The Experts below are selected from a list of 165 Experts worldwide ranked by ideXlab platform

Eduardo M Krieger - One of the best experts on this subject based on the ideXlab platform.

  • restoration of arterial Blood Oxygen Tension increases arterial pressure in sinoaortic denervated rats
    American Journal of Physiology-heart and Circulatory Physiology, 1994
    Co-Authors: K G Franchini, I A Cestari, Eduardo M Krieger
    Abstract:

    The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypo...

  • Restoration of arterial Blood Oxygen Tension increases arterial pressure in sinoaortic-denervated rats
    American Journal of Physiology-Heart and Circulatory Physiology, 1994
    Co-Authors: K G Franchini, I A Cestari, Eduardo M Krieger
    Abstract:

    The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypoxemia and hypercapnia were observed in acute (1 day) and chronic (20 days) SAD rats [arterial PO2 (PaO2) = 65 +2- 1.6 and 71 +2- 2.2 mmHg and arterial PCO2 (PaCO2) = 46 +/- 1.3 and 37 +/- 1.8 mmHg, respectively] compared with control rats (PaO2 = 85 +/- 1.6 mmHg, PaCO2 = 31 +/- 1.07 mmHg). Increasing inspired PO2 (PIO2) from 138 mmHg (room air) to 155 mmHg restored the PaO2 of SAD rats to control levels (acute = 81 +/- 2.21 mmHg, chronic = 85 +/- 2.35 mmHg). PaO2. restoration produced pronounced elevation of mean arterial pressure (MAP) of acute (from 121 +/- 4 to 147 +/- 3.5 mmHg) and chronic (from 121 +/- 3 to 134 +/- 3.5 mmHg) SAD rats. Progressive stepwise increase of PIO2 (from 138 to 175, 210, and 235 mmHg) produced no additional elevation of MAP of acute (113 +/- 4, 137 +/- 5, 143 +/- 5, and 147 +/- 5 mmHg) and chronic (111 +/- 3.6, 131 +/- 7.4, 130 +/- 8.7, and 130 +/- 7 mmHg) SAD rats. Otherwise, the arterial pressure of control rats remained unchanged to progressive stepwise increase of PIO2 (118 +/- 5, 117 +/- 4, 118 +/- 4, 116 +/- 4 mmHg). These data suggest that the elimination of chemoreceptors in SAD rats produces hypoxemia responsible for hypotensive influences that counteract the pressor effects produced by baroreceptor elimination.

Michel Duvelleroy - One of the best experts on this subject based on the ideXlab platform.

  • mechanisms of coronary vasoconstriction induced by high arterial Oxygen Tension
    American Journal of Physiology-heart and Circulatory Physiology, 1997
    Co-Authors: Stéphane Mouren, Michel Duvelleroy, R Souktani, M Beaussier, L Abdenour, M Arthaud, Eric Vicaut
    Abstract:

    In isolated rabbit hearts perfused with suspension of red Blood cells, we investigated the role of the endothelium and of several substances in the coronary vasoconstriction induced by a high arterial Blood Oxygen Tension (PaO2). Red Blood cells in Krebs-Henseleit buffer were Oxygenated to obtain control and high-PaO2 perfusates. Arterial Oxygen content was kept constant in both perfusates by reducing hemoglobin concentration in the high-PaO2 perfusate. Coronary Blood flow was kept constant so that Oxygen supply would not vary with the rise in PaO2. Increases in perfusion pressure therefore reflected increased coronary resistance. The high PaO2-induced coronary vasoconstriction was not affected by administration of indomethacin, nordihydroguaiaretic acid, NG-nitro-L-arginine, or superoxide dismutase and catalase but was abolished after endothelium damage or by cromakalim. These results demonstrate that 1) the endothelium contributes to the high PaO2-induced coronary vasoconstriction; 2) this effect is independent of cycloOxygenase or lipOxygenase products, nitric oxide, or free radicals; and 3) the closure of ATP-sensitive K+ channels mediates this vasoconstriction.

  • Amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial Blood Oxygen Tension
    Cardiovascular research, 1994
    Co-Authors: Stéphane Mouren, Eric Vicaut, Olivier Charansonney, Michel Duvelleroy
    Abstract:

    Objective: The aim was to investigate the effect on the coronary network of the interaction between high arterial Blood Oxygen Tension (Pao2) and stimulation by the α adrenergic agonist phenylephrine or by serotonin in an isolated, Blood perfused rabbit heart preparation. Methods: Fresh pig erythrocytes in Krebs-Henseleit buffer were Oxygenated to reach normal Pao2 [19.4(SEM 0.7) kPa] or high Pao2 [53.2(5.5) kPa]. Blood Oxygen content was kept constant despite the higher Pao2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g·100 ml−1 (p < 0.01). Coronary Blood flow was kept constant throughout the study, so that the Oxygen supply would not vary with the rise in Pao2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. Results: Switching from normal to high Pao2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the α adrenergic agonist phenyleprine, perfusion of a high Pao2 solution increased coronary resistance by +35(7)% (p

  • amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial Blood Oxygen Tension
    Cardiovascular Research, 1994
    Co-Authors: Stéphane Mouren, Eric Vicaut, Olivier Charansonney, Michel Duvelleroy
    Abstract:

    Objective: The aim was to investigate the effect on the coronary network of the interaction between high arterial Blood Oxygen Tension (Pao2) and stimulation by the α adrenergic agonist phenylephrine or by serotonin in an isolated, Blood perfused rabbit heart preparation. Methods: Fresh pig erythrocytes in Krebs-Henseleit buffer were Oxygenated to reach normal Pao2 [19.4(SEM 0.7) kPa] or high Pao2 [53.2(5.5) kPa]. Blood Oxygen content was kept constant despite the higher Pao2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g·100 ml−1 (p < 0.01). Coronary Blood flow was kept constant throughout the study, so that the Oxygen supply would not vary with the rise in Pao2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. Results: Switching from normal to high Pao2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the α adrenergic agonist phenyleprine, perfusion of a high Pao2 solution increased coronary resistance by +35(7)% (p<0.05), a value significantly higher than that found without phenylephrine. Oxygen consumption and myocardial performance did not vary throughout the study. To determine whether this amplification of the response, we applied the same protocol using serotonin instead of phenylephrine. Here again, coronary vasoconstriction rose in response to high Pao2 after serotonin infusion [+25(5)% versus +59(10)%]. Conclusions: The response of the coronary network to high Pao2 is amplified by pretreatment with the α adrenergic agonist phenylephrine or with serotonin, regardless of any changes in metabolic status. Cardiovascular Research 1994; 28 :1326-1330

Eric Vicaut - One of the best experts on this subject based on the ideXlab platform.

  • mechanisms of coronary vasoconstriction induced by high arterial Oxygen Tension
    American Journal of Physiology-heart and Circulatory Physiology, 1997
    Co-Authors: Stéphane Mouren, Michel Duvelleroy, R Souktani, M Beaussier, L Abdenour, M Arthaud, Eric Vicaut
    Abstract:

    In isolated rabbit hearts perfused with suspension of red Blood cells, we investigated the role of the endothelium and of several substances in the coronary vasoconstriction induced by a high arterial Blood Oxygen Tension (PaO2). Red Blood cells in Krebs-Henseleit buffer were Oxygenated to obtain control and high-PaO2 perfusates. Arterial Oxygen content was kept constant in both perfusates by reducing hemoglobin concentration in the high-PaO2 perfusate. Coronary Blood flow was kept constant so that Oxygen supply would not vary with the rise in PaO2. Increases in perfusion pressure therefore reflected increased coronary resistance. The high PaO2-induced coronary vasoconstriction was not affected by administration of indomethacin, nordihydroguaiaretic acid, NG-nitro-L-arginine, or superoxide dismutase and catalase but was abolished after endothelium damage or by cromakalim. These results demonstrate that 1) the endothelium contributes to the high PaO2-induced coronary vasoconstriction; 2) this effect is independent of cycloOxygenase or lipOxygenase products, nitric oxide, or free radicals; and 3) the closure of ATP-sensitive K+ channels mediates this vasoconstriction.

  • Amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial Blood Oxygen Tension
    Cardiovascular research, 1994
    Co-Authors: Stéphane Mouren, Eric Vicaut, Olivier Charansonney, Michel Duvelleroy
    Abstract:

    Objective: The aim was to investigate the effect on the coronary network of the interaction between high arterial Blood Oxygen Tension (Pao2) and stimulation by the α adrenergic agonist phenylephrine or by serotonin in an isolated, Blood perfused rabbit heart preparation. Methods: Fresh pig erythrocytes in Krebs-Henseleit buffer were Oxygenated to reach normal Pao2 [19.4(SEM 0.7) kPa] or high Pao2 [53.2(5.5) kPa]. Blood Oxygen content was kept constant despite the higher Pao2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g·100 ml−1 (p < 0.01). Coronary Blood flow was kept constant throughout the study, so that the Oxygen supply would not vary with the rise in Pao2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. Results: Switching from normal to high Pao2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the α adrenergic agonist phenyleprine, perfusion of a high Pao2 solution increased coronary resistance by +35(7)% (p

  • amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial Blood Oxygen Tension
    Cardiovascular Research, 1994
    Co-Authors: Stéphane Mouren, Eric Vicaut, Olivier Charansonney, Michel Duvelleroy
    Abstract:

    Objective: The aim was to investigate the effect on the coronary network of the interaction between high arterial Blood Oxygen Tension (Pao2) and stimulation by the α adrenergic agonist phenylephrine or by serotonin in an isolated, Blood perfused rabbit heart preparation. Methods: Fresh pig erythrocytes in Krebs-Henseleit buffer were Oxygenated to reach normal Pao2 [19.4(SEM 0.7) kPa] or high Pao2 [53.2(5.5) kPa]. Blood Oxygen content was kept constant despite the higher Pao2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g·100 ml−1 (p < 0.01). Coronary Blood flow was kept constant throughout the study, so that the Oxygen supply would not vary with the rise in Pao2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. Results: Switching from normal to high Pao2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the α adrenergic agonist phenyleprine, perfusion of a high Pao2 solution increased coronary resistance by +35(7)% (p<0.05), a value significantly higher than that found without phenylephrine. Oxygen consumption and myocardial performance did not vary throughout the study. To determine whether this amplification of the response, we applied the same protocol using serotonin instead of phenylephrine. Here again, coronary vasoconstriction rose in response to high Pao2 after serotonin infusion [+25(5)% versus +59(10)%]. Conclusions: The response of the coronary network to high Pao2 is amplified by pretreatment with the α adrenergic agonist phenylephrine or with serotonin, regardless of any changes in metabolic status. Cardiovascular Research 1994; 28 :1326-1330

Stéphane Mouren - One of the best experts on this subject based on the ideXlab platform.

  • mechanisms of coronary vasoconstriction induced by high arterial Oxygen Tension
    American Journal of Physiology-heart and Circulatory Physiology, 1997
    Co-Authors: Stéphane Mouren, Michel Duvelleroy, R Souktani, M Beaussier, L Abdenour, M Arthaud, Eric Vicaut
    Abstract:

    In isolated rabbit hearts perfused with suspension of red Blood cells, we investigated the role of the endothelium and of several substances in the coronary vasoconstriction induced by a high arterial Blood Oxygen Tension (PaO2). Red Blood cells in Krebs-Henseleit buffer were Oxygenated to obtain control and high-PaO2 perfusates. Arterial Oxygen content was kept constant in both perfusates by reducing hemoglobin concentration in the high-PaO2 perfusate. Coronary Blood flow was kept constant so that Oxygen supply would not vary with the rise in PaO2. Increases in perfusion pressure therefore reflected increased coronary resistance. The high PaO2-induced coronary vasoconstriction was not affected by administration of indomethacin, nordihydroguaiaretic acid, NG-nitro-L-arginine, or superoxide dismutase and catalase but was abolished after endothelium damage or by cromakalim. These results demonstrate that 1) the endothelium contributes to the high PaO2-induced coronary vasoconstriction; 2) this effect is independent of cycloOxygenase or lipOxygenase products, nitric oxide, or free radicals; and 3) the closure of ATP-sensitive K+ channels mediates this vasoconstriction.

  • Amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial Blood Oxygen Tension
    Cardiovascular research, 1994
    Co-Authors: Stéphane Mouren, Eric Vicaut, Olivier Charansonney, Michel Duvelleroy
    Abstract:

    Objective: The aim was to investigate the effect on the coronary network of the interaction between high arterial Blood Oxygen Tension (Pao2) and stimulation by the α adrenergic agonist phenylephrine or by serotonin in an isolated, Blood perfused rabbit heart preparation. Methods: Fresh pig erythrocytes in Krebs-Henseleit buffer were Oxygenated to reach normal Pao2 [19.4(SEM 0.7) kPa] or high Pao2 [53.2(5.5) kPa]. Blood Oxygen content was kept constant despite the higher Pao2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g·100 ml−1 (p < 0.01). Coronary Blood flow was kept constant throughout the study, so that the Oxygen supply would not vary with the rise in Pao2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. Results: Switching from normal to high Pao2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the α adrenergic agonist phenyleprine, perfusion of a high Pao2 solution increased coronary resistance by +35(7)% (p

  • amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial Blood Oxygen Tension
    Cardiovascular Research, 1994
    Co-Authors: Stéphane Mouren, Eric Vicaut, Olivier Charansonney, Michel Duvelleroy
    Abstract:

    Objective: The aim was to investigate the effect on the coronary network of the interaction between high arterial Blood Oxygen Tension (Pao2) and stimulation by the α adrenergic agonist phenylephrine or by serotonin in an isolated, Blood perfused rabbit heart preparation. Methods: Fresh pig erythrocytes in Krebs-Henseleit buffer were Oxygenated to reach normal Pao2 [19.4(SEM 0.7) kPa] or high Pao2 [53.2(5.5) kPa]. Blood Oxygen content was kept constant despite the higher Pao2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g·100 ml−1 (p < 0.01). Coronary Blood flow was kept constant throughout the study, so that the Oxygen supply would not vary with the rise in Pao2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. Results: Switching from normal to high Pao2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the α adrenergic agonist phenyleprine, perfusion of a high Pao2 solution increased coronary resistance by +35(7)% (p<0.05), a value significantly higher than that found without phenylephrine. Oxygen consumption and myocardial performance did not vary throughout the study. To determine whether this amplification of the response, we applied the same protocol using serotonin instead of phenylephrine. Here again, coronary vasoconstriction rose in response to high Pao2 after serotonin infusion [+25(5)% versus +59(10)%]. Conclusions: The response of the coronary network to high Pao2 is amplified by pretreatment with the α adrenergic agonist phenylephrine or with serotonin, regardless of any changes in metabolic status. Cardiovascular Research 1994; 28 :1326-1330

K G Franchini - One of the best experts on this subject based on the ideXlab platform.

  • restoration of arterial Blood Oxygen Tension increases arterial pressure in sinoaortic denervated rats
    American Journal of Physiology-heart and Circulatory Physiology, 1994
    Co-Authors: K G Franchini, I A Cestari, Eduardo M Krieger
    Abstract:

    The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypo...

  • Restoration of arterial Blood Oxygen Tension increases arterial pressure in sinoaortic-denervated rats
    American Journal of Physiology-Heart and Circulatory Physiology, 1994
    Co-Authors: K G Franchini, I A Cestari, Eduardo M Krieger
    Abstract:

    The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypoxemia and hypercapnia were observed in acute (1 day) and chronic (20 days) SAD rats [arterial PO2 (PaO2) = 65 +2- 1.6 and 71 +2- 2.2 mmHg and arterial PCO2 (PaCO2) = 46 +/- 1.3 and 37 +/- 1.8 mmHg, respectively] compared with control rats (PaO2 = 85 +/- 1.6 mmHg, PaCO2 = 31 +/- 1.07 mmHg). Increasing inspired PO2 (PIO2) from 138 mmHg (room air) to 155 mmHg restored the PaO2 of SAD rats to control levels (acute = 81 +/- 2.21 mmHg, chronic = 85 +/- 2.35 mmHg). PaO2. restoration produced pronounced elevation of mean arterial pressure (MAP) of acute (from 121 +/- 4 to 147 +/- 3.5 mmHg) and chronic (from 121 +/- 3 to 134 +/- 3.5 mmHg) SAD rats. Progressive stepwise increase of PIO2 (from 138 to 175, 210, and 235 mmHg) produced no additional elevation of MAP of acute (113 +/- 4, 137 +/- 5, 143 +/- 5, and 147 +/- 5 mmHg) and chronic (111 +/- 3.6, 131 +/- 7.4, 130 +/- 8.7, and 130 +/- 7 mmHg) SAD rats. Otherwise, the arterial pressure of control rats remained unchanged to progressive stepwise increase of PIO2 (118 +/- 5, 117 +/- 4, 118 +/- 4, 116 +/- 4 mmHg). These data suggest that the elimination of chemoreceptors in SAD rats produces hypoxemia responsible for hypotensive influences that counteract the pressor effects produced by baroreceptor elimination.