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G K Asimakis

Publications and source records attributed to G K Asimakis.

30 records · Page 2Linked to original sources
PubMed1984

Myocardial ischemia: correlation of mitochondrial adenine nucleotide and respiratory function.

State 3 respiration of rat heart mitochondria decreased approximately 60% after 20 min normothermic in vitro ischemia. After 20 min ischemia, the levels of intramitochondrial adenine nucleotides (ATP + ADP + AMP) decreased to approximately 20% of control values, with a rapid loss between 10 and 20 min. Also, the exchangeable adenine pool of the mitochondria decreased 60% after 20 min ischemia. State 4 respiration was not affected by the ischemic insult. The adenine nucleotide translocase activities of mitochondria from control and ischemic hearts were too high to measure accurately. Therefore, the effects of ischemia on adenine nucleotide translocase activity could not be established. However, 1 microM carboxyatractyloside did not impair state 3 respiration of control mitochondria, but did inhibit the adenine translocase activity by at least 80%. Moreover, titration of state 3 respiration with carboxyatractyloside produced sigmoidal curves for mitochondria from control and ischemic tissue. State 3 respiration correlated well with the total mitochondrial adenine nucleotides and the exchangeable adenine pool (r = 0.63 and 0.78, respectively). Data collected from isolated perfused rat hearts also showed a good correlation between state 3 respiration and the exchangeable adenine nucleotides (r = 0.92). In this study, mitochondria were isolated from hearts that were either perfused, made ischemic for 30 min by aortic cross-clamp, or reperfused for 10 min after the aortic cross-clamp. The slopes and y-intercepts of the regression lines were similar for the in vitro ischemic and the perfusion studies. There was no significant difference between the effects of ischemia on the state 3 and uncoupled respiratory rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1981

Intramitochondrial adenine nucleotides and energy-linked functions of heart mitochondria.

Isolated rabbit heart mitochondria were incubated with varying amounts of inorganic pyrophosphate in 250 mM sucrose to specifically decrease the pool size of endogenous adenine nucleotides. The endogenous adenine nucleotide content decreased by as much as 80% as a result of this treatment. Phosphorylating respiration (state 3) declined from about 340 to 180 nAtoms O . min-1 . mg protein-1 over the full range of intramitochondrial adenine nucleotides measured (approx 7.5-1.5 nmol/mg protein). Uncoupled and nonphosphorylating (state 4) rates of respiration were not greatly affected by adenine nucleotide depletion. Respiratory activity of the adenine nucleotide-depleted mitochondria was enhanced by addition of exogenous adenosine 5'-triphosphate (ATP). Partial depletion (approx 40%) of the intramitochondrial adenine nucleotides resulted in an impaired ability of heart mitochondria to retain Ca2+. Premature Ca2+ efflux was associated with organelle swelling and altered energy coupling. Exogenous ATP or adenosine 5'-diphosphate (ADP) added prior to Ca2+ efflux restored Ca2+ retention in these mitochondria. Atractyloside inhibited the restoration of Ca2+ retention. This study indicates a significant role for endogenous adenine nucleotides in maintaining oxidative phosphorylation and Ca2+ transport in heart mitochondria. The results are discussed with regard to significance in ischemic heart damage.

Adenine Nucleotides↗
PubMed1977

Functions of selected biochemical systems from the exercised-trained dog heart.

Mitochondria and sarcoplasmic reticulum (SR) fractions were isolated from exercised-trained (E-T) and sedentary control dog hearts. Measurements of mitochondrial respiratory functions indicated no changes in energy-producing (ATP synthesis) capacity in mitochondria from E-T compared to control dog hearts. However, the ability of isolated mitochondria from E-T hearts to retain accumulated calcium was markedly decreased compared to controls. Inhibition of mitochondrial rates of calcium uptake with the inhibitor, ruthenium red, revealed fewer binding and/or transport sites in mitochondrial membranes from exercised-trained heart preparations. ATP-dependent binding (- oxalate) and uptake (+ oxalate) of calcium by SR preparations from E-T hearts were unchanged compared to controls. In contrast, significant differences in the rates of release of bound calcium were found in SR isolated from E-T hearts. Total myocardial protein, nucleic acids, and connective tissue levels were unchanged in E-T hearts compared to controls. The results suggest subtle changes are occurring in the energy-utilizing mechanism(s) involving calcium transport of the myocardial cell during exercise training. These changes may be related to alterations in the performance of the exercised-trained heart.

Animals↗
PubMed1977

Contractile function and myofibrillar ATPase activity in the exercise-trained dog heart.

Myocardial contractility and the enzymatic (ATPase) activity of cardiac contractile proteins were examined after exercise training using the chronically instrumented, unanesthetized dog as an experimental model. Before training, heart rate and the maximum rate of left ventricular pressure development (max dP/dt) were measured at rest and during submaximal exercise. Animals were then subjected to an 8- to 10-wk treadmill running program. Training was verified by the establishment of a 10- to 20-beat/min reduction in heart rate during submaximal exercise. After training max dP/dt was within normal limits at rest, but significantly elevated during submaximal exercise. When max dP/dt was plotted as a function of heart rate, either with the animal standing quietly on the treadmill or during submaximal exercise, a marked elevation in max dP/dt at any given heart rate was observed following training. Myofibrillar protein yield and ATPase activity values were nearly identical in left ventricles from exercise-trained and sedentary control dogs. Although exercise training by treadmill running improved contractile function in the unanesthetized dog myocardium, this response does not appear to involve alterations in myofibrillar ATPase activity.

Adenosine Triphosphatases↗
PubMedDate not supplied

Recovery of nonbeating donor hearts.

BACKGROUND: Use of hearts from non-heart-beating donors could greatly increase the pool of cardiac homografts. This hypothesis was investigated in a model of traumatic death with New Zealand rabbits which were exsanguinated after 10 minutes of hypotension. METHODS: The hearts were left in situ at normothermia until just before the onset of contracture, were surgically exposed, given either blood cardioplegic, crystalloid cardioplegic, or University of Wisconsin cardioplegic solution, and then stored for 1 hour at 4 degrees C in the respective solutions. The hearts were reperfused for 20 minutes with a Langendorff apparatus. A balloon was placed in the left ventricle, and peak developed pressure and diastolic pressure-volume relationship data were collected over a range of balloon volumes. Control data was obtained from nonischemic rabbit hearts. RESULTS: Blood cardioplegic solution preserved peak developed pressure and the slope of diastolic pressure-volume relationship at control levels, whereas crystalloid cardioplegic and University of Wisconsin solutions showed significant deterioration in both of these indexes. The total adenine nucleotide pool was significantly improved with the use of blood cardioplegic solution compared with crystalloid cardioplegic and University of Wisconsin solutions although all groups were significantly depressed compared with control values. CONCLUSIONS: This study indicates that hearts harvested from non-heart-beating donors can have function that is not statistically different from controls if preserved with blood cardioplegic solution and that University of Wisconsin and crystalloid cardioplegic solutions are inadequate for preserving hearts harvested under these unique conditions.

Adenosine↗