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Resulting from the electrocardiographic investigations in dynamics, in 7 patients with purulent-inflammatory complications of surgical diseases of the abdominal organs, the positive effect of intravascular laser irradiation of the blood on the function of cardiovascular system is shown.
Amiloride has previously been shown to facilitate receptor binding of atrial natriuretic factor (ANF) to membranes of adrenal cortex and to enhance ANF induced inhibition of steroid secretion in vitro. This interaction of amiloride and ANF also holds true for the cardiovascular system. In precontracted rabbit aortic strips the relaxing effect induced by the combination of ANF (10(-10) mol/l) and amiloride (10(-5) mol/l) was overadditional. The production of cyclic guanosine monophosphate (cGMP), which parallels ANF induced relaxations of vascular strips, was not affected by amiloride alone up to 10(-3) mol/l, but was concentration-dependently increased in the presence of ANF (10(-8) mol/l). In spontaneously hypertensive rats ANF-induced decreases in blood pressure were potentiated by amiloride. Post ischemia reperfusion arrhythmias in isolated rat hearts were reduced by ANF. Amiloride increased this effect. The binding experiments revealed an interaction of amiloride and ANF on the receptor level. Binding of labeled ANF to aortic tissue was concentration-dependently increased by amiloride. Addition of ATP had the opposite effect. Therefore it can be suggested that amiloride and ATP interfere with a mechanism regulating the sensitivity of the vascular ANF-receptor for its ligand regarding binding and signal transforming presumably by a kinase mediated phosphorylation/dephosphorylation process.
In 34 patients, 25 males and 9 females, aged 12-24 years (mean 15.9) 3-5 years after the completion of acute lymphoblastic leukemia treatment the non-invasive evaluation of cardiovascular system was done with the use of electrocardiography, echocardiography and treadmill stress test. The cumulative anthracycline doses varied from 149 to 417 mg/m2, mean 250 mg/m2. The control group consisted of 28 healthy volunteers, 15 males and 13 females aged 9-25 years (mean 17.0). The history, physical examination and non-invasive tests' results did not revealed the cardiomyopathy signs, left ventricle contractility in the study and control groups did not differ significantly. Treadmill stress test showed lower maximal heart rate achieved and deeper ST segment depression in the study group. We conclude that the patients after leukemia treatment need further careful investigations.
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Like human chymase, hamster chymase is an ANG II-forming enzyme, but pathophysiological roles of chymase are still unknown. We determined the functional conversion of ANG I and [Pro11, D-Ala12]ANG I, a chymase-selective substrate, to ANG II in the hamster cardiovascular system. ANG I and [Pro11, D-Ala12]ANG I produced similar dose-dependent pressor responses in conscious hamsters. Captopril and CV-11974, an ANG II type 1 (AT1)-receptor antagonist, inhibited the responses to ANG I; in contrast, the pressor responses to [Pro11, D-Ala12]ANG I were suppressed only by CV-11974. In the isolated aorta, captopril suppressed ANG I-induced contraction by 84%; administration of captopril with either chymostatin or aprotinin eliminated the contraction. [Pro11, D-Ala12]ANG I-induced contraction was not affected by captopril but was attenuated by chymostatin (71%) and aprotinin (57%). CV-11974 abolished the responses to both substrates, whereas PD-123319, an AT2-receptor antagonist, had no effect. In homogenates of the aorta and heart, soybean trypsin inhibitor-inhibitable ANG II formation predominated over captopril- or aprotinin-inhibitable ANG II formation. These data suggest that [Pro11,D-Ala12]ANG I and part of ANG I were functionally converted to ANG II by chymase and other serine protease(s) in hamster vessels, inducing AT1-receptor-mediated vasoconstriction. Biochemical data supported a role for chymase in the alternative pathway.
From 1984 to 1992 in Japan, 37 cases, including 2 cases of our own, have been reported to involve the percutaneous removal of foreign bodies from the cardiovascular system by catheter. We reviewed the cases of these foreign bodies and the locations, approaches and types of catheters used for removal. The reported foreign bodies were usually iatrogenic in origin and were approximately two times larger than those found in patients who had self-dislodged catheters. The most common catheter approaches were from either the right femoral or saphenous veins.
Endothelin (ET) is a peptide synthetized by endothelial cells (EC), smooth-muscle cells (SMC), cardiomyocytes and endocardial cells in response to the effects of mechanical factors and some biologically active substances--angiotensin 11, interleykin-1, the transforming growth factor-alpha and tumor necrosis factor alpha(TNF-alpha). ET possesses significant constrictor action on vessels (100 times more than angiotensin), positive inotropic action on the heart and stimulates proliferation. Increase of the endogenous endothelin concentration has been shown in many pathological states of the cardiovascular system. By inhibiting ET receptors it has been proved EN involvement in the pathogenesis of some of these states--systemic hypertension, myocardial infarction, vasospasm and cardiac failure.
This review will discuss the in vivo physical chemical relaxation properties of superparamagnetic iron oxide particles. Various parameters such as size, magnetization, compartmentalization and water exchange effects and how these alter the behavior of the iron oxide particles in an in vitro vs an in vivo situation with special reference to the cardiovascular system will be exemplified. Furthermore, applications using iron oxide particles for vascular, perfusion and viability imaging as well as assessment of the inflammatory status of a given tissue will be discussed.
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Knowledge of the sympathetic system is a basic element in the understanding of numerous physiological and physiopathological phenomena. In the two last decades, new pharmacological, biochemical and molecular tools have changed our approach to the roles of beta-adrenoceptors in the cardiovascular system. In the heart, the positive inotropic effect of predominant beta 1-adrenoceptor stimulation is classically recognised. Several studies reveal a significant physiological relevance of the beta 2-adrenoceptor which could activate different signalling pathways in addition to that of cAMP. Moreover, the detection of a third beta-adrenoceptor subtype, beta 3, in human heart, responsible for a negative inotropic effect through a NO signalling pathway, has changed the classically admitted paradigm on the regulation of heart function by the beta-adrenergic system. The identification of atypical beta-adrenoceptors, based on pharmacological tools, led to the discovery of "putative" beta 4-adrenoceptors, which constituted a low affinity state of the beta 1-adrenoceptors. In vessels, all beta-adrenoceptors subtypes, beta 1, beta 2 and beta 3, mediated a vasodilation, but the signalling pathway involved in this effect was variable according to their localization (endothelial or smooth muscle cells), the species and the vascular bed. beta-adrenoceptors are involved in several cardiovascular disease and could constitute a determinant therapeutic target. The efficiency of some beta-blockers used in the treatment of heart failure could result from action on beta 3-adrenoceptors. Moreover, a mutation of the beta-adrenoceptor subtype suggested a role in hypertension and diabetes mellitus.
Metoprolol, a beta 1 blocking agent, is being used with increasing frequency during pregnancy for treatment of disorders such as hypertension or beta-mimetic induced tachycardia. Since it is well documented that beta-blocking agents are able to cross the placenta, the question arises whether these drugs have any adverse effect on the fetal metabolic or cardiovascular system. It was the aim of this animal experimental study to investigate the following questions: 1. Does metoprolol exert a negative influence on fetal metabolic and cardiovascular functions during normoxia? 2. Is the fetal reaction to an acute short period of hypoxemia altered by metoprolol? To answer these questions, experiments were carried out in 6 pregnant sheep at 110-130 days of gestation. In 8 experiments metoprolol was infused into a fetal vein in increasing dosage (0,04-0,32 mg/min). In a second series of experiments (n = 8), an acute hypoxemia was induced by complete reduction of uterine blood flow for 1 minute, and the results obtained with or without metoprolol were compared. Metoprolol does not exert a negative influence on fetal oxygenation, acid-base balance, lactate concentration and blood pressure, although the metoprolol concentration measured in fetal plasma was relatively high (two - to threefold above therapeutic metoprolol levels). Thus, definitive adverse effects on the fetus induced by metoprolol are not recognizable. The fetal sympathoadrenal reaction to an acute hypoxemia, as measured by the concentration of the free catecholamines epinephrine, norepinephrine and dopamine in the fetal plasma, is also unchanged by metoprolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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A number of physiological, pharmacological and pathological stimuli initiate cardiac hypertrophy. The intracellular signalling events activated by these stimuli are equally complex. Our ability to treat the hypertrophic and failing myocardium effectively will require clarification of which signalling events regulate growth, remodelling and failure. Much recent attention has focused on the regulation of the mitogen-activated protein kinase cascades (MAPKs), with the importance of these cascades in the development of cardiovascular diseases being extensively explored. These signalling pathways may provide one link from the diverse stress and pharmacological extracellular stimuli to the regulation of gene expression, contractile protein regulation and protein function. This review focuses on the recent progress made in the understanding of the regulation and function of MAPKs in the cardiovascular system, with particular emphasis being placed on the events in the cardiac ventricular myocyte.
ATP is normally available in cells at millimolar concentrations and is "buffered" by intracellular pools of other high-energy phosphates, such as creatine phosphate. Thus intracellular [ATP] [( ATP]i) may seem an unlikely candidate for a regulatory signal inside cells. Recent evidence suggests, however, that [ATP]i regulates the behavior of a class of potassium (KATP) channels that are found throughout the cardiovascular system. KATP channels are present in cardiac, skeletal, and vascular smooth muscle. The channels are inhibited by micromolar [ATP]i, and this inhibition is relieved by micromolar [ADP]i. We present evidence in support of the idea that variations of [ATP]i and [ADP]i, even within normal concentration ranges, may influence cellular function in the heart and vascular system via a direct action on the KATP channel. Furthermore, very specific modulators of KATP channel activity are available. We discuss the mechanism of action of these agents and their interaction with endogenous modulators and consider their potential roles in cardiovascular therapy.
It has been slightly more than 10 years since the first proof-of-concept studies were performed, which demonstrated the feasibility of gene transfer into the heart and vasculature of experimental animals. Since that time there has been a dramatic increase in the nature and sophistication of gene transfer techniques and also in the number of cardiovascular diseases that are potential targets for gene-based therapies. In this article, the authors review the current strategies for gene delivery, including viral and nonviral approaches. The authors also highlight several biologic processes within the cardiovascular system, including restenosis, experimental angiogenesis, heart failure, and atherosclerosis-conditions for which gene therapy shows promise. It is hoped that this will provide an update of this therapeutic strategy for the year 2000.