Cardiac Mechanical Dysfunction Induced by Ischemia‐reperfusion in Perfused Heart Isolated from Stroke‐prone Spontaneously Hypertensive Rats

2004 ◽  
Vol 26 (6) ◽  
pp. 485-498 ◽  
Author(s):  
Tetsuji Itoh ◽  
Kohji Abe ◽  
Miwa Tokumura ◽  
Satoru Hirono ◽  
Masao Haruna ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Perfused Heart ◽  
Spontaneously Hypertensive

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 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

scholarly journals Treatment of spontaneously hypertensive rats with rosiglitazone ameliorates cardiovascular pathophysiology via antioxidant mechanisms in the vasculature

2009 ◽  
Vol 297 (3) ◽  
pp. E685-E694 ◽  
Author(s):  
Maria A. Potenza ◽  
Sara Gagliardi ◽  
Leonarda De Benedictis ◽  
Addolorata Zigrino ◽  
Edy Tiravanti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
Lipid Peroxidation Product ◽  
Hypertensive Rats ◽  
Sod Activity ◽  
Insulin Sensitizer ◽  
Spontaneously Hypertensive

Oxidative stress contributes to cardiovascular complications of diabetes, in part, by reducing the bioavailability of nitric oxide (NO). We investigated the mechanisms whereby the insulin sensitizer rosiglitazone may ameliorate oxidative stress in the vasculature of spontaneously hypertensive rats (SHR). Nine-week-old SHR were treated by gavage for 7 wk with rosiglitazone (5 mg·kg−1·day−1) or vehicle control. Treatment of SHR with rosiglitazone lowered systolic blood pressure, reduced fasting plasma insulin and asymmetrical dimethylarginine, and increased insulin sensitivity (when compared with vehicle treatment). In vessel homogenates and serum from rosiglitazone-treated SHR, SOD activity was enhanced, while 8-iso-PGF2α (lipid peroxidation product) was reduced (when compared with samples from vehicle-treated SHR). Moreover, expression of p22phox (catalytic subunit of NADPH oxidase) as well as nitrotyrosine and superoxide content were all reduced in the aortas of rosiglitazone-treated SHR. In mesenteric vascular beds (MVB) isolated ex vivo from rosiglitazone-treated SHR, NO-dependent vasodilator actions of insulin were improved when compared with MVB from vehicle-treated SHR. Acute pretreatment of MVB from vehicle-treated SHR with apocynin (NADPH oxidase inhibitor) enhanced vasodilator actions of insulin (results comparable to those in MVB from rosiglitazone-treated SHR). In Langendorff heart preparations from rosiglitazone-treated SHR, ischemia/reperfusion injury caused infarcts 40% smaller than in hearts from vehicle-treated SHR. Acute pretreatment of hearts from vehicle-treated SHR with apocynin produced similar results. Finally, rosiglitazone treatment of endothelial cells in primary culture reduced superoxide induced by insulin-resistant conditions. We conclude that rosiglitazone therapy in SHR increases SOD activity and decreases p22phox expression in the vasculature to reduce oxidant stress leading to an improved cardiovascular phenotype.

P0551THE EFFECTS OF HYPERBARIC OXYGEN PRECONDITIONING AND APOCYNIN TREATMENT IN POSTISCHEMIC ACUTE KIDNEY INJURY INDUCED IN SPONTANEOUSLY HYPERTENSIVE RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sanjin Kovacevic ◽  
Milan Ivanov ◽  
Zoran Miloradovic ◽  
Predrag Brkic ◽  
Una-Jovana Vajic ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Mortality Rates ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tubular Necrosis ◽  
Renal Ischemia Reperfusion Injury

Abstract Background and Aims Acute kidney injury (AKI) is associated with significant in-hospital morbidity and mortality, particularly in those admitted to the Intensive care units, where mortality rates may exceed 50%. Besides increased mortality rates, there are chronic consequences that carry high risk of developing or exacerbating chronic kidney disease and accelerated development of the end-stage renal disease. Renal ischemia/reperfusion injury is a common cause of AKI and hypertension might contribute to the increased incidence of AKI. The purpose of this study was to investigate the effects of combined hyperbaric oxygen (HBO) preconditioning and apocynin treatment on kidney hemodynamics, function and structure in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. Method Male SHR were randomly selected in three experimental groups: sham-operated group (SHAM, n=9), AKI control group (AKI, n=11) and AKI group with HBO preconditioning and apocynin treatment (AKI+APO+HBO, n=13). HBO preconditioning was performed by exposing to pure oxygen (2.026 bar) twice a day for two consecutive days for 60 minutes and day before AKI induction. All surgical procedures were performed in anaesthetized rats and AKI was induced by removal of the right kidney and atraumatic clamp occlusion of the left renal artery for 45 minutes. NADPH oxidase inhibitor, apocynin (40 mg/kg b.m., intravenously) was applied as a bolus injection 5 minutes before clamp removal. All hemodynamic parameters were measured 24 hours after reperfusion. After hemodynamic measurements, blood samples were collected and used for further analysis. Animals were sacrificed by pentobarbital overdose injection. Kidney tissue was removed and then prepared for histological examination. Results AKI significantly increased renal vascular resistance (RVR, p&lt;0.001) and reduced renal blood flow (RBF, p&lt;0.001), which were significantly improved in group with HBO preconditioning with apocynin treatment (RVR, p&lt;0.05; RBF, p&lt;0,01). AKI induction significantly increased plasma creatinine (p&lt;0.001), urea (p&lt;0.001), phosphate (p&lt;0.001) levels. Remarkable improvement, with decrease in creatinine (p&lt;0.001), urea (p&lt;0.01) and phosphate (p&lt;0.001) levels was observed in treated group. While AKI induction significantly increased plasma KIM – 1 levels (p&lt;0.001), HBO preconditioning with apocynin treatment decreased its levels (p&lt;0.05). Considering renal morphology, in SHAM operated rats, normal morphology of glomeruli, tubulointerstitium, and blood vessels were observed including rare kidney specimens with a few PAS positive casts in the lumen of the tubules. In animals with AKI significant morphological alterations were present: tubular cells necrosis, dilatation of certain segments of the proximal and distal tubules, mostly with loss of brush-border. The most notable changes were present in the cortico-medullary zone, where the broad areas of tubular necrosis and a large number of PAS positive casts in the collecting ducts were observed. In treated animals degrees of morphological changes were significantly lower compared to AKI control. There were reduced tubular dilatation, tubular necrosis in the cortico-medullary zone and PAS positive cast formation. Conclusion HBO preconditioning and apocynin treatment improve renal hemodynamics, function and in SHR which suffer AKI. These results suggest that it is reasonable to assume that HBO preconditioning and NADPH oxidase inhibition potentially may have beneficial effects, but further comprehensive experimental and clinical studies are needed to confirm these promising results.

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