Effect of Peroxide, Sodium, and Calcium on Brain Mitochondrial Respiration In Vitro: Potential Role in Cerebral Ischemia and Reperfusion

Vlessis, Angelo A.; Widener, Linda L.; Bartos, Dagmar

doi:10.1111/j.1471-4159.1990.tb01977.x

Cited by 44 publications

(20 citation statements)

References 36 publications

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“…Furthermore, sodium itself can potentiate calcium inhibition of state 3 respiration in isolated mitochondria. 30 This analysis of the free energies involved in sodium transport does not explain the apparent decrease in the sodium gradient before significant loss of ATP. Perhaps there is a large increase in inward Na + permeability preceding the full loss of ATP during ischemia.…”

mentioning

confidence: 99%

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Eleff

Maruki

Monsein

et al. 1991

Stroke

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We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 ±5 to 0-3 ±0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4±4.8 minutes) than either adenosine triphosphate (16.5±3.7 minutes) or intracellular pH (38.9±1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient (Stroke 1991^2:233-241) T he application of magnetic resonance spectroscopy (MRS) to in situ brain allows the time course of ischemically perturbed cerebral bioenergetics as reflected by adenosine triphosphate (ATP), phosphocreatine, and intracellular pH 1 -2 and transcellular sodium gradient 3 to be examined. The potential interactions of brain sodium gradients, intracellular pH, and bioenergetics are many. Maintenance of a normal sodium gradient, necessary for normal neurologic function, is an ATP- Received May 25, 1990; accepted October 17, 1990. dependent process and accounts for 40% of the metabolic demand of the brain as assessed by highdose lidocaine during barbiturate coma. 4 Maintenance of a normal intracellular pH is critical for proper functioning of most enzymatic processes. With the onset of complete ischemia, intracellular pH falls as glucose stores are converted to lactic acid and ATP is hydrolyzed.5 Soon after ATP depletion, extracellular Na + activity decreases. 6 However, Na + influx may precede the sudden decrease in extracellular Na + activity as measured by microelectrodes if this early Na + influx is accompanied by sufficient water to maintain a constant sodium activity. On reperfusion, limited ATP generation may be diverted into restoring ionic gradients instead of main...

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confidence: 99%

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Eleff

Maruki

Monsein

et al. 1991

Stroke

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“…It has been reported that the high metabolic rates associated with reperfusion injury can lead to excess oxygen radical production (Vlessis et al, 1990). At the onset of ischemia there is an accumulation of hypoxanthine due to breakdown of adenine nucleotides.…”

Section: Factors Associated With Excess Formation Of Cerebral Reactivmentioning

confidence: 99%

Oxidative damage and cerebral aging

LeBel

Bondy

1992

Progress in Neurobiology

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“…As described above, many studies have demonstrated that reactive oxygen species (ROS) and the resulting oxidative stress play a pivotal role in neuronal cell death (Flamm et al, 1978;Fridovich, 1979;Hall and Braughler, 1993;Kontos, 1989;Siesjo et al, 1985;Vlessis et al, 1990). There are two major regions in the electron transport chain where ROS are produced.…”

Section: Ipc and Mitochondrial Protection In The 2nd Windowmentioning

confidence: 99%

“…This hyperoxidation of electron carriers is indicative of either a response to decreased substrate availability and/or a reaction of mitochondrial complexes to reactive oxygen species (ROS) (Perez-Pinzon et al, 1997b). Postischemic mitochondrial may also be a major source of ROS, and free radical-mediated damage has been linked to reperfusion injury following brain ischemia (Flamm et al, 1978;Fridovich, 1979;Hall and Braughler, 1993;Kontos, 1989;Siesjo et al, 1985;Vlessis et al, 1990). However, recent findings suggest that this hyperoxidation may result from loss of electron carriers from mitochondria following cerebral ischemia, such as cytochrome c and NADH (Perez-Pinzon et al, 1999c).…”

Section: Neuroprotective Effects Of Ischemic Preconditioning In Brainmentioning

confidence: 99%

Perioperative Neuroprotection Symposium

Fiskum¹

2004

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Public reporting burden for this collection of information is estimated to average 1 hour par the data needed, and completing and reviewing this collection of information. Send conranls reducing this burden to Washington Headquarters Services. Directorate for Information Operations Management and Budget, Paperwork Reduction Protect (0704-01681. Washington, DC 20803Indudkig the «ma for reviewing instructions, searching existing data sources, gathering and maintaining tMs burden estimate or any other aspect of this ooHecMon of information, including suggestions for 1218 Jefferson Davis Highway, Suite 1204, Arttngton, VA 22202-4302, and to the Office of AGENCY USE ONLY (Leave blank) REPORT DATE June 2004 REPORT TYPE AND DATES COVERED Final Proceedings (13 Sep 03-22 May 04) TITLE AND SUBTITLE Perioperative Neuroprotection Symposium AUTHOR(S)Gary Fiskum, Ph.D. S. FUNDING NUMBERS DAMD17-03-1-0500 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Maryland, Baltimore Baltimore, MD 21201 E-Mail: gfisk001@umaryland.edu PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSORING / MONITORING AGENCY REPORT NUMBER SUPPLEMENTARY NOTESOriginal contains color plates: ALL DTIC reproductions will be in black and white 12a. DISTRIBUTION / AVAILABILITY STATEMENT Approved for Public Release; Distribution Unlimited 12b. DISTRIBUTION CODE A-TRACT IMaiiliwyiH 200 VVwW)The Perioperative Neuroprotection Symposium was held on April 16-19 in Ft. Lauderdale, Fl. The meeting was attended by approximately 140 registrant». Twenty four invited speakers made presentations in five sessions. An additional 40 poster presentations were^available for discussion throughout the meeting. Each participant received a symposium abstract book that included mini-reviews from each of the speakers and the short abstracts from the posters. The speakers also submitted formal manuscripts for peer-reviewed publication.Five of the poster presenters were also invited to submit short research manuscripts. Mitochondria and Neuroprotection Symposium April [16][17][18][19] 2004 Albert Lester Lehninger February 17,1917-March4,1986 Albert Lehninger was born in Bridgeport, Connecticut and received a B.A. in English from Wesleyan University in 1939. He received his Ph.D. in Physiological Chemistry from the University of Wisconsin in 1942. Lehninger stayed on at the Univ. of Wisconsin as an Instructor until 1945, when he was appointed Assistant Professor of Biochemistry and Surgery at the University of Chicago. At this juncture he had published 11 research articles. From 1945From -1952, he published an additional 33 articles. These studies included the discovery that fatty acid oxidation, ketone body metabolism, and the TCA cycle occur in the mitochondrion, some of the first investigations employing isolation of this organelle (see e.g., JBC1949 and 1950). Thus, while Lehninger was a chemist at heart, he was one of the founding father...

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Effect of Peroxide, Sodium, and Calcium on Brain Mitochondrial Respiration In Vitro: Potential Role in Cerebral Ischemia and Reperfusion

Cited by 44 publications

References 36 publications

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

Oxidative damage and cerebral aging

Perioperative Neuroprotection Symposium

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