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M A Duvelleroy

Publications and source records attributed to M A Duvelleroy.

12 recordsLinked to original sources
PubMed1985

Coronary response to large decreases of hemoglobin-O2 affinity in isolated rat heart.

In this study, the consequences of large increases of P50 (O2 partial pressure at 50% oxyhemoglobin saturation) on coronary blood flow (CBF) were investigated in isolated Wistar rat heart. Rightward shifts of the O2 dissociation curve (ODC), obtained by lysing and resealing erythrocytes to encapsulate inositol hexaphosphate (IHP), led to a very large increase in P50 without side effects. Each heart was perfused alternatively with control stored human blood [P50 = 18.8 +/- 0.3 (SE) mmHg] and IHP-treated human blood (P50 = 47.1 +/- 1.7 mmHg), according to the technique of Langendorff (mean perfusion pressure 80 mmHg; hematocrit 25%). Arterial PO2 of 180 mmHg was maintained to keep arterial O2 content identical for both types of blood. When hemoglobin affinity was lowered, CBF decreased from 5.32 +/- 0.20 to 3.40 +/- 0.14 ml X min-1 X g-1, coronary sinus PO2 (PcsO2) rose from 39.9 +/- 0.9 to 69.9 +/- 4.2 mmHg, and myocardial O2 consumption (MVO2) rose slightly from 0.125 +/- 0.005 to 0.149 +/- 0.010 ml O2 X min-1 X g-1 (P less than 0.05). A significant negative correlation was found between CBF and P50 (r = -0.90; n = 32) and a significant positive correlation between PcsO2 and P50 (r = +0.84; n = 28). The coronary blood flow response to high P50 values was not abolished when maximal dilation was induced by adenosine, so this response seems independent of metabolic needs. These experiments have demonstrated that if O2 uptake by erythrocytes remains constant, in the presence of a high P50, sufficient O2 supply may be achieved with substantially less blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1984

Role of oxygen radicals in cardiac injury due to reoxygenation.

The ability of oxygen derived free radicals to induce irreversible cellular injuries during reoxygenation was studied on isolated potassium-arrested heart preparation. Enzymatic scavengers of hydrogen peroxide (H2O2) and superoxide anion (O-2), catalase and superoxide dismutase, were not effective in reversing the cardiac alterations induced by hypoxia. Cellular injuries induced by reoxygenation, 'Oxygen paradox', were partially prevented by scavengers of H2O2 (glutathione reduced form, catalase) and O-2 (superoxide dismutase). The 'oxygen paradox' was associated with a release of malonaldehyde. The inhibition of lipid peroxidation by alpha-tocopherol prevented the toxic effect of molecular oxygen on hypoxic hearts. The specific quenchers of singlet oxygen (histidine) and hydroxyl radical (mannitol) reduced the peroxidation of unsaturated lipids and the intensity of the 'oxygen paradox' phenomenon. The results indicate that in cardiac muscle (i) oxygen derived free radicals are important byproducts of abnormal oxidative metabolism present during the post hypoxic period; (ii) the 'oxygen paradox' phenomenon is related to the formation of lipid hydroperoxides leading to the cellular membrane disruption and to the irreversible alteration of cardiac integrity.

Adenosine Triphosphate↗
PubMed1983

Dependency of O2-affinity effects on O2 consumption in the isolated rat heart.

We have studied the effect of a decrease in hemoglobin-O2 affinity (increased P50) on O2 delivery in the non-paced, isolated, blood-perfused rat heart before and after coronary vasodilatation with and without an increase in myocardial O2 consumption (MVO2) produced with isoproterenol. Changes in perfusate P50 were produced with orthoiodosodium benzoate (OISB). Low concentrations of isoproterenol (0.74 micrograms/liter) caused no significant changes in coronary blood flow (QCOR) or MVO2 per beat. Perfusion with OISB-treated (8 mM) blood increased P50 from 29 to 33 mmHg at constant pH. MVO2 per beat increased significantly, QCOR did not change, and the ratio QCOR/MVO2, a reflection of the flow/metabolism distribution, decreased to values obtained in the absence of isoproterenol. With high doses of isoproterenol (5.0 micrograms/liter), MVO2 per beat and QCOR/MVO2 increased. Addition of OISB (13 mM) increased P50 from 29 to 39 mmHg, with no significant reduction in either QCOR or the QCOR/MVO2 ratio. Our data suggest that a decrease in blood-O2 affinity affects myocardial O2 delivery depending on the initial metabolic requirement: at basal MVO2 changes in the distribution of myocardial blood flow are probably secondary to the effects of PO2 on vessels that supply metabolically less active regions; at high MVO2 and following a maximum increase in capillary density, changes in vascular PO2 appear less effective than locally generated metabolic vasodilators, and distribution of blood flow is unaffected.

Animals↗
PubMed1976

Blood-perfused working isolated rat heart.

We describe a method for perfusion of a working isolated rat heart with washed erythrocytes suspended in a Krebs-Henseleit bicarbonate buffer containing bovine albumin (fraction V). With washed pig red cells, as hematocrit was varied between 0 and 40%, coronary flow (CF), aortic flow (AF), external work (W), and myocardial oxygen consumption (MVO2) were measured. Hemodynamic data at a hematocrit of 30% (CF = 5.4 +/- 0.7 ml/min per g, AF = 75 +/- 8 ml/min per g) were identical with those reported for the intact animal. Coronary sinus PO2 was highest with a red cell-free perfusate suggesting that coronary flow is partially shunted. Human red cells obtained from banked blood, were tried also with success. With careful filtration, the preparation is stable for 2 h and well suited for study of the dynamics of myocardial oxygen delivery.

Animals↗