Cardiac surgical implications of calcium dyshomeostasis in the heart

Meldrum, Daniel R.; Cleveland, Joseph C.; Sheridan, Brett C.; Rowland, Robert T.; Banerjee, Anirban; Harken, Alden H.

doi:10.1016/0003-4975(95)00952-3

Cited by 60 publications

(39 citation statements)

References 48 publications

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“…After hyperkalemic arrest, endothelium-dependent relaxation is moderately impaired (7), possibly due to changes in membrane potential (11,12), NOS substrate and cofactor depletion, alterations in concentration or compartmentalization of intracellular calcium (13,14), or injury to the cell membranes and associated enzymes and ion pumps. In addition, the release of NO from the constitutive isoform of NOS (eNOS) is reduced after ischemia and cardioplegia, as determined by direct measurement (15).…”

Section: Cardioplegia and Endothelial Function Effects On Nitric Oxidmentioning

confidence: 99%

Vascular changes after cardiopulmonary bypass and ischemic cardiac arrest: roles of nitric oxide synthase and cyclooxygenase

Sellke

1999

Braz J Med Biol Res

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Cardiac surgery involving ischemic arrest and extracorporeal circulation is often associated with alterations in vascular reactivity and permeability due to changes in the expression and activity of isoforms of nitric oxide synthase and cyclooxygenase. These inflammatory changes may manifest as systemic hypotension, coronary spasm or contraction, myocardial failure, and dysfunction of the lungs, gut, brain and other organs. In addition, endothelial dysfunction may increase the occurrence of late cardiac events such as graft thrombosis and myocardial infarction. These vascular changes may lead to increased mortality and morbidity and markedly lengthen the time of hospitalization and cost of cardiac surgery. Developing a better understanding of the vascular changes operating through nitric oxide synthase and cyclooxygenase may improve the care and help decrease the cost of cardiovascular operations. Correspondence

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Section: Cardioplegia and Endothelial Function Effects On Nitric Oxidmentioning

confidence: 99%

Vascular changes after cardiopulmonary bypass and ischemic cardiac arrest: roles of nitric oxide synthase and cyclooxygenase

Sellke

1999

Braz J Med Biol Res

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“…[27][28][29] Consequently, one of the important issues for the preservation of cardiac function is the inhibition of cytokine production.…”

Section: Discussionmentioning

confidence: 99%

The Suppression of Proinflammatory Cytokines Improves Heart Function From Non-Heart-Beating Donors Following Transplantation in a Canine Model

et al. 2009

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SummaryWe evaluated the effectiveness of a suppressant of the production of proinflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)-α on a canine heart transplantation model with non-heart-beating donors (NHBDs).Adult mongrel dogs were divided into 3 groups of 5: a control group; FR-1 in which donors were given FR167653, a potent suppressant of IL-1 β and TNF-α production; and FR-2 in which both donors and recipients were given FR167653. After measuring the baseline hemodynamic parameters, including cardiac output (CO), left ventricular pressure (LVP), and maximum and minimum rates of increase in LVP (± LVdp/dt), FR167653 was administered continuously for 30 minutes before ischemia in the FR-1 and FR-2 groups. Cardiac arrest was obtained by rapid exsanguination from the abdominal aorta and inferior vena cava. The organ was left in the cadaver for 30 minutes. The coronary vascular beds were washed out with 4°C Celsior solution, and then the donor heart was preserved in 4°C Celsior solution for 4 hours. The donor heart was transplanted orthotopically with cardiopulmonary bypass (CPB). FR167653 was administered intravenously from 15 minutes before aortic-cross clamping until the end of the experiment in the FR-2 group. The recipient was weaned from CPB 1 hour after reperfusion. We compared the hemodynamic parameters at 3 hours after reperfusion with the preoperative values in donor animals with the right atrial pressure at 10 mmHg and a 5 μg/kg/min dopamine infusion. Histopathological analysis was also performed.There were no significant differences in the recovery rates of the hemodynamic parameters between the control and FR-1 groups and between the FR-1 and FR-2 groups. However, the recovery rates of CO and -LVdp/dt in the FR-2 group were significantly (P < 0.05) higher than those in the control group. Histopathological analysis showed that myofilaments were better preserved in the FR-2 group compared with the control group.The administration of a suppressant of proinflammatory cytokines before both ischemia and reperfusion effectively preserves donor heart function after transplantation with NHBDs. (Int Heart J 2009; 50: 235-245) From the

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“…Calcium regulatory proteins such as sarcolemmal Ca 2ϩ -ATPase or sarcoplasmatic reticulum Ca 2ϩ -ATPase show energy dependency. Their impairment can cause a decrease in contractile performance (12). Alterations of myocardial energy-dependent processes after administration of TNF-␣ might therefore contribute to impaired force development.…”

Section: Discussionmentioning

confidence: 99%

Increased myocardial oxygen consumption by TNF-α is mediated by a sphingosine signaling pathway

Hofmann

Domeier

Frantz

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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The present study investigated the effect of tumor necrosis factor (TNF)-␣ on myocardial energy metabolism as estimated by myocardial oxygen consumption (MV O2). MV O2 of electrically stimulated isolated trabeculae of right ventricular Wistar rat myocardium was analyzed using a Clark-type oxygen probe. After the initial data collection in the absence of TNF-␣, measurements were repeated after TNF-␣ stimulation. In separate experiments, pretreatment with the nitric oxide (NO) synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME) or the ceramidase inhibitor n-oleoylethanolamine (NOE) was done to investigate NO/sphingosine-related effects. TNF-␣ impaired myocardial economy at increasing stimulation frequencies without altering baseline MV O2. Incubation with TNF-␣ in the presence of L-NAME further impaired myocardial economy. NOE preincubation abrogated the TNF-␣ effect on myocardial economy. Moreover, the negative inotropic effect of TNF-␣ was observed in NOE-pretreated but not L-NAME-pretreated muscle fibers. Exogenous sphingosine mimicked the TNF-␣ effect on mechanics and energetics. We conclude that TNF-␣ impairs the economy of chemomechanical energy transduction primarily through a sphingosine-mediated pathway. cytokines; nitric oxide; myocardial energy metabolism; tumor necrosis factor-␣

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Cardiac surgical implications of calcium dyshomeostasis in the heart

Cited by 60 publications

References 48 publications

Vascular changes after cardiopulmonary bypass and ischemic cardiac arrest: roles of nitric oxide synthase and cyclooxygenase

Vascular changes after cardiopulmonary bypass and ischemic cardiac arrest: roles of nitric oxide synthase and cyclooxygenase

The Suppression of Proinflammatory Cytokines Improves Heart Function From Non-Heart-Beating Donors Following Transplantation in a Canine Model

Increased myocardial oxygen consumption by TNF-α is mediated by a sphingosine signaling pathway

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