Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats

2009 ◽  
Vol 11 (2) ◽  
pp. 152-162 ◽  
Author(s):  
Chung-Jen Lee ◽  
Ru-Ping Lee ◽  
Yi-Maun Subeq ◽  
Chia-Chi Lee ◽  
Tai-Chu Peng ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Spontaneously Hypertensive Rats ◽  
Low Dose ◽  
Organ Damage ◽  
Interleukin 10 ◽  
High Dose ◽  
Hypertensive Rats ◽  
Total Blood ◽  
Spontaneously Hypertensive ◽  
Blood Withdrawal

Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor a (TNF-a) and interleukin 10 (IL-10) can be produced by HS and lead to multiple organ dysfunction and death. We investigated the effects of high dose (10 mg/kg/hr) and low dose (1 mg/kg/hr) propofol treatment after HS in conscious spontaneously hypertensive rats (SHRs). By withdrawing 40% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight [BW]) for more than 30 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 24 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, and 24 hr after the 30-min blood withdrawal period. Cytokine levels, including TNF-a and IL-10 in the serum, were measured 1 hr after HS. The kidney, liver, and lung were removed for pathology assessment at 48 hr after HS. HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-a, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-a level, increased serum IL-10 level, attenuated the severity of organ damage, and improved survival rate after HS. This treatment protected SHRs against HS-induced organ damage. Moreover, high-dose propofol had a more protective effect than low-dose propofol against HS in conscious SHRs.

Effects of low-dose ketanserin on blood pressure variability, baroreflex sensitivity and end-organ damage in spontaneously hypertensive rats

2005 ◽  
Vol 108 (6) ◽  
pp. 547-552 ◽  
Author(s):  
He-Hui XIE ◽  
Fu-Ming SHEN ◽  
Yong-Bing CAO ◽  
Hui-Lin LI ◽  
Ding-Feng SU
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Variability ◽  
Spontaneously Hypertensive Rats ◽  
Baroreflex Sensitivity ◽  
Low Dose ◽  
Organ Damage ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Organ Protection ◽  
Spontaneously Hypertensive

The present study was designed to investigate the effects of low-dose ketanserin on BPV (blood pressure variability), BRS (baroreflex sensitivity) and organ damage in SHR (spontaneously hypertensive rats). Ketanserin was mixed in rat chow at an estimated dose of 0.1 mg·kg−1 of body weight·day−1. SHR were treated for 4 months. BP (blood pressure) was then recorded continuously for 24 h in a conscious state. After determination of BRS, rats were killed for organ damage evaluation. It was found that long-term treatment with low-dose ketanserin did not lower BP levels, but significantly decreased BPV, enhanced BRS and reduced organ damage in SHR. Multiple regression analysis showed that the decrease in left ventricular hypertrophy was most closely correlated (or associated) with the increase in BRS, whereas the decrease in aortic hypertrophy was most closely associated with the decrease in diastolic BPV and the amelioration in renal lesion, with the increase in BRS and the decrease in diastolic BPV. In conclusion, low-dose ketanserin produces organ protection independently of its BP-lowering action in SHR, and this organ protection was importantly attributable to the enhancement of BRS and decrease in BPV.

Effect of chronic NG-nitro-L-arginine methyl ester (L-NAME) on blood pressure and renal function in conscious uninephrectomized spontaneously hypertensive rats

1998 ◽  
Vol 76 (1) ◽  
pp. 63-67 ◽  
Author(s):  
María Reverte ◽  
Olga Flores ◽  
Belén Gallego ◽  
Antonio Lestón ◽  
José Miguel López-Novoa
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Renal Function ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Low Dose ◽  
Potassium Excretion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sodium And Potassium

We have studied during 30 days the effect of a low dose of NG-nitro-L-arginine methyl ester (1 mg ·kg-1 ·day-1 in drinking water) in the presence of D- or L-arginine (1 mg ·kg-1 ·day-1 in drinking water) in comparison with D- or L-arginine alone on blood pressure and renal function in conscious uninephrectomized female spontaneously hypertensive rats. At the end of the study, there was a significant increase in systolic blood pressure in the NG-nitro-L-arginine methyl ester + D-arginine group (307 ± 6 mmHg (1 mmHg = 133.3 Pa), n = 14, p << 0.05) in comparison with NG-nitro-L-arginine methyl ester + L-arginine (281 ± 6 mmHg, n = 14), L-arginine (262 ± 5 mmHg, n = 13), and D-arginine (258 ± 7 mmHg, n = 12) groups. There were no changes in diuresis, proteinuria, or sodium and potassium excretion between differently treated animals during this study. These results suggest that in uninephrectomized female spontaneously hypertensive rats, after 1 month blockade of NO synthesis with a low dose of NG-nitro-L-arginine methyl ester, vasculature is under tonic control by NO and it is not correlated with renal dysfunction.Key words: Key words: NG -nitro-L-arginine methyl ester (L-NAME), kidney, hypertension, spontaneously hypertensive rats, renaldysfunction, uninephrectomy.

scholarly journals Brain Overexpression of Uncoupling Protein-2 (UCP2) Delays Renal Damage and Stroke Occurrence in Stroke-Prone Spontaneously Hypertensive Rats

2020 ◽  
Vol 21 (12) ◽  
pp. 4289
Author(s):  
Carla L. Busceti ◽  
Maria Cotugno ◽  
Franca Bianchi ◽  
Maurizio Forte ◽  
Rosita Stanzione ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Lentiviral Vector ◽  
Uncoupling Protein ◽  
Organ Damage ◽  
Kidney Damage ◽  
Uncoupling Protein 2 ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Protein Levels

The downregulation of uncoupling protein-2 (UCP2) is associated with increased brain and kidney injury in stroke-prone spontaneously hypertensive rats (SHRSP) fed with a Japanese style hypersodic diet (JD). Systemic overexpression of UCP2 reduces organ damage in JD-fed SHRSP. We examined the effect of brain-specific UCP2 overexpression on blood pressure (BP), stroke occurrence and kidney damage in JD-fed SHRSP. Rats received a single i.c.v. injection of a lentiviral vector encoding UCP2 (LV-UCP2), or an empty vector. The brain delivery of LV-UCP2 significantly delayed the occurrence of stroke and kidney damage. The large reduction of proteinuria observed after LV-UCP2 injection was unexpected, because BP levels were unchanged. At the time of stroke, rats treated with LV-UCP2 still showed a large UCP2 upregulation in the striatum, associated with increases in OPA1 and FIS1 protein levels, and reductions in PGC1-α, SOD2, TNFα mRNA levels and NRF2 protein levels. This suggested UCP2 overexpression enhanced mitochondrial fusion and fission and reduced oxidative damage and inflammation in the striatum of JD-fed SHRSP rats. Our data suggest the existence of central mechanisms that may protect against hypertension-induced organ damage independently of BP, and strengthen the suitability of strategies aimed at enhancing UCP2 expression for the treatment of hypertensive damage.

Dexamethasone and Training-Induced Cardiac Remodeling Improve Cardiac Function and Arterial Pressure in Spontaneously Hypertensive Rats

2020 ◽  
pp. 107424842095327
Author(s):  
Francine Duchatsch ◽  
Lidieli P. Tardelli ◽  
Naiara A. Herrera ◽  
Thalles F. R. Ruiz ◽  
Carlos A. Vicentini ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Cardiac Remodeling ◽  
Spontaneously Hypertensive Rats ◽  
Low Dose ◽  
Collagen Deposition ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Deposition Area ◽  
Systolic And Diastolic Function ◽  
And Training

Introduction: Dexamethasone (DEX)-induced hypertension and cardiac remodeling are still unclear, especially in spontaneously hypertensive rats (SHR). On the other side, exercise training is a good strategy to control hypertension. Therefore, this study investigated the effects of DEX treatment and physical training on arterial pressure and cardiac remodeling in SHR. Material and Methods: SHR underwent treadmill training (5 days/week, 1h/session, at 50-60% of maximal capacity, 0% degree, 75 days) and received low-dose of DEX (50µg/kg, s.c.) during the last 15 days. Sedentary Wistar rats (W) were used as control. Echocardiography and artery catheterization were performed for cardiac remodeling and function, arterial pressure and autonomic nervous system analyses. In addition, left ventricle (LV) capillary density, myocyte diameter and collagen deposition area were analyzed using specific histological staining. Results: Low-dose of DEX treatment did not exacerbate arterial pressure of SHR and trained groups had lower values, regardless of DEX. DEX and training decreased relative left ventricle wall thickness (RWT) and determined LV angiogenesis (+19%) and lower collagen deposition area (−22%). In addition, it determined increased left ventricular diastolic diameter. These changes were followed by improvements on systolic and diastolic function, since it was observed increased posterior wall shortening velocity (PWSV) and reduced isovolumetric relaxation time (IVRT). Conclusion: In conclusion, this study is unique to indicate that low-dose of DEX treatment does not exacerbate arterial pressure in SHR and, when associated with training, it improves LV systolic and diastolic function, which may be due to LV angiogenesis and reduction of wall collagen deposition area.

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