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At least 1,495 records · Page 83Linked to original sources
PubMed1996

Improved cardiac function after prolonged hypothermic ischemia with the Na+/H+ exchange inhibitor HOE 694.

BACKGROUND: Na+/H+ exchange represents an important mechanism for pH regulation in the cardiac cell that, however, may paradoxically mediate tissue damage in the reperfused myocardium. We investigated whether inhibition of the exchanger can protect the heart against damage after prolonged hypothermic storage with the use of the selective inhibitor 3-methylsulfonyl-4-piperidinobenzoyl-guanidine methanesulfonate (HOE 694). METHODS: After equilibration, isolated rabbit hearts were arrested with a 3 minute infusion of modified St. Thomas' cardioplegic solution and subsequently maintained in ischemic arrest at 4 degrees C for 12 hours before reperfusion at 37 degrees C for 60 minutes. Left ventricular function and creatine kinase release were measured at intervals throughout reperfusion. High-energy phosphate and adenine nucleotide content were determined in hearts before cardioplegia, at the end of the 12-hour storage period, and at the end of reperfusion. HOE 694 (1 mumol/L) was administered either with cardioplegia and throughout reperfusion (study 1) or selectively with either cardioplegia or reperfusion only (study 2). RESULTS: In study 1, systolic function in untreated hearts recovered to less than 40% of preischemic values and was associated with a greater than 1,000% percent sustained elevation in left ventricular end-diastolic pressure. In contrast, systolic recovery in HOE 694-treated hearts was significantly accelerated and improved to approximately 80%, whereas left ventricular end-diastolic pressure increased to only 300% of baseline. Significant protection also occurred in those hearts in which HOE 694 was administered only at reperfusion while the drug was less effective if given only during cardioplegia. Creatine kinase release was not significantly affected except in study 2, where it was significantly lower after 60 minutes of reperfusion in hearts where HOE 694 was added at the time of reperfusion. Tissue metabolite content was not affected by drug treatment. CONCLUSIONS: This study shows a marked protective effect of the Na+/H+ exchange inhibitor HOE 694 in rabbit hearts subjected to 12 hours of hypothermic ischemia and strongly suggests that antiport inhibitors could play an effective role in myocardial preservation.

Animals↗
PubMed1992

The influence of vasodilating beta-blockers on cardiac function and vascular resistance in essential hypertension.

In nearly all forms of established hypertension, the cardinal hemodynamic disturbance is an increased total peripheral resistance, while cardiac output is abnormally low, particularly during exercise. When left untreated, total peripheral resistance increases, cardiac output falls, and blood pressure increases over time. The coronary reserve is reduced, and renal as well as cerebral resistance increases and blood flow falls. Antihypertensive agents effect central hemodynamics differently. Ordinary beta-blockers do usually not reduce total peripheral resistance much below pretreatment level, and cardiac output is chronically depressed, particularly during exercise. However, the beta-blockers greatly reduce the workload on the heart by decreasing the heart rate-pressure product. Modern beta-blockers with vasodilating activity--like carvedilol--are based on a combination of beta-blockade and vasodilatation. Such beta-blockers also induce a marked decrease in the pressure-heart rate product, and some reduction in total peripheral resistance. They cause less depression of exercise cardiac output than ordinary beta-blockers. Blood flow to the kidneys and the brain is maintained. From a theoretical point of view, this type of antihypertensive treatment should maintain good blood pressure control, reduce cardiac workload and be associated with less side-effects than ordinary beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1989

Delta and Mu receptor agonists correlate with greater depression of cardiac function than morphine sulfate in perfused rat hearts.

In previous studies done in our laboratory, we demonstrated that morphine sulfate could depress heart rate and cardiac output when added to the perfusate of a working rat heart model using a modified Langendorff preparation. In this study we investigated three different delta agonists and a mu agonist by adding each to the perfusate in a fashion similar to the experiments done with morphine sulfate. We found that all three delta agonists, leu-enkephalin, D-ala-D-leu-enkephalin (DADL), and D-Pen enkephalin, would significantly decrease cardiac output. In the case of D-Pen enkephalin, heart rate and stroke volume were also significantly decreased. Additionally the mu agonist Tyr-D-ala-gly-N-met-phe-gly-ol (DAGO) also caused a significant decrease in heart rate, cardiac output, and stroke volume. The data suggest that all three delta agonists and DAGO are capable of depressing heart rate, cardiac output, and stroke volume at concentrations between 10(3) and 10(4) lower than those used in studies with morphine sulfate.

Animals↗
PubMed1978

Serial studies of cardiac function in patients receiving adriamycin.

A total of 283 adult and pediatric patients treated with drug combinations which include adriamycin (ADM) had at least one cardiac evaluation; 103 patients had two or more serial studies after a baseline evaluation. Changes in systolic time intervals, echocardiographically determined ejection fractions, and electrocardiographic voltage correlated with increasing cumulative ADM dosage. However, the incidence of congestive heart failure among these patients was less than 2%. It is estimated that 22%-31% of these patients would not have completed a cumulative dose of greater than 450 mg/m2 of ADM if the drug had been discontinued on the basis of these tests, using previously published criteria for cessation of treatment. Thus far, however, no adverse effects have been observed from the completion of planned courses of therapy. The clinical significance of serial changes in noninvasive tests is therefore uncertain. While such changes may reflect subclinical anthracycline cardiotoxicity and clinical cardiotoxicity can reliably be diagnosed, the utility of routine, serial noninvasie testing in planning conventional-dose anthracycline therapy is questionable.

Adolescent↗
PubMed2005

Evaluation of cardiac function by tissue Doppler echocardiography: hemodynamic determinants and clinical application.

A total of 32 patients without regional wall motion abnormality of the left ventricle underwent sequential tissue Doppler echocardiography and cardiac catheterization. Peak velocities of systolic (Sa), early diastolic (Ea), and late diastolic (Aa) motion of the mitral annulus were measured. Normal references for Sa, Ea and Aa were obtained from 138 volunteers. Indices of left ventricular (LV) systolic and diastolic function were evaluated using high-fidelity LV pressure and volume signals. By multivariate analysis, Sa, Ea and As were significantly and independently related to the maximum of the first derivative of pressure over time (dP/dt(max)), LV relaxation time constant (tau), and LV ejection fraction (EF), respectively. Using the fifth percentiles of the age-stratified normal references as cut-offs, low Sa, low Ea and low Aa identified declined dP/dt(max), prolonged tau and reduced EF, respectively, with good sensitivities and specificities. In conclusion, mitral annulus velocities by tissue Doppler echocardiography can be used to identify patients with declined dP/dt(max), prolonged tau and reduced EF.

Adult↗
PubMed1999

Haemoglobin, blood volume, cardiac function, and aerobic power.

Alterations in [Hb], which are mediated through changes in arterial oxygen content, and alterations in BV, which are mediated through changes in cardiac output (Q), have a significant effect on both VO2max and aerobic performance. If BV is held constant, a decrease in [Hb] (anaemia) causes a decrease in VO2max and aerobic performance, while an increase in [Hb] (blood doping) causes an increase in VO2max and aerobic performance. If [Hb] is held constant, an increase in BV can cause and increase in both VO2max and aerobic performance, while a decrease in BV can cause a decrease in VO2max and aerobic performance. In addition, an increase in BV can compensate for moderate reductions in [Hb] through increase in Q, allowing VO2max to remain unchanged or even increase. Also, a large portion of the difference in the enhanced cardiovascular function of endurance athletes is due to their high BV and the resultant enhancement of diastolic function. Hence, optimizing both [Hb] and BV is a very important consideration for endurance performance.

Anemia, Iron-Deficiency↗
PubMed1998

Central venous pressure and cardiac function during spaceflight.

Early in spaceflight, an apparently paradoxical condition occurs in which, despite an externally visible headward fluid shift, measured central venous pressure is lower but stroke volume and cardiac output are higher, and heart rate is unchanged from reference measurements made before flight. This paper presents a set of studies in which a simple three-compartment, steady-state model of cardiovascular function is used, providing insight into the contributions made by the major mechanisms that could be responsible for these events. On the basis of these studies, we conclude that, during weightless spaceflight, the chest relaxes with a concomitant shape change that increases the volume of the closed chest cavity. This leads to a decrease in intrapleural pressure, ultimately causing a shift of blood into the vessels of the chest, increasing the transmural filling pressure of the heart, and decreasing the central venous pressure. The increase in the transmural filling pressure of the heart is responsible, through a Starling-type mechanism, for the observed increases in heart size, left ventricular end-diastolic volume, stroke volume, and cardiac output.

Blood Pressure↗
PubMed2002

Cardiac function: MR evaluation in one breath hold with real-time true fast imaging with steady-state precession.

In 12 healthy volunteers and eight patients with cardiac disease, cine magnetic resonance (MR) imaging in the heart was performed with real-time true fast imaging with steady-state precession (FISP), which permitted evaluation of the entire left ventricle in one breath hold (91 msec per frame, 13 frames per section position, nine short-axis section positions per breath hold). Contrast-to-noise ratios (CNRs) and left ventricular mass and function measurements with this technique were compared in all subjects with single-section true FISP imaging and, in the volunteers only, with segmented fast low-angle shot (FLASH) MR imaging. Myocardium-to-blood CNR was significantly higher for both true FISP sequences compared with the FLASH sequence. Measurements of resting left ventricular function with real-time true FISP imaging were comparable with those derived from a series of separate breath-hold single-section true FISP acquisitions.

Adult↗
PubMed1990

Effects of beta-adrenoceptor antagonists on cardiac function in ischemic-reperfused myocardium of the isolated working rabbit heart.

The effects of beta-adrenoceptor antagonists (dl-nebivolol, atenolol and propranolol) and of 1-nebivolol on cardiodynamics and mitochondrial oxidative phosphorylation were studied in the isolated working rabbit heart subjected to normothermic global ischemia, followed, in some cases, by reperfusion. The hearts were pretreated with the different drugs (0.32 mg/l) 30 min before the start of ischemia, dl-Nebivolol and propranolol provided protection for both cardiodynamic and mitochondrial functions, as did l-nebivolol, which lacks beta-adrenoceptor blocking properties, while atenolol failed to protect mechanical activity and cardiac mitochondria against the effects of ischemia and post-ischemic reperfusion. Catecholamine depletion with reserpine did not have a beneficial effect on the recovery of cardiodynamic and mitochondrial function during post-ischemic reperfusion. It is concluded that the beneficial effects of beta-blockers on the ischemic and reperfused myocardium can not be explained by a specific beta-blocking action alone.

Adrenergic beta-Antagonists↗