scholarly journals IMM-H004, a coumarin derivative, attenuated brain ischemia/reperfusion injuries and subsequent inflammation in spontaneously hypertensive rats through inhibition of VCAM-1

RSC Advances ◽  
2017 ◽  
Vol 7 (44) ◽  
pp. 27480-27495 ◽  
Author(s):  
Peng-Fei Yang ◽  
Xiu-Yun Song ◽  
Ting Zeng ◽  
Qi-Di Ai ◽  
Dan-Dan Liu ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Spontaneously Hypertensive Rats ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Coumarin Derivative ◽  
Dependent Manner ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Dose Dependent

We studied the effect of IMM-H004 in treating brain I/R injury in spontaneously hypertensive rats and showed that IMM-H004 could efficiently ameliorate neurological defects and infarct volume in a time and dose dependent manner.

α1-Adrenoceptor subtypes mediating contraction of the femoral artery in spontaneously hypertensive rats

1994 ◽  
Vol 72 (8) ◽  
pp. 862-869 ◽  
Author(s):  
Seigo Fujimoto
Keyword(s):  
Blood Vessels ◽  
Femoral Artery ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Dose Dependent

α1-Adrenoceptors (ARs) were divided into α1H and α1L subtypes by their different affinities for bunazosin or prazosin. α1H-ARs were further subdivided into α1A, α1B, and α1C subtypes. Therefore, this study was undertaken to determine which α1-AR subtypes were involved in the activation of femoral artery preparations by α1-AR agonists in spontaneously hypertensive rats (SHR). For comparison, aortic strips were also incorporated in the present study. In the presence of propranolol, deoxycorticosterone, and desipramine, norepinephrine (NE) contracted the vascular strips in a dose-dependent manner. Negative log EC50 values and maximum responses of NE-induced contraction of the SHR femoral artery were unchanged and increased, respectively, compared with those of Sprague–Dawley and Wistar–Kyoto rats (WKY). Contractile responses of the SHR aortae to NE were similar to those of the normotensive tissues. Schild plot data for α1-AR antagonists indicated that α1-AR subtypes mediating contraction of the aorta were homogeneous and had high affinities for bunazosin (pA2 9.4, α1H subtype) and WB 4101 (pA2 9.3) and a low affinity for 5-methylurapidil (pA2 7.7). In the femoral artery, because Schild plots for bunazosin had slopes of less than 1.0, there were α1H and α1L subtypes. Bunazosin, at 10−9 M, which could mask the α1H subtype, yielded a Schild plot for bunazosin with a slope not different from unity and decreased the pA2 value for bunazosin (pA2 9.4 vs. 8.5). Chlorethylclonidine inhibited the response of the aortic and femoral preparations to NE but did not change Schild plot data for 5-methylurapidil. It was suggested that in the rat femoral artery, α1C and α1L subtypes mediated the contractile response to NE. The α1-AR subtype in the aorta was essentially identical with the α1H subtype in the femoral artery. α1-AR subtypes mediating contraction in the SHR blood vessels were identical with those in the WKY tissues.Key words: α1-adrenoceptor subtype, blood vessels, spontaneously hypertensive rat.

Changes of Blood Pressure Rhythm and Clock Protein Expression Levels in Spontaneously Hypertensive Rats After Ischemia-Reperfusion

2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Circadian Clock ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
The Relationship ◽  
Clock Protein

Abstract Objective A variety of circadian patterns of blood pressure after ischemic stroke in patients with essential hypertension appear to be a potential risk of stroke recurrence, but the mechanism is still unclear. This study intends to reveal the changes in blood pressure rhythm and circadian clock protein expression levels in spontaneously hypertensive rats (SHR) after ischemia-reperfusion, and the relationship between the two. Methods Using the SHR middle cerebral artery occlusion experimental model, the systolic blood pressure was continuously monitored for 24 hours after the operation to observe the blood pressure rhythm. The rat tail vein blood was taken every 3h, and the serum CLOCK, BMAL1, PER1 and CRY1 protein expression levels were detected by Elisa. Pearson correlation analysis counted the relationship between SHR blood pressure rhythm and circadian clock protein fluctuation after ischemia-reperfusion. Results The proportion of abnormal blood pressure patterns in the SHR + tMCAO group was significantly higher than that in the SHR group, the serum CLOCK expression was relatively constant, and the circadian rhythm of BMAL1, PER1 and CRY1 protein expression changed significantly. Pearson analysis showed that PER1 protein level was negatively correlated with dipper (r = -0.565, P = 0.002) and extreme-dipper (r = -0.531, P = 0.001) blood pressure, and was significantly positively correlated with non-dipper blood pressure (r = 0.620, P < 0.001). Conclusion The rhythm pattern of blood pressure after ischemia-reperfusion in SHR is obviously disordered, and it is closely related to the regulation of Per1 gene.

scholarly journals Rapamycin Induces an eNOS (Endothelial Nitric Oxide Synthase) Dependent Increase in Brain Collateral Perfusion in Wistar and Spontaneously Hypertensive Rats

Stroke ◽  
2020 ◽  
Vol 51 (9) ◽  
pp. 2834-2843
Author(s):  
Daniel J. Beard ◽  
Zhaojin Li ◽  
Anna M. Schneider ◽  
Yvonne Couch ◽  
Marilyn J. Cipolla ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Infarct Volume ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background and Purpose: Rapamycin is a clinically approved mammalian target of rapamycin inhibitor that has been shown to be neuroprotective in animal models of stroke. However, the mechanism of rapamycin-induced neuroprotection is still being explored. Our aims were to determine if rapamycin improved leptomeningeal collateral perfusion, to determine if this is through eNOS (endothelial nitric oxide synthase)-mediated vessel dilation and to determine if rapamycin increases immediate postreperfusion blood flow. Methods: Wistar and spontaneously hypertensive rats (≈14 weeks old, n=22 and n=15, respectively) were subjected to ischemia by middle cerebral artery occlusion (90 and 120 minutes, respectively) with or without treatment with rapamycin at 30-minute poststroke. Changes in middle cerebral artery and collateral perfusion territories were measured by dual-site laser Doppler. Reactivity to rapamycin was studied using isolated and pressurized leptomeningeal anastomoses. Brain injury was measured histologically or with triphenyltetrazolium chloride staining. Results: In Wistar rats, rapamycin increased collateral perfusion (43±17%), increased reperfusion cerebral blood flow (16±8%) and significantly reduced infarct volume (35±6 versus 63±8 mm 3 , P <0.05). Rapamycin dilated leptomeningeal anastomoses by 80±9%, which was abolished by nitric oxide synthase inhibition. In spontaneously hypertensive rats, rapamycin increased collateral perfusion by 32±25%, reperfusion cerebral blood flow by 44±16%, without reducing acute infarct volume 2 hours postreperfusion. Reperfusion cerebral blood flow was a stronger predictor of brain damage than collateral perfusion in both Wistar and spontaneously hypertensive rats. Conclusions: Rapamycin increased collateral perfusion and reperfusion cerebral blood flow in both Wistar and comorbid spontaneously hypertensive rats that appeared to be mediated by enhancing eNOS activation. These findings suggest that rapamycin may be an effective acute therapy for increasing collateral flow and as an adjunct therapy to thrombolysis or thrombectomy to improve reperfusion blood flow.

scholarly journals Exaggerated Liver Injury Induced by Ischemia–Reperfusion in Spontaneously Hypertensive Rats

2005 ◽  
Vol 18 (10) ◽  
pp. 1335-1339 ◽  
Author(s):  
M OHMORI ◽  
N ARAKI ◽  
K HARADA ◽  
T SUDOH ◽  
K SUGIMOTO ◽  
...  
Keyword(s):  
Liver Injury ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Brain ischemia and gastric mucosal damage in spontaneously hypertensive rats

1996 ◽  
Vol 41 (12) ◽  
pp. 2383-2391 ◽  
Author(s):  
Keishi Kawakubo ◽  
Setsuro Ibayashi ◽  
Tetsuhiko Nagao ◽  
Kosei Doi ◽  
Kunihiko Aoyagi ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Spontaneously Hypertensive Rats ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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