coronary interventions for acute myocardial ischemia, cardiac surgery in the setting of cardiopulmonary bypass, and cardiac transplantation. While the pathogenesis of I/R injury in these settings is multifactorial, it is clear that activation of the innate immune system and the resulta...

متن کامل

Role of carbon monoxide and biliverdin in renal ischemia/reperfusion injury.

Heme oxygenase (HO) isoforms catalyze the conversion of heme to carbon monoxide (CO) and biliverdin/bilirubin with a concurrent release of iron. There is strong evidence that HO activity and products play a major role in renoprotection, however the exact molecular mechanisms underlying the beneficial effects exerted by this pathway are not fully understood. This review is aimed at illustrating ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Fìzìologì?nij žurnal

سال: 2021

ISSN: ['2522-9028', '2522-9036']

DOI: https://doi.org/10.15407/fz67.05.030