Decrease In Diastolic Arterial Pressure Research Articles

Показатели суточного мониторинга артериального давления у лиц старческого возраста c хронической сердечной недостаточностью в зависимости от жесткости сосудов

INTRODUCTION: Measurement of arterial pressure (AP) is a standard method for assessing the risk of developing cardiovascular diseases. Analysis of systolic and diastolic pressure, as well as their ratio, can help determine the risk of developing cardiovascular diseases. One of the ways to diagnose elevatedarterial pressure is daily monitoring of arterial pressure (DMAP). An increase in AP in the elderly is usually associated with an increase in the stiffness of the vascular walls. This leads to an increase in systolic arterial pressure (SAP) and pulse pressure (PP), as well as a decrease in diastolic arterial pressure (DAP). Elevated arterial pressure enhances the load on the heart and can lead to its pathological alterations. A decrease in DAP impairs the blood supply to the heart, which can cause ischemia and fibrosis; the result isdevelopment of diastolic dysfunction, which is the main cause of chronic heart failure (CHF). Currently, a promising way to determine the arterial stiffness is measurement of a cardio-ankle vascular index.The prognostic and diagnostic value of this parameter has been confirmed by numerous studies. It is important to study the parameters of the daily AP profile and arterial stiffness in older patients with CHF. This permits to identify malignant forms of elevated blood pressure, which can lead to cardiovascular complications. AIM: To study the characteristics of the parameters of the daily arterial pressure profile in elderly patients with CHF, depending on the vascular stiffness determined by volume sphygmography. MATERIALS AND METHODS: One hundred and twenty elderly patients with CHF undergoing treatment in a cardiology hospital were examined. By the method of volume sphygmography, the patients were divided into groups with ‘vessels of normal stiffness’ (group 1) and ‘stiff vessels’ (group 2), with subsequentDMAP. A statistical analysis of the parameters of the daily AP profile in the groups was performed. RESULTS: In patients of group 1, both daytime and nighttime SAP, DAP and PP, were significantly higher than in patients of group 2. Besides, in group 1, there was a nighttime decrease in SAP and DAP, while the morning rise of SAP was statistically higher in group 2, and no differences were recorded between the groups in the morning rise of DAP. When assessing the ankle-brachial index in patients of group 2, daytime and nighttime SAP and DAP were statistically higher. In group 1 (with probable peripheral atherosclerosis), PP was higher both during the day and at night. The nocturnal decrease in SAP was statistically higher in group 2, while the nocturnal decrease in DAP prevailed in group 1. The morning rise of SAP and DAP was higher in group 1. CONCLUSION: The DMAP data may indicate to some extent the severity of hypertension in patients with CHF, and this probably depends on the ‘stiffness of the vessels’. In elderly patients with CHF with ‘normal stiffness’ of vessels, the parameters of the daily arterial pressure profile were higher than in patients with ‘stiff vessels’. However, the daily range of parameters of the daily arterial pressure profile was greater in the group of patients with ‘stiff vessels’ (group 2).

Effect of omeprazole on antihypertensive efficacy of amlodipine in patients with comorbid pathology – arterial hypertension and acid-dependent disease

Objective:The problem of drug interactions is increasingly important today because they may induce serious adverse events as well as interfere with efficacy of pharmacotherapy. Combinations of drugs are most often prescribed to patients presenting with comorbid pathology. The incidence of a combination of arterial hypertension (AH) and acid-dependent diseases (ADDs) varies widely ranging from 11.6 to 50%. One of combinations of drugs prescribed to such patients is a combination of calcium channel blocker amlodipine and proton pump inhibitor omeprazole. The latter in the human body undergoes biotransformation mediated at the level of cytochrome P450 by isoenzymes CYP2C19 and CYP3A4. Amlodipine is a substrate of the isoenzyme CYP3A4, which increases the probability of the development of interaction between these drugs. The purpose of our study was to investigate antihypertensive efficacy of amlodipine in patients suffering from arterial hypertension combined with acid-dependent diseases and additionally taking omeprazole.Method:Study included a total of 150 patients with AH and ADD. Antihypertensive therapy was evaluated by means of office measuring of arterial pressure (AP) and circadian monitoring of AP (CMAP). The followed-up patients with AH and ADD were divided into 2 groups. Group One was composed of hypertensive patients undergoing pharmacotherapy with 10 mg amlodipine, whose condition required due to exacerbation of ADD administration of omeprazole at a dose of 20 mg for a period from 3 to 4 weeks. Group Two comprised hypertensive patients receiving antihypertensive therapy consisting of 10 mg amlodipine, who were found to have remission of acid-dependent diseases, with no additional medication taken.Results:The obtained findings demonstrated that one of the commonly used drug combinations in treatment of patients with AH and ADD in ambulatory conditions was a combination of omeprazole and amlodipine, accounting for 7.1%. The results of office measurement of arterial pressure (AP) 2 weeks after initiating pharmacotherapy with omeprazole in patients with AH and ADD demonstrated that the patients receiving omeprazole in addition to antihypertensive therapy were found to have a statistically significant decrease in systolic arterial pressure (SAP) and statistically significantly more pronounced dynamics of a decrease in diastolic arterial pressure (SAP) (p<0.05) compared with those not receiving therapy with omeprazole. Also, in the group of patients taking omeprazole, the findings of circadian monitoring of blood pressure (CMAP) showed a statistically significant decrease in average circadian SAP, average circadian DAP, mean value of daytime SAP and mean value of nighttime SAP (p<0.05).Conclusion:The obtained findings demonstrated that simultaneous prescription of amlodipine and omeprazole to patients with concomitant pathology, i.e., AH and ADD, turned out to enhance the antihypertensive affect of amlodipine, which probably resulted from substrate competition of amlodipine and omeprazole at the level isoenzyme CYP 3A4 of cytochrome P450.

Benidipine, a Long-Acting Calcium Channel Blocker, Inhibits Oxidative Stress in Polymorphonuclear Cells in Patients with Essential Hypertension

To study the relationship between blood pressure and oxidative stress in leukocytes, the effect of benidipine on these variables was compared with that of a placebo. Hypertensive patients were randomly assigned benidipine 4 mg (n=40) or placebo (n=40), and treated for 6 months. Oxidative stress in polymorphonuclear cells (PMNs) was measured by gated flow cytometry. There was a significant relationship between systolic or diastolic arterial pressure and reactive oxygen species (ROS) formation by PMNs in the benidipine group (r=0.61, p<0.01) and in the placebo group (r=0.58, p<0.01). After administration of 4 mg benidipine, ROS formation by PMNs fell by 32 arbitrary units (n=40, p<0.01). After administration of placebo, ROS formation by PMNs decreased by 0.6 arbitrary units (n=40, p=0.31) (p<0.01 for differing treatment effects). There was a significant relationship between the decrease in systolic arterial pressure and the decrease in ROS formation by PMNs in the benidipine group (r=0.52, p<0.01), but not in the placebo group (r=-0.08, p=0.61). There was also a significant relationship between the decrease in diastolic arterial pressure and decrease in ROS formation by PMNs in the benidipine group (r=0.65, p<0.01) but not in the placebo group (r=-0.09, p=0.59). In hypertensive patients, we observed a significant relationship between systolic or diastolic blood pressure and ROS formation by PMNs, and found that benidipine decreased oxidative stress in PMNs of hypertensive patients, at least in part by decreasing blood pressure.

Heat stress modifies human baroreflex function independently of heat-induced hypovolemia.

Since human thermoregulatory heat loss responses, cutaneous vasodilation and sweating, cause hypovolemia, they should resultantly stimulate human baroreflexes. However, it is possible that the thermoregulatory system directly interacts with the baroreflex system through central neural connections independently of the heat-induced hypovolemia. We hypothesized that heat stress modifies the baroreflex control of sympathetic nerve activity independently of heat-induced hypovolemia in humans. We made whole-body heating with tube-lined suits perfused with warm water (46-47 degrees C) on 10 healthy male subjects. The heating increased skin and tympanic temperatures by 10.0 and 0.4 degrees C, respectively. It increased resting total muscle sympathetic nerve activity (MSNA, microneurography) by 94 +/- 9% and decreased central venous pressure (CVP, dependent arm technique) by 2.6 +/- 0.9 mmHg. The heating increased arterial baroreflex gain by 193%, assessed as a response of MSNA to a decrease in diastolic arterial pressure during Valsalva's maneuver, but it did not change threshold arterial pressure for MSNA activation. Although the heating did not change the cardiopulmonary baroreflex gain assessed as a response of MSNA to a change in estimated central venous pressure (CVP) during a 10 degrees head-down and -up tilt test, it upwardly shifted the stimulus-response baroreflex relationship. These changes in baroreflex functions during heating were not restored by an intravenous infusion of warmed isotonic saline (37 degrees C, 15 ml/kg) that restored the heat-induced reduction of CVP. Our results support our hypothesis that heat stress modifies the baroreflex control of MSNA independently of heat-induced hypovolemia in humans. Our results also suggest that the hyperthermal modification of baroreflex results from central neural interaction between thermoregulatory and baroreflex systems.

Evidence that ranolazine behaves as a weak β 1 - and β 2 -adrenoceptor antagonist in the rat cardiovascular system

The clinical anti-anginal effectiveness of ranolazine is currently being evaluated. However, the mechanism of its anti-ischaemic action is still unclear. The aim of this work was to establish whether ranolazine exerts functional beta-adrenoceptor antagonist activity in the rat cardiovascular system. Radioligand binding studies were performed in rat hearts and guinea-pig lungs for beta1- and beta2-adrenoceptor affinity, respectively. Ranolazine had micromolar affinity for both beta,- and beta2-adrenoceptors (pKi5.8 and 6.3, respectively). Developed tension was measured in isolated rat left atria (electrically driven at 4 Hz) and cumulative concentration/response curves to (+/-)isoprenaline (0.01-1,000 nM) constructed. Ranolazine (0.32-10 microM) surmountably but weakly antagonised isoprenaline-induced positive inotropic responses, with an apparent pA2 of 5.85 (5.69-6.00) and a slope of -0.74 (-0.70 to -0.77). In bivagotomised, atropinised pithed rats, ranolazine per se evoked marked bradycardia at doses above 10 mg/kg i.v. (maximum variation at 80 mg/kg -125+/-15 bpm, n=6, P<0.001) by a mechanism apparently unrelated to blockade of beta1- or beta2-adrenoceptors. Cumulative incremental doses of (+/-)isoprenaline (0.63 ng/kg to 0.16 mg/kg i.v.) administered to pithed rats induced concomitant depressor and chronotropic responses. Animals received either vehicle (saline 0.9% i.v., n=12), atenolol (0.04-2.5 mg/kg i.v., n=6 per dose), ICI 118551 (0.01-0.63 mg/kg i.v., n=6 or 7 per dose), (+/-)propranolol (0.01-0.63 mg/kg i.v., n=6 per dose) or ranolazine (2.5-80 mg/kg i.v., n=6 or 7 per dose) 10 min prior to isoprenaline. Ranolazine dose-dependently and competitively antagonised isoprenaline-induced decreases in diastolic arterial pressure (DAP, dose ratio 12.2 with 80 mg/kg ranolazine) and increases in heart rate (HR, dose ratio 20.3 with 80 mg/kg ranolazine). Collectively, these results demonstrate that ranolazine behaves as a weak beta1- and beta2-adrenoceptor antagonist in the rat cardiovascular system.

Approaches to the Prevention of Perioperative Myocardial Ischemia

Goals for the perioperative management of patients with coronary artery disease include: * Prevent increases in sympathetic nervous system activity: reduce anxiety preoperatively; prevent stress response and release of catecholamines by appropriate use of opioids or volatile anesthetics and beta-adrenoceptor antagonists; beta-blocker therapy should be initiated before and continued during and after the surgical procedure. * Decrease heart rate: reduction in heart rate increases oxygen supply to ischemic myocardium and reduces oxygen demand; the use of beta-blockers is the most effective means to reduce or attenuate deleterious increases in heart rate. * Preserve coronary perfusion pressure: decreases in diastolic arterial pressure in the presence of severe coronary artery stenoses will lead to decreases in blood flow; preservation of perfusion pressure by administration of fluid or phenylephrine or a reduction in anesthetic concentration may be critical. * Decrease myocardial contractility: reduces myocardial oxygen demand and can be accomplished with beta-adrenoceptor antagonists or volatile anesthetics. * Precondition myocardium against stunning and infarction: in the future, this may accomplished by stimulating the adenosine triphosphate- dependent potassium channel with agents such as volatile anesthetics and opioid delta1-receptor agonists.

Approaches to the prevention of perioperative myocardial ischemia.

Goals for the perioperative management of patients with coronary artery disease include: * Prevent increases in sympathetic nervous system activity: reduce anxiety preoperatively; prevent stress response and release of catecholamines by appropriate use of opioids or volatile anesthetics and beta-adrenoceptor antagonists; beta-blocker therapy should be initiated before and continued during and after the surgical procedure. * Decrease heart rate: reduction in heart rate increases oxygen supply to ischemic myocardium and reduces oxygen demand; the use of beta-blockers is the most effective means to reduce or attenuate deleterious increases in heart rate. * Preserve coronary perfusion pressure: decreases in diastolic arterial pressure in the presence of severe coronary artery stenoses will lead to decreases in blood flow; preservation of perfusion pressure by administration of fluid or phenylephrine or a reduction in anesthetic concentration may be critical. * Decrease myocardial contractility: reduces myocardial oxygen demand and can be accomplished with beta-adrenoceptor antagonists or volatile anesthetics. * Precondition myocardium against stunning and infarction: in the future, this may accomplished by stimulating the adenosine triphosphate- dependent potassium channel with agents such as volatile anesthetics and opioid delta1-receptor agonists.

Inhibition of Nitric Oxide Synthase Causes Profound Enhancement of the Bezold-Jarisch Reflex

The Bezold-Jarisch reflex function was evaluated in rats made hypertensive by the chronic oral intake of a nitric oxide synthase inhibitor N ω-nitro- l-arginine methyl ester (L-NAME, averaging 35 mg/kg/day), for 3, 6, and 12 days (n = 9/group) and in untreated control rats (CR, n = 9/group). L-NAME–treated rats showed a marked hypertension (MAP: 148 ± 3, 182 ± 4, and 179 ± 4 mm Hg, respectively) compared with CR (110 ± 2 mm Hg). The 6- and 12-day groups showed tachycardia (447 ± 20 and 466 ± 13 beats/min, respectively) when compared with CR (355 ± 10 beats/min). When compared with CR, left ventricular hypertrophy was observed in rats treated with L-NAME for 6 and 12 days. The Bezold-Jarisch reflex, a decrease in heart rate (HR) accompanied by a decrease in diastolic arterial pressure (DAP), was evoked in a dose dependent manner by the intravenous injection of 5-hydroxytryptamine (5-HT, 5 to 10 μg/kg). Relative to responses observed in CR, 5-HT at 10 μg/kg caused a four- to fivefold greater decrease in HR and a two- to threefold greater decrease in DAP in all the L-NAME treatment groups. Using a Langendorff technique, we observed a significant increase in the responsiveness of the pacemaker to acetylcholine (1.25 to 80 μg/mL). These data suggest that the pharmacological inhibition of the nitric oxide synthase causes profound changes in the mechanisms of cardiovascular regulation as shown by a marked enhancement of the Bezold-Jarisch reflex in L-NAME-treated rats. The enhancement of this reflex seems to be in great part due to the hyperresponsiveness of the cardiac pacemaker to cholinergic stimulation.

Enoximone versus Dopamine in Patients Being Weaned from Cardiopulmonary Bypass

The efficacy of acute haemodynamic support with intravenous enoximone (2 X bolus 0.5 mg/kg; infusion 5.0 micrograms/kg/min) versus dopamine (3.0-4.0 micrograms/kg/min), over an 18-hour period, was investigated in patients to be weaned from cardiopulmonary bypass (placebo-controlled trial). Under steady-state conditions, enoximone produced a substantial increase in cardiac index (20.6 +/- 1.7%), but no change in heart rate. The improvement in cardiac index with time until constant values were reached (6 h) was not directly paralleled by the plasma concentration of enoximone. Pharmacodynamically relevant concentrations were already present after 1 h of infusion (480 +/- 68 ng/ml) and comparable with the value determined after 6 h (442 +/- 37 ng/ml). After 18 h of infusion, plasma concentration had reached 742 +/- 47 ng/ml without a further improvement in cardiac function. The augmentation of stroke volume index (23.3 +/- 2.5%) occurred concomitantly with a decrease in systemic vascular resistance (-23.1 +/- 0.6%), obviously due to a decrease in diastolic arterial pressure (-12.0 +/- 3.8%). The pulmonary capillary wedge pressure remained unaffected. There was only a slight decrease in pulmonary vascular resistance (-9.3 +/- 3.2%). During both enoximone infusion and dopamine infusion, right atrial pressure increased (10.0 +/- 3.1 and 9.0 +/- 1.8%, respectively), in contrast to the untreated control group. This is contradictory to the drugs' described effect in patients suffering from congestive heart failure. At a concentration which would not normally cause cardiac acceleration, dopamine provided minor haemodynamic support in the period after cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of nitroglycerin on exercise-induced regional myocardial contractile dysfunction are not diminished by pretreatment with dihydroergotamine.

1 Because controversy exists regarding the effects of dihydroergotamine (DHE) on the performance of underperfused myocardium, the effects of DHE were investigated in a model of exercise-induced regional myocardial dysfunction in conscious dogs. 2 We also investigated a possible functional antagonism between DHE and nitroglycerin that might reduce the latter drug's antianginal efficacy. 3 Investigations were carried out in conscious dogs. After stenosis of the circumflex branch of the left coronary artery that minimally affected resting myocardial function, treadmill exercise induced transient regional contractile dysfunction. Heart rate, arterial blood pressure, left ventricular dp/dtmax and left ventricular end-diastolic pressure were registered. Regional contractile performance was assessed by ultrasonic distance measurement in the underperfused and in a normally perfused area. 4 DHE (5 micrograms kg-1, i.v.) induced a decrease in left ventricular dp/dtmax at rest and during exercise. DHE did not cause a deterioration in contractile function in the ischaemic myocardium, but led to a slight although not significant improvement in regional myocardial function. 5 After pretreatment with DHE, infusion of nitroglycerin (15 micrograms kg-1, i.v.) induced an improvement in the underperfused myocardial area during treadmill exercise, accompanied by a decrease in diastolic arterial pressure and left ventricular end-diastolic pressure and an increase in left ventricular dp/dtmax. 6 These results suggest that DHE will not worsen exercise-induced angina pectoris, and that the antianginal efficacy of nitroglycerin will not be neutralized by pretreatment with DHE.

Effets hémodynamiques du propofol utilisé comme agent unique pour l'induction de l'anesthésie

Haemodynamic effects of propofol were studied during induction of anaesthesia, in 20 patients undergoing abdominal aortic replacement. Eight of them suffered from coronary arterial disease. Propofol was used at a dose of 2 mg · kg −1. During 5 min after propofol administration, no drug was administered. Neither plasma expansion nor tracheal intubation were carried out. Haemodynamic changes were : 17% decrease in systolic arterial pressure, and 13% decrease in diastolic arterial pressure, associated with a 12% decrease in cardiac output and 7% decrease in systemic vascular resistances; no change in heart rate in spite of the decrease in arterial pressure; and a mild increase in diastolic pulmonary arterial pressure. Left ventricular systolic work and rate pressure product decreased, suggesting a favourable incidence in coronary disease by lowering myocardial oxygen consumption. Nevertheless, it must be considered that, in the group studied, patients with coronary disease receiving beta-blocking drugs were excluded. So, mild haemodynamic changes observed here have to be confirmed in patients suffering from more severe coronary arterial disease.

BUPRENORPHINE: A NEW POTENT LONG-ACTING SYNTHETIC ANALGESIC. COMPARISON WITH MORPHINE

A new thebaine derivative, buprenorphine, 0.6 mg, was compared with morphine 15 mg in a double-blind trial, in patients recovering from elective Caesarean section. Within 1 h of administration analgesia was obtained with both drugs and was sustained for 7-8 h with buprenorphine, and 3-4 h with morphine. Buprenorphine caused a greater decrease in diastolic arterial pressure than did morphine, but arterial systolic pressure and heart rate were not influenced by either drug. No serious side-effects were encountered in this study.

Hemodynamic effects of noninvasive systolic unloading (nitroprusside) and diastolic augmentation (external counterpulsation) in patients with acute myocardial infarction

The two major beneficial hemodynamic effects of invasive circulatory assistance (intraaortic balloon pumping) are (1) left ventricular systolic unloading, and (2) diastolic augmentation of aortic pressure. In this study, these effects were produced noninvasively in 17 patients (13 with acute myocardial infarction, 5 of whom had cardiogenic shock). Systolic unloading produced by the constant intravenous infusion of sodium nitroprusside (16 to 200 μg/min) caused a reduction in pulmonary capillary wedge pressure (27 to 19 mm Hg), a rise in cardiac index (1.71 to 2.25 liters/min per m 2), and a reduction in mean arterial pressure (81 to 73 mm Hg). Diastolic augmentation with external counterpulsation produced a 20 mm Hg increase in peak, and a 7 mm Hg increase in mean diastolic arterial pressure. Cardiac index rose 14 percent after external counterpulsation in the patients with acute myocardial infarction. The results of combined use of these two modes of therapy (nitroprusside plus external counterpulsation) were better than those of either alone, in that external counterpulsation reversed the decrease in diastolic arterial pressure produced by nitroprusside, and also increased cardiac index further in six of nine patients. Thus it is feasible to utilize the principles of invasive circulatory assistance in a noninvasive way to produce hemodynamic improvement in patients with acute myocardial infarction.