ABSTRACT
Objectives: To investigate whether remote ischemic conditioning (RIC) applied to patients with ST-segment elevation myocardial infarction (STEMI) before percutaneous coronary intervention (PCI) could affect circulating miR-208b level or not. Methods:Patients diagnosed with STEMI undergoing PCI from January 2016 to July 2017 were enrolled from the Department of Cardiology, Affiliated Zhongshan Hospital of Dalian University.The patients were randomly allocated to two groups: (1) control group (n=25), PCI alone; (2) RIC group (n=50), PCI combined with RIC (three cycles of 5 min inflation and 5 min deflation of the right lower limb with blood pressure cuff performed before reperfusion). Serum miR-208b was measured before and immediately, at 24 h, and 48 h after PCI with real-time quantitative polymerase chain reaction. Results: The expression of miR-208b was significantly higher immediately post PCI than that before operation in the control group (84.1±9.0 vs 77.8±9.4; P=0.032), while it was significantly lower immediately post PCI than that before operationin RIC group (71.0±9.3 vs 77.4±8.8; P=0.028).miR-208b level was similar before PCI between the control and RIC groups (P=0.874), which was significantly reduced immediately post PCI in RIC group as compared with the control group (P=0.021).The peak value of creatine kinase isoenzyme (CK-MB) in the limb RIC group was significantly lower than that in the control group ([135.2±18.6] U/L vs [167.7±17.2] U/L; P=0.038).The area under the CK-MB curve of the RIC group was significantly smaller than that of the control group ([3 060.7±17.1] U/L vs [3 635.9±15.1] U/L); P=0.047]. The left ventricular ejection fraction (LVEF) in RIC group was significantly higher than that in the control group ([57.8±7.8]% vs [51.9±7.9]%; P=0.003) post PCI. The expression level of serum miR-208b was positively correlated with CK-MB AUC in RIC group (r=0.498, P<0.001). Conclusions: RIC of the lower limb prior to PCI could reduce miR-208b level and improve cardiac functionin STEMI patients.
ABSTRACT
<p><b>OBJECTIVE</b>Vasoconstriction and vascular hypersensitivity to serotonin were previously shown in animal models of adventitia injury. We investigated the contribution of angiotensin II (AngII)/AngII receptors and oxidative stress to vascular contractility and reactivity in this model.</p><p><b>METHODS</b>Wistar Kyoto rats were divided into 3 groups: normal (n = 6, no any intervention, only for measuring the serum AngII concentration), vehicle (n = 12, collared), and valsartan (n = 12, collared + valsartan 30 mg×kg(-1)×d(-1)). After one week of treatment, adventitia injury was induced by positioning a silicone collar around the right carotid artery for one week. Blood flow and vascular reactivity to serotonin were determined one week after injury, the blood from left ventricle was taken to measure the serum AngII concentration by ELISA, and carotids were harvested for morphometry and Western blot analysis.</p><p><b>RESULTS</b>Adventitia injury induced lumen cross-sectional area reduction (-44% vs. -5%), media diameter increase (62% vs. 10%), blood flow reduction [(2.79 ± 0.22) vs. (4.33 ± 0.84) ml/min] were significantly attenuated by valsartan. The increased vascular reactivity sensitivity to serotonin in vehicle group was also significantly reduced in valsartan group. Serum AngII concentration was significantly increased in vehicle group [(45.21 ± 4.52) pg/ml vs. (19.83 ± 0.5) pg/ml in normal rats, P = 0.0148] and the expression of AngII type 1 (AT(1)) receptor, AngII type 2 (AT(2)) receptor, as well as p22(phox) in collared arteries were significantly upregulated. Valsartan did not affect the AT(1) receptor expression but further increased serum AngII concentration [(89.73 ± 20.44) pg/ml vs. (45.21 ± 4.52) pg/ml, P = 0.001], and AT(2) receptor expression, while downregulated p22(phox) expressions.</p><p><b>CONCLUSIONS</b>Collar-induced adventitia injury resulted in chronic vasoconstriction and vascular hypersensitivity to serotonin via increased serum AngII level, upregulated AngII receptors expression in the vascular well, and activated local oxidative stress. These changes could be blocked by valsartan suggesting a crucial role of AngII/AngII receptors on vascular contractility and reactivity changes in this model.</p>