Mitochondrial function, oxygen extraction, epicardial S-T segment changes and tritiated digoxin distribution after reperfusion of ischemic myocardium

Kane, James J.; Murphy, Marvin L.; Bisset, Joe K.; deSoyza, Neil; Doherty, James E.; Straub, K. D.

doi:10.1016/0002-9149(75)90530-5

Cited by 109 publications

(21 citation statements)

References 16 publications

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“…A produção de lactato continuou a aumentar durante os primeiros dez minutos de reperfusão. Este metabolismo anaeróbico, na presença de uma provável liberação de oxigênio, pode indicar a presença de uma disfunção temporária das células miocárdicas (27,28) . Somente aos 60 minutos de reperfusão cessou-se a produção de lactato.…”

Section: Níveis Plasmáticos Da Enzima Ck-mbunclassified

Metabolismo miocárdico após cardioplegia sangüínea hipotérmica retrógrada contínua

Sobrosa¹,

Jansson²,

Kaijser³

et al. 2000

Rev Bras Cir Cardiovasc

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INTRODUÇÃOO grande desenvolvimento da cirurgia cardíaca nos últimos trinta anos se deve muito à reintrodução da cardioplegia cristalóide hiperpotássica no final da Sobrosa C G, Jansson E, Kaijser L, Bomfim V -Metabolismo miocárdico após cardioplegia sangüínea hipotérmica retrógrada contínua. Rev Bras Cir Cardiovasc 2000; 15 (3): 219-26.RESUMO: Casuística e Métodos: Realizamos uma análise metabólica da cardioplegia sangüínea hipotérmica retrógrada contínua em um estudo prospectivo de 15 pacientes consecutivos encaminhados para operação eletiva de revascularização miocárdica. Os critérios de inclusão foram doença coronária bi ou triarterial e função ventricular preservada (FE > 40%). Os critérios de exclusão foram angina instável, diabéticos insulino-dependentes e operações associadas. Três pacientes foram excluídos do trabalho (operação associada e deslocamento do cateter de cardioplegia retrógrada). Amostras de sangue arterial e do seio coronário foram simultaneamente colhidas: antes do início da CEC, na abertura da aorta e com 10, 30 e 60 minutos de reperfusão, para análise do conteúdo de oxigênio e da concentração de lactato. Quatro biópsias miocárdicas foram obtidas do ápice do ventrículo esquerdo: (1) após instalação da CEC (mas antes do pinçamento aórtico), (2) imediatamente após o término da indução cardioplégica, (3) antes do despinçamento aórtico e (4) com 30 minutos de reperfusão, para análise dos níveis de ATP, ADP, AMP e lactato no miocárdio. A isoenzima CK-MB foi analisada no sangue venoso.Resultados: Não houve mortalidade no grupo. Houve uma diminuição da extração artério-venosa do lactato e do oxigênio pelo coração durante a reperfusão, somente havendo uma recuperação parcial ao final de 60 minutos de reperfusão. O ATP e os outros nucleotídeos tiveram os seus níveis mantidos no miocárdio durante o pinçamento aórtico, mas estes caíram nos primeiros 30 minutos de reperfusão. O lactato acumulouse no músculo cardíaco durante o pinçamento aórtico e diminuiu durante a reperfusão. Houve um aumento da enzima CK-MB, principalmente entre a terceira e sexta horas de pós-operatório.Conclusões: Do ponto de vista metabólico, o método não evitou o metabolismo anaeróbico durante o período de pinçamento aórtico e que somente com 60 minutos de reperfusão houve uma recuperação metabólica parcial. Essas alterações são, provavelmente, o reflexo da injúria isquêmica celular ocorrida durante o pinçamento aórtico e são de efeito transitório. DESCRITORES: Miocárdio, metabolismo. Parada cardíaca induzida, métodos. Hipotermia induzida, métodos. Miocárdio, metabolismo. Miocárdio, efeito de drogas. Reperfusão miocárdica. Coração, fisiologia. Revascularização miocárdica. década de sessenta. O desafio de realizar cirurgias mais complexas em pacientes mais idosos e mais graves e melhorar as técnicas cirúrgicas e conseqüentemente com tempo de pinçamento aórtico mais prolongado, estimulou muito as pesquisas no campo

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Section: Níveis Plasmáticos Da Enzima Ck-mbunclassified

Metabolismo miocárdico após cardioplegia sangüínea hipotérmica retrógrada contínua

Sobrosa¹,

Jansson²,

Kaijser³

et al. 2000

Rev Bras Cir Cardiovasc

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“…Excess succinate, a substrate for complex II, has been shown to support ETC activity (Kane et al, 1975;Melnick and Schiller, 1985;Hekman et al, 1988;Takehara et al, 1995). Therefore, the effect of 5 mM succinate on mitochondrial calcium buffering was examined in mitochondrial-defective AD cybrid lines.…”

Section: Effect Of the Complex II Substrate Succinate On The Recoverymentioning

confidence: 99%

Calcium Homeostasis and Reactive Oxygen Species Production in Cells Transformed by Mitochondria from Individuals with Sporadic Alzheimer’s Disease

Sheehan

Swerdlow

Miller³

et al. 1997

J. Neurosci.

241

140

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Alzheimer's disease (AD) is associated with defects in mitochondrial function. Mitochondrial-based disturbances in calcium homeostasis, reactive oxygen species (ROS) generation, and amyloid metabolism have been implicated in the pathophysiology of sporadic AD. The cellular consequences of mitochondrial dysfunction, however, are not known. To examine these consequences, mitochondrially transformed cells (cybrids) were created from AD patients or disease-free controls. Mitochondria from platelets were fused to 0 cells created by depleting the human neuroblastoma line SH-SY5Y of its mitochondrial DNA (mtDNA). AD cybrids demonstrated a 52% decrease in electron transport chain (ETC) complex IV activity but no difference in complex I activity compared with control cybrids or SH-SY5Y cells. This mitochondrial dysfunction suggests a transferable mtDNA defect associated with AD. ROS generation was elevated in the AD cybrids. AD cybrids also displayed an increased basal cytosolic calcium concentration and enhanced sensitivity to inositol-1,4,5-triphosphate (InsP 3 )-mediated release. Furthermore, they recovered more slowly from an elevation in cytosolic calcium induced by the InsP 3 agonist carbachol. Mitochondrial calcium buffering plays a major role after this type of perturbation. ␤-amyloid (25-35) peptide delayed the initiation of calcium recovery to a carbachol challenge and slowed the recovery rate. Nerve growth factor reduced the carbachol-induced maximum and moderated the recovery kinetics. Succinate increased ETC activity and partially restored the AD cybrid recovery rate. These subtle alterations in calcium homeostasis and ROS generation might lead to increased susceptibility to cell death under circumstances not ordinarily toxic.

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“…On the other hand, only scattered and conflicting information regarding the status of mitochondrial function with respect to their respiratory and oxidative phosphorylation activities in the I/R hearts is available in the literature (3,19). It is pointed out that, whereas prolonged ischemia has been reported to depress mitochondrial state 3 respiration and slightly reduce their ability to generate ATP (8,23), reperfusion of the ischemic heart has been shown to produce no change (1,45), further depression (17,22), or increase in the oxidative phopshorylation rate (OPR) (24,35). In addition, some investigators (13,16) have shown depressions in both mitochondrial state 3 and state 4 respiration without any change in respiratory control index (RCI), whereas others (9) have reported no change in state 3 respiration but an increase in state 4 respiration in I/R hearts.…”

mentioning

confidence: 99%

Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts

Makazan¹,

Saini²,

Dhalla³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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Makazan Z, Saini HK, Dhalla NS. Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts. Am J Physiol Heart Circ Physiol 292: H1986 -H1994, 2007. First published December 15, 2006; doi:10.1152/ajpheart.01214.2006.-To study the mechanisms of mitochondrial dysfunction due to ischemiareperfusion (I/R) injury, rat hearts were subjected to 20 or 30 min of global ischemia followed by 30 min of reperfusion. After recording both left ventricular developed pressure (LVDP) and end-diastolic pressure (LVEDP) to monitor the status of cardiac performance, mitochondria from these hearts were isolated to determine respiratory and oxidative phosphorylation activities. Although hearts subjected to 20 min of ischemia failed to generate LVDP and showed a marked increase in LVEDP, no changes in mitochondrial respiration and phosphorylation were observed. Reperfusion of 20-min ischemic hearts depressed mitochondrial function significantly but recovered LVDP completely and lowered the elevated LVEDP. On the other hand, depressed LVDP and elevated LVEDP in 30-min ischemic hearts were associated with depressions in both mitochondrial respiration and oxidative phosphorylation. Reperfusion of 30-min ischemic hearts elevated LVEDP, attenuated LVDP, and decreased mitochondrial state 3 and uncoupled respiration, respiratory control index, ADP-to-O ratio, as well as oxidative phosphorylation rate. Alterations of cardiac performance and mitochondrial function in I/R hearts were attenuated or prevented by pretreatment with oxyradical scavenging mixture (superoxide dismutase and catalase) or antioxidants [N-acetyl-L-cysteine or N-(2-mercaptopropionyl)-glycine]. Furthermore, alterations in cardiac performance and mitochondrial function due to I/R were simulated by an oxyradical-generating system (xanthine plus xanthine oxidase) and an oxidant (H 2O2) either upon perfusing the heart or upon incubation with mitochondria. These results support the view that oxidative stress plays an important role in inducing changes in cardiac performance and mitochondrial function due to I/R. cardiac performance; oxidative phosphorylation; mitochondrial respiration; oxyradicals; antioxidants BY VIRTUE OF THEIR ABILITY to carry on the processes of oxidative phosphorylation and electron transport, mitochondria are the major source of energy production in the form of ATP, which is required for cardiac contraction and relaxation (19,26,46). Mitochondria are also known to accumulate a substantial amount of Ca 2ϩ and are considered to serve as a sink to maintain the intracellular concentration of free Ca 2ϩ within certain limits (18,19,26). However, an excessive amount of intracellular Ca 2ϩ results in the overloading of mitochondria with Ca 2ϩ

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Mitochondrial function, oxygen extraction, epicardial S-T segment changes and tritiated digoxin distribution after reperfusion of ischemic myocardium

Cited by 109 publications

References 16 publications

Metabolismo miocárdico após cardioplegia sangüínea hipotérmica retrógrada contínua

Metabolismo miocárdico após cardioplegia sangüínea hipotérmica retrógrada contínua

Calcium Homeostasis and Reactive Oxygen Species Production in Cells Transformed by Mitochondria from Individuals with Sporadic Alzheimer’s Disease

Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts

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