Blood pressure-lowering did not improve short-term mortality or dependency in acute stroke and hypertension

2009 ◽  
Vol 14 (5) ◽  
pp. 145-145
Author(s):  
M. J Alberts
PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97917 ◽  
Author(s):  
Hongxuan Wang ◽  
Yamei Tang ◽  
Xiaoming Rong ◽  
Hui Li ◽  
Rui Pan ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammad M. Naderali ◽  
Imose Itua ◽  
Abdul-Razak Abubakari ◽  
Ebrahim K. Naderali

A number of preclinical and clinical studies have reported blood-pressure-lowering benefits of thiazolidinediones in diabetic subjects and animal models of diabetes. This study was designed to further elucidate vascular effects of rosiglitazone, on healthy nonobese, lean animals. Adult male Wistar rats were randomized and assigned to control and rosiglitazone-treated groups and were dosed daily with either vehicle or rosiglitazone (10 mg kg−1 day−1) by oral gavage for 5 days. Compared with control group, rosiglitazone treatment significantly reduced plasma levels of triglycerides (>240%) and nonesterified free fatty acids (>268%) (both, P<0.001). There were no changes in vascular contractility to KCl or noradrenaline between two groups. However, rosiglitazone therapy improved carbamylcholine-induced vasorelaxation (93±3 % versus control 78±2, P<0.01) an effect which was abolished by L-NAME. There was no difference in sodium nitroprusside-induced vasorelaxation between the control and rosiglitazone-treated animals. These results indicate that short-term rosiglitazone therapy improves both metabolic profile and vascular function in lean rats. The vascular effect of rosiglitazone appears to be mediated by alteration in NO production possibly by activation of endothelial PPARγ. This increased NO production together with improved lipid profile may explain mechanism(s) of blood-pressure-lowering effects of thiazolidinediones on both human and experimental animals.


2012 ◽  
Vol 30 ◽  
pp. e103
Author(s):  
Eivind Berge ◽  
Astrid G. Hornslien ◽  
Else C. Sandset ◽  
Philip M. Bath

2018 ◽  
Vol 13 (7) ◽  
pp. 759-765 ◽  
Author(s):  
Else Charlotte Sandset ◽  
Nerses Sanossian ◽  
Lisa J Woodhouse ◽  
Craig Anderson ◽  
Eivind Berge ◽  
...  

Rationale Despite several large clinical trials assessing blood pressure lowering in acute stroke, equipoise remains particularly for ischemic stroke. The “Blood pressure in Acute Stroke Collaboration” commenced in the mid-1990s focussing on systematic reviews and meta-analysis of blood pressure lowering in acute stroke. From the start, Blood pressure in Acute Stroke Collaboration planned to assess safety and efficacy of blood pressure lowering in acute stroke using individual patient data. Aims To determine the optimal management of blood pressure in patients with acute stroke, including both intracerebral hemorrhage and ischemic stroke. Secondary aims are to assess which clinical and therapeutic factors may alter the optimal management of high blood pressure in patients with acute stroke and to assess the effect of vasoactive treatments on hemodynamic variables. Methods and design Individual patient data from randomized controlled trials of blood pressure management in participants with ischemic stroke and/or intracerebral hemorrhage enrolled during the ultra-acute (pre-hospital), hyper-acute (<6 h), acute (<48 h), and sub-acute (<168 h) phases of stroke. Study outcomes The primary effect variable will be functional outcome defined by the ordinal distribution of the modified Rankin Scale; analyses will also be carried out in pre-specified subgroups to assess the modifying effects of stroke-related and pre-stroke patient characteristics. Key secondary variables will include clinical, hemodynamic and neuroradiological variables; safety variables will comprise death and serious adverse events. Discussion Study questions will be addressed in stages, according to the protocol, before integrating these into a final overreaching analysis. We invite eligible trials to join the collaboration.


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