Abstract-Although the differences between central and peripheral blood pressure (BP) values have been known for decades, the consequences of decision making based on peripheral rather than central BP have only recently been recognized. There are only a few studies assessing the relationship between intraaortic BP and cardiovascular risk. In addition, the relationship between central BP and the risk of cardiovascular events in a large group of coronary patients has not yet been evaluated. Therefore, the aim of the study was to determine the prognostic significance of central BP-derived indices in patients undergoing coronary angiography. Invasive central BPs were taken at baseline, and study end points were ascertained during over a 4. Key Words: blood pressure Ⅲ central pulse pressure Ⅲ pulsatility Ⅲ cardiovascular risk Ⅲ atherosclerosis Ⅲ coronary artery disease D iastolic blood pressure (DBP) was previously believed to be the only meaningful predictor of cardiovascular events; however, systolic blood pressure (SBP) is now being considered an even more important cardiovascular risk factor. 1 Recently, the prospective and retrospective epidemiological studies have demonstrated that elevated pulse pressure (PP, the difference between systolic and diastolic pressure) is independently related to the risk of cardiovascular events, especially in the elderly. 1,2 Furthermore, new parameters (pulsatility and pulsatility index) of the pulsatile component of blood pressure (BP) have been developed. 3,4 Pulsatility is calculated as PP divided by mean blood pressure (MBP). 3 Unlike SBP, DBP, and PP, this new parameter is not correlated with MBP, and thus it may be very useful in research on atherosclerosis pathogenesis and its complications development. 5,6 Pulsatility may be seen as indicator of the relative changes of blood pressure in opposition to pulse pressure which is an index of absolute blood pressure changes.Although the differences between central and peripheral BP values have been known for decades, the consequences of decision making based on peripheral rather than central BP have only recently been recognized. 6 -9 As central BP directly affects heart and coronary as well as carotid arteries and is directly related to the incidence of major cardiovascular complications, more and more attention is being given to the ascending aortic BP measurements. 6,7 There are only a few studies assessing the relationship between central BP and cardiovascular risk. The relationship between pulsatility (as measured invasively in the ascending aorta) and the risk of cardiovascular events has not yet been evaluated. Therefore, the present study was designed for the assessment of the relationship between prognosis and the steady and pulsatile components of central BP. Methods Study PopulationConsecutive patients suspected of having coronary artery disease (CAD) who were undergoing nonemergency coronary angiography from
Our experiment has shown that metformin administration is followed by H2S tissue concentrations increase in mouse brain, heart, kidney and liver.
To achieve better long-term outcomes in CRT patients the antero-apical pattern of LV QRS complexes and apical or paraseptal LV lead position should be avoided.
Hydrogen sulfide (H2S) is a crucial co-modulator of cardiovascular, nervous, digestive and excretory systems function. The pleiotropic action of atorvastatin exceeds simple 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibition and involves multiple biological mechanisms. This study assesses the influence of atorvastatin on the H2S tissue concentration in mouse brain, liver, heart and kidney. Twenty-four female CBA strain mice received an intraperitoneal injection. The mice were given one of the following solutions: 0.1 mg atorvastatin (5 mg/kg of body weight (b.w.)/day--group D1, n=8), 0.4 mg atorvastatin (20 mg/kg b.w./day--group D2, n=8) or a saline physiological control (0.2 ml--group C, n=8). A modified Siegel spectrophotometric method was used for the H2S tissue concentration measurements. There was a remarkable rise in the H2S concentration [μg/g] in the kidney (C: 5.26±0.09, D1: 5.77±0.11, p=0.0003; D2: 7.48±0.09, p<0.0001). There were also slight H2S tissue level changes in the brain (C: 1.61±0.01, D1: 1.75±0.03, p=0.0001; D2: 1.78±0.03, p<0.0001), the heart (C: 4.54±0.08, D1: 4.86±0.10, p=0.0027; D2: 4.56±0.07, p=0.6997) and the liver (C: 3.45±0.03, D1: 3.27±0.02, p=0.0001; D2: 3.31±0.02, p=0.0003). Our study supports the influence of atorvastatin on H2S tissue concentration in kidneys and other mouse organs.
Carvedilol induces endogenous hydrogen sulfide tissue concentration changes in various mouse organs. Folia biologica (Kraków) 59: 151-155. Carvedilol, a third generation non-selective adrenoreceptor blocker, is widely used in cardiology. Its action has been proven to reach beyond adrenergic antagonism and involves multiple biological mechanisms. The interaction between carvedilol and endogenous gasotransmitter hydrogen sulfide (H S) is unknown. The aim of the study is to assess the influence of carvedilol on the H S tissue level in mouse brain, liver, heart and kidney. Twenty eight SJL strain female mice were administered intraperitoneal injections of 2.5 mg/kg b.w./d (group D1, n = 7), 5 mg/kg b.w./d (group D2, n = 7) or 10 mg/kg b.w./d of carvedilol (group D3, n = 7). The control group (n = 7) received physiological saline in portions of the same volume (0.2 ml). Measurements of the free tissue H S concentrations were performed according to the modified method of Siegel. A progressive decline in H S tissue concentration along with an increase in carvedilol dose was observed in the brain (12.5%, 13.7% and 19.6%, respectively). Only the highest carvedilol dose induced a change in H S tissue level in the heart an increase by 75.5%. In the liver medium and high doses of carvedilol increased the H S level by 48.1% and 11.8%, respectively. In the kidney, group D2 showed a significant decrease of H S tissue level (22.5%), while in the D3 group the H S concentration increased by 12.9%. Our study has proven that carvedilol affects H S tissue concentration in different mouse organs.
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