Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction
| العنوان: | Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction |
|---|---|
| المؤلفون: | Abdelkarim Sabri, Akinyemi Bajulaiye, Geetha Muthukumaran, Sarah Mann, Joseph R. Libonati, Kathleen M. Sturgeon |
| المصدر: | Journal of the Renin-Angiotensin-Aldosterone System, Vol 16 (2015) |
| بيانات النشر: | Hindawi - SAGE Publishing, 2015. |
| سنة النشر: | 2015 |
| مصطلحات موضوعية: | Male, medicine.medical_specialty, Medicine (General), Cell Survival, Primary Cell Culture, Ischemia, Myocardial Infarction, Myocardial Reperfusion Injury, In Vitro Techniques, Rats, Sprague-Dawley, Endocrinology, R5-920, Internal medicine, Renin–angiotensin system, Internal Medicine, medicine, Animals, Myocytes, Cardiac, Myocardial infarction, Rats, Wistar, Acidosis, Ultrasonography, Ventricular Remodeling, business.industry, Angiotensin II, Body Weight, medicine.disease, Blockade, Rats, Animals, Newborn, Cardiology, medicine.symptom, business, Reperfusion injury, Hormone |
| الوصف: | Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to subsequent ischemic events. While chronic angiotensin II blockade is cardioprotective post-MI, the acute effects of angiotensin II in ischemia-reperfusion injury (IR) remains unclear. In the present study, we tested whether angiotensin II administration altered recovery of left ventricular (LV) function to IR in hearts from sham and MI rats. Echocardiography, LV pressure-volume relationships, and IR performance were established in subsets of sham ( N = 27) and MI hearts ( N = 41). IR was conducted in red-cell-perfused Langendorff hearts (60 minutes of low-flow ischemia; 30 minutes of reperfusion) during vehicle or angiotensin II infusions (10 −7 M). MI hearts were dilated and had reduced fractional shortening and blunted systolic elastance ( p < 0.05). Despite systolic dysfunction in MI, functional recovery to IR was similar to sham. Angiotensin II significantly worsened IR performance in sham ( p < 0.05), but not MI. The effect of angiotensin II on in vitro cardiomyocyte survival under various pH conditions was also tested. Acidosis increased cardiomyocyte death and angiotensin II potentiated this effect. We conclude that IR performance is similar between sham and MI hearts and that MI hearts are resistant to angiotensin II-induced cardiac dysfunction in response to IR. |
| اللغة: | English |
| تدمد: | 1752-8976 1470-3203 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cc388bee75285a1017a90210914fb5c7Test https://doaj.org/article/3f0dfe26297a4e6caf8f699607f04323Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....cc388bee75285a1017a90210914fb5c7 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 17528976 14703203 |
|---|