ABSTRACT
Objective:To investigate the blood pressure variability and its clinical significance in patients with acute cerebral infarction who combined with H type hypertension.Methods: 95 patients with acute cerebral infarction who combined with H type hypertension were enrolled in the perspective study. According to the homocysteine(Hcy) level of patients, they were divided into observation group ( Hcy ≥10mmol/L, 51cases) and control group (Hcy<10mmol/L, 44cases). The blood pressure variability and main clinical features of these patients in the two groups in 24h were observed. At the same time, the correlation between blood pressure variability and main clinical feature in observation group were analyzed.Results: The 24h systolic pressure variability, 24h diastolic pressure variability, carotid intima-media thickness and national institute of health stroke scale (NIHSS) of observation group were 14.57±4.62, 18.57±5.38, 13.39±4.85 mm and 1.27±0.17, respectively. While they were 12.48±3.78, 16.12±5.74, 11.34±4.32 mm and 1.09±0.13 in the control group, respectively. And the differences of them between the two groups were statistical significance (t=2.389,t=2.146,t=2.160,t=5.725,P<0.05). Besides, there was obvious positive correlation between 24h systolic pressure variability and NIHSS of patients with acute cerebral infarction (r=0.254,P<0.05), and there was also obvious positive correlation between 24h systolic pressure variability and thickness of carotid intima-media (r=0.256,P<0.05).Conclusion: Increased blood pressure variability in patients with acute hypertensive cerebral infarction combined with H type hypertension may be related to poor prognosis of patients and vascular intima thickness.
ABSTRACT
<p><b>BACKGROUND</b>Lactate dehydrogenase (LDH) is a crucial regulator of energy metabolism in many organs including the heart. Lovastatin is widely used in prevention and treatment of coronary heart disease and is a drug with substantial metabolic influences. Our study aimed to determine the activities of the lactate dehydrogenase A and B (LDHA and LDHB) genes following lovastatin treatment.</p><p><b>METHODS</b>The rat myocardial cell line H9c2(2-1) in culture was exposed to 100 nmol/L lovastatin for 24 hours or for five days. The functions of the LDHA and LDHB genes were examined at the transcriptional (mRNA) level with quantitative real-time polymerase chain reaction (Q-RT-PCR), and at the translational (protein) level with immunoblotting.</p><p><b>RESULTS</b>When compared with control levels, the LDHA mRNA went up by (151.65 ± 16.72)% (P = 0.0132) after 24 hours and by (175.28 ± 56.54)% (P = 0.0366) after five days of lovastatin treatment. Although 24 hours of lovastatin treatment had no significant effects on LDHB mRNA levels, when the treatment was extended to five days, LDHB mRNA levels were significantly down-regulated to (63.65 ± 15.21)% of control levels (P = 0.0117). After 24 hours of treatment with lovastatin, there were no significant changes in protein levels of either LDHA or LDHB. When treatment time was extended to five days, the protein levels of LDHA were up-regulated by (148.65 ± 11.81)% (P = 0.00969), while the protein levels of LDHB were down-regulated to (64.91 ± 5.47)% of control levels (P = 0.0192).</p><p><b>CONCLUSIONS</b>Lovastatin affects gene activities of LDHA and LDHB differently, which may reveal novel pharmacological effects of lovastatin.</p>
Subject(s)
Animals , Rats , Anticholesteremic Agents , Pharmacology , Blotting, Western , Cell Line , Isoenzymes , Genetics , Metabolism , L-Lactate Dehydrogenase , Genetics , Metabolism , Lovastatin , Pharmacology , Myocytes, Cardiac , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
<p><b>BACKGROUND</b>Glucocorticoid signaling exerts major roles in inflammation, metabolism and depression, which are three crucial factors accompanying or underlying coronary heart disease. Although accumulating evidence indicates the influence of glucocorticoids on the pathology and treatment of coronary heart disease, there is still a dearth of pharmaceutical mechanisms for this relationship. This study aimed to investigate the influence of drug treatment on glucocorticoid receptor levels in coronary heart disease.</p><p><b>METHODS</b>Eighty hospitalized patients (average age (59.0 +/- 7.5) years, 46 male and 34 female) with coronary heart disease were categorized into four groups with 20 members in each according to one of the four drugs they were treated with. The four drugs were: nitrated derivative isosorbide dinitrate, the beta-adrenergic receptor blocker metoprolol, the calcium antagonist nifedipine, and the HMG-CoA reductase inhibitor lovastatin. Glucocorticoid receptor protein levels of peripheral blood lymphocytes were tested using immunoblotting analysis before and after one month of treatment.</p><p><b>RESULTS</b>Immunoblotting analysis showed increased glucocorticoid receptor levels after treatment with metoprolol and nifedipine. There were no statistically significant changes of glucocorticoid receptor levels after treatment with isosorbide dinitrate or lovastatin, although there were trends of up-regulation of glucocorticoid receptor expression after both treatments.</p><p><b>CONCLUSIONS</b>Both the beta-blocker and the calcium blocker can increase glucocorticoid receptor levels after chronic administration. This effect suggests a mechanism for their anti-inflammatory and other therapeutic roles for coronary heart disease and comorbid disorders.</p>