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Lester Packer - One of the best experts on this subject based on the ideXlab platform.
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Nitecapone protects the Langendorff perfused Heart against ischemia-reperfusion injury.
Biochemistry and molecular biology international, 1993Co-Authors: M. Valenza, Elena Serbinova, S Khwaja, Lester Packer, Judith D. CatudiocAbstract:We assessed the protection afforded against myocardial ischemia/reperfusion by nitecapone in the Langendorff Heart model using male Sprague-Dawley rats. We found that when present in the perfusate 10 microM nitecapone improved the mechanical function of the Heart and lowered the enzyme leakage of lactate dehydrogenase after 40 minutes of global ischemia. In nitecapone treated Hearts the content of oxidized proteins and lipids (carbonyl groups and endogenous lipid fluorescent products) decreased. Nitecapone partially prevented the loss of total sulfhydryl groups and vitamin E after ischemia and reperfusion. We suggest that the mechanism of nitecapone protection most likely involves direct antioxidant action and enhancing the activity of other antioxidants.
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Palm oil vitamin E protects against ischemia/reperfusion injury in the isolated perfused Langendorff Heart
Nutrition Research, 1992Co-Authors: Elena Serbinova, S Khwaja, Judith D. Catudioc, J Ericson, Z Torres, A Gapor, Valerian E. Kagan, Lester PackerAbstract:Abstract We studied the effect of palm oil vitamin E on Langendorff perfused rat Hearts subjected to 40 minutes of global ischemia. Our results demonstrated that palm oil vitamin E was more efficient in the protection of isolated Langendorff Heart against ischemia/reperfusion injury than tocopherol as measured by its mechanical recovery. Palm oil vitamin E completely suppressed LDH enzyme leakage from ischemic Hearts, prevented the decrease in ATP and creatine phosphate levels and inhibited the formation of endogenous lipid peroxidation products. Our data indicate that a palm oil vitamin E mixture containing both alpha-tocopherol and alpha-tocotrienol may be more efficient than alpha-tocopherol alone in the protection of the Heart against oxidative stress induced by ischemia-reperfusion.
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palm oil vitamin e protects against ischemia reperfusion injury in the isolated perfused Langendorff Heart
Nutrition Research, 1992Co-Authors: Elena Serbinova, S Khwaja, Judith D. Catudioc, J Ericson, Z Torres, A Gapor, Valerian E. Kagan, Lester PackerAbstract:Abstract We studied the effect of palm oil vitamin E on Langendorff perfused rat Hearts subjected to 40 minutes of global ischemia. Our results demonstrated that palm oil vitamin E was more efficient in the protection of isolated Langendorff Heart against ischemia/reperfusion injury than tocopherol as measured by its mechanical recovery. Palm oil vitamin E completely suppressed LDH enzyme leakage from ischemic Hearts, prevented the decrease in ATP and creatine phosphate levels and inhibited the formation of endogenous lipid peroxidation products. Our data indicate that a palm oil vitamin E mixture containing both alpha-tocopherol and alpha-tocotrienol may be more efficient than alpha-tocopherol alone in the protection of the Heart against oxidative stress induced by ischemia-reperfusion.
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THIOCTIC ACID PROTECTS AGAINST ISOLATED PERFUSED Langendorff Heart ISCHEMIA-REPERFUSION INJURY IN THE
1992Co-Authors: Elena Serbinova, S Khwaja, Lester PackerAbstract:Antioxidant properties of thioctic and dihydrolipoic acid have been demonstrated in membranes and low density lipoproteins (LDL) in vitro. In vivo studies with dietary supplementation of thioctic acid to rats showed that it can also protect tissues against oxidative damage. Presumably, this action is due to a thioctic acid dihydrolipoic acid (TA/DHLA) coupled antioxidant mechanism, which enhances the activity of other antioxidants (i.e. ascorbate, a-tocopherol) by regenerating them from their radical form. In the present study, thioctic acid proved to protect against ischemia/reperfusion injury to Langendofi perfused Hearts. Hearts isolated from rats fed thioctic acid and subjected to ischemia exhibited better mechanical recovery (left ventricular developed pressure) after reperfusion and lower lactate dehydrogenase leakage. Thioctic acid supplementation also decreased the appearance of fluorescent lipid peroxidation products after ischemia/reperfusion, lowered the rate of 2,2’-azobis-(2,4-dimethylvaleronitrile) (AMVN) induced lipid peroxidation in Heart homogenates, and prevented the loss of a-tocopherol. The total sulfhydryl group content in thioctic acid fed animals was higher and the decrease due to ischemiareperfusion was not as marked in this group as observed in the control. These results show that dietary supplementation with thioctic acid in vivo provides protection against ischemia/reperfusion injury in the Langendorff Heart model.
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Thioctic acid protects against ischemia-reperfusion injury in the isolated perfused Langendorff Heart.
Free radical research communications, 1992Co-Authors: Elena Serbinova, S Khwaja, Abraham Z. Reznick, Lester PackerAbstract:Antioxidant properties of thioctic and dihydrolipoic acid have been demonstrated in membranes and low density lipoproteins (LDL) in vitro. In vivo studies with dietary supplementation of thioctic acid to rats showed that it can also protect tissues against oxidative damage. Presumably, this action is due to a thioctic acid dihydrolipoic acid (TA/DHLA) coupled antioxidant mechanism, which enhances the activity of other antioxidants (i.e. ascorbate, α-tocopherol) by regenerating them from their radical form.In the present study, thioctic acid proved to protect against ischemia/reperfusion injury to Langendorff perfused Hearts. Hearts isolated from rats fed thioctic acid and subjected to ischemia exhibited better mechanical recovery (left ventricular developed pressure) after reperfusion and lower lactate dehydrogenase leakage. Thioctic acid supplementation also decreased the appearance of fluorescent lipid peroxidation products after ischemia/reperfusion, lowered the rate of 2,2′-azobis-(2,4-dimethylvaleron...
Elena Serbinova - One of the best experts on this subject based on the ideXlab platform.
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Nitecapone protects the Langendorff perfused Heart against ischemia-reperfusion injury.
Biochemistry and molecular biology international, 1993Co-Authors: M. Valenza, Elena Serbinova, S Khwaja, Lester Packer, Judith D. CatudiocAbstract:We assessed the protection afforded against myocardial ischemia/reperfusion by nitecapone in the Langendorff Heart model using male Sprague-Dawley rats. We found that when present in the perfusate 10 microM nitecapone improved the mechanical function of the Heart and lowered the enzyme leakage of lactate dehydrogenase after 40 minutes of global ischemia. In nitecapone treated Hearts the content of oxidized proteins and lipids (carbonyl groups and endogenous lipid fluorescent products) decreased. Nitecapone partially prevented the loss of total sulfhydryl groups and vitamin E after ischemia and reperfusion. We suggest that the mechanism of nitecapone protection most likely involves direct antioxidant action and enhancing the activity of other antioxidants.
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Palm oil vitamin E protects against ischemia/reperfusion injury in the isolated perfused Langendorff Heart
Nutrition Research, 1992Co-Authors: Elena Serbinova, S Khwaja, Judith D. Catudioc, J Ericson, Z Torres, A Gapor, Valerian E. Kagan, Lester PackerAbstract:Abstract We studied the effect of palm oil vitamin E on Langendorff perfused rat Hearts subjected to 40 minutes of global ischemia. Our results demonstrated that palm oil vitamin E was more efficient in the protection of isolated Langendorff Heart against ischemia/reperfusion injury than tocopherol as measured by its mechanical recovery. Palm oil vitamin E completely suppressed LDH enzyme leakage from ischemic Hearts, prevented the decrease in ATP and creatine phosphate levels and inhibited the formation of endogenous lipid peroxidation products. Our data indicate that a palm oil vitamin E mixture containing both alpha-tocopherol and alpha-tocotrienol may be more efficient than alpha-tocopherol alone in the protection of the Heart against oxidative stress induced by ischemia-reperfusion.
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palm oil vitamin e protects against ischemia reperfusion injury in the isolated perfused Langendorff Heart
Nutrition Research, 1992Co-Authors: Elena Serbinova, S Khwaja, Judith D. Catudioc, J Ericson, Z Torres, A Gapor, Valerian E. Kagan, Lester PackerAbstract:Abstract We studied the effect of palm oil vitamin E on Langendorff perfused rat Hearts subjected to 40 minutes of global ischemia. Our results demonstrated that palm oil vitamin E was more efficient in the protection of isolated Langendorff Heart against ischemia/reperfusion injury than tocopherol as measured by its mechanical recovery. Palm oil vitamin E completely suppressed LDH enzyme leakage from ischemic Hearts, prevented the decrease in ATP and creatine phosphate levels and inhibited the formation of endogenous lipid peroxidation products. Our data indicate that a palm oil vitamin E mixture containing both alpha-tocopherol and alpha-tocotrienol may be more efficient than alpha-tocopherol alone in the protection of the Heart against oxidative stress induced by ischemia-reperfusion.
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THIOCTIC ACID PROTECTS AGAINST ISOLATED PERFUSED Langendorff Heart ISCHEMIA-REPERFUSION INJURY IN THE
1992Co-Authors: Elena Serbinova, S Khwaja, Lester PackerAbstract:Antioxidant properties of thioctic and dihydrolipoic acid have been demonstrated in membranes and low density lipoproteins (LDL) in vitro. In vivo studies with dietary supplementation of thioctic acid to rats showed that it can also protect tissues against oxidative damage. Presumably, this action is due to a thioctic acid dihydrolipoic acid (TA/DHLA) coupled antioxidant mechanism, which enhances the activity of other antioxidants (i.e. ascorbate, a-tocopherol) by regenerating them from their radical form. In the present study, thioctic acid proved to protect against ischemia/reperfusion injury to Langendofi perfused Hearts. Hearts isolated from rats fed thioctic acid and subjected to ischemia exhibited better mechanical recovery (left ventricular developed pressure) after reperfusion and lower lactate dehydrogenase leakage. Thioctic acid supplementation also decreased the appearance of fluorescent lipid peroxidation products after ischemia/reperfusion, lowered the rate of 2,2’-azobis-(2,4-dimethylvaleronitrile) (AMVN) induced lipid peroxidation in Heart homogenates, and prevented the loss of a-tocopherol. The total sulfhydryl group content in thioctic acid fed animals was higher and the decrease due to ischemiareperfusion was not as marked in this group as observed in the control. These results show that dietary supplementation with thioctic acid in vivo provides protection against ischemia/reperfusion injury in the Langendorff Heart model.
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Thioctic acid protects against ischemia-reperfusion injury in the isolated perfused Langendorff Heart.
Free radical research communications, 1992Co-Authors: Elena Serbinova, S Khwaja, Abraham Z. Reznick, Lester PackerAbstract:Antioxidant properties of thioctic and dihydrolipoic acid have been demonstrated in membranes and low density lipoproteins (LDL) in vitro. In vivo studies with dietary supplementation of thioctic acid to rats showed that it can also protect tissues against oxidative damage. Presumably, this action is due to a thioctic acid dihydrolipoic acid (TA/DHLA) coupled antioxidant mechanism, which enhances the activity of other antioxidants (i.e. ascorbate, α-tocopherol) by regenerating them from their radical form.In the present study, thioctic acid proved to protect against ischemia/reperfusion injury to Langendorff perfused Hearts. Hearts isolated from rats fed thioctic acid and subjected to ischemia exhibited better mechanical recovery (left ventricular developed pressure) after reperfusion and lower lactate dehydrogenase leakage. Thioctic acid supplementation also decreased the appearance of fluorescent lipid peroxidation products after ischemia/reperfusion, lowered the rate of 2,2′-azobis-(2,4-dimethylvaleron...
Mikko Nikinmaa - One of the best experts on this subject based on the ideXlab platform.
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hypoxia exposure and b type natriuretic peptide release from Langendorff Heart of rats
Acta Physiologica, 2017Co-Authors: Katja Anttila, Tomi Streng, Johanna Pispa, Minna Vainio, Mikko NikinmaaAbstract:Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B-type natriuretic peptide (BNP) from Langendorff Heart. Methods Rat Hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set-up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P < 0.001). Heart rate decreased when the oxygen concentration in the perfusate reached 9.1 ± 0.02 mg L−1 and continued to fall in lower oxygen concentrations (F = 14.8, P < 0.001). There was also a significant but inverse correlation between BNP and oxygen in the coronary flow (R2 = 0.27, P < 0.001). Conclusion In the spontaneously beating Langendorff rat Heart, a decreasing concentration of oxygen in the ingoing perfusion increased the secretion of BNP. The effect of oxygen was independent of mechanical stretch of the Heart as it occurred even when the Heart rate decreased but the pressure conditions remained constant. The difference in the oxygen capacitance of blood and Krebs–Henseleit solution appears to be a major factor affecting secretion of BNP, which is correlated with the oxygen tension of myocardial cells and affected both by the oxygen concentration and capacitance of solution perfusing the Heart and by the coronary flow.
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Hypoxia exposure and B-type natriuretic peptide release from Langendorff Heart of rats
Acta physiologica (Oxford England), 2016Co-Authors: Katja Anttila, Tomi Streng, Johanna Pispa, Minna Vainio, Mikko NikinmaaAbstract:Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B-type natriuretic peptide (BNP) from Langendorff Heart. Methods Rat Hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set-up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P
S Khwaja - One of the best experts on this subject based on the ideXlab platform.
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Nitecapone protects the Langendorff perfused Heart against ischemia-reperfusion injury.
Biochemistry and molecular biology international, 1993Co-Authors: M. Valenza, Elena Serbinova, S Khwaja, Lester Packer, Judith D. CatudiocAbstract:We assessed the protection afforded against myocardial ischemia/reperfusion by nitecapone in the Langendorff Heart model using male Sprague-Dawley rats. We found that when present in the perfusate 10 microM nitecapone improved the mechanical function of the Heart and lowered the enzyme leakage of lactate dehydrogenase after 40 minutes of global ischemia. In nitecapone treated Hearts the content of oxidized proteins and lipids (carbonyl groups and endogenous lipid fluorescent products) decreased. Nitecapone partially prevented the loss of total sulfhydryl groups and vitamin E after ischemia and reperfusion. We suggest that the mechanism of nitecapone protection most likely involves direct antioxidant action and enhancing the activity of other antioxidants.
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Palm oil vitamin E protects against ischemia/reperfusion injury in the isolated perfused Langendorff Heart
Nutrition Research, 1992Co-Authors: Elena Serbinova, S Khwaja, Judith D. Catudioc, J Ericson, Z Torres, A Gapor, Valerian E. Kagan, Lester PackerAbstract:Abstract We studied the effect of palm oil vitamin E on Langendorff perfused rat Hearts subjected to 40 minutes of global ischemia. Our results demonstrated that palm oil vitamin E was more efficient in the protection of isolated Langendorff Heart against ischemia/reperfusion injury than tocopherol as measured by its mechanical recovery. Palm oil vitamin E completely suppressed LDH enzyme leakage from ischemic Hearts, prevented the decrease in ATP and creatine phosphate levels and inhibited the formation of endogenous lipid peroxidation products. Our data indicate that a palm oil vitamin E mixture containing both alpha-tocopherol and alpha-tocotrienol may be more efficient than alpha-tocopherol alone in the protection of the Heart against oxidative stress induced by ischemia-reperfusion.
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palm oil vitamin e protects against ischemia reperfusion injury in the isolated perfused Langendorff Heart
Nutrition Research, 1992Co-Authors: Elena Serbinova, S Khwaja, Judith D. Catudioc, J Ericson, Z Torres, A Gapor, Valerian E. Kagan, Lester PackerAbstract:Abstract We studied the effect of palm oil vitamin E on Langendorff perfused rat Hearts subjected to 40 minutes of global ischemia. Our results demonstrated that palm oil vitamin E was more efficient in the protection of isolated Langendorff Heart against ischemia/reperfusion injury than tocopherol as measured by its mechanical recovery. Palm oil vitamin E completely suppressed LDH enzyme leakage from ischemic Hearts, prevented the decrease in ATP and creatine phosphate levels and inhibited the formation of endogenous lipid peroxidation products. Our data indicate that a palm oil vitamin E mixture containing both alpha-tocopherol and alpha-tocotrienol may be more efficient than alpha-tocopherol alone in the protection of the Heart against oxidative stress induced by ischemia-reperfusion.
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THIOCTIC ACID PROTECTS AGAINST ISOLATED PERFUSED Langendorff Heart ISCHEMIA-REPERFUSION INJURY IN THE
1992Co-Authors: Elena Serbinova, S Khwaja, Lester PackerAbstract:Antioxidant properties of thioctic and dihydrolipoic acid have been demonstrated in membranes and low density lipoproteins (LDL) in vitro. In vivo studies with dietary supplementation of thioctic acid to rats showed that it can also protect tissues against oxidative damage. Presumably, this action is due to a thioctic acid dihydrolipoic acid (TA/DHLA) coupled antioxidant mechanism, which enhances the activity of other antioxidants (i.e. ascorbate, a-tocopherol) by regenerating them from their radical form. In the present study, thioctic acid proved to protect against ischemia/reperfusion injury to Langendofi perfused Hearts. Hearts isolated from rats fed thioctic acid and subjected to ischemia exhibited better mechanical recovery (left ventricular developed pressure) after reperfusion and lower lactate dehydrogenase leakage. Thioctic acid supplementation also decreased the appearance of fluorescent lipid peroxidation products after ischemia/reperfusion, lowered the rate of 2,2’-azobis-(2,4-dimethylvaleronitrile) (AMVN) induced lipid peroxidation in Heart homogenates, and prevented the loss of a-tocopherol. The total sulfhydryl group content in thioctic acid fed animals was higher and the decrease due to ischemiareperfusion was not as marked in this group as observed in the control. These results show that dietary supplementation with thioctic acid in vivo provides protection against ischemia/reperfusion injury in the Langendorff Heart model.
-
Thioctic acid protects against ischemia-reperfusion injury in the isolated perfused Langendorff Heart.
Free radical research communications, 1992Co-Authors: Elena Serbinova, S Khwaja, Abraham Z. Reznick, Lester PackerAbstract:Antioxidant properties of thioctic and dihydrolipoic acid have been demonstrated in membranes and low density lipoproteins (LDL) in vitro. In vivo studies with dietary supplementation of thioctic acid to rats showed that it can also protect tissues against oxidative damage. Presumably, this action is due to a thioctic acid dihydrolipoic acid (TA/DHLA) coupled antioxidant mechanism, which enhances the activity of other antioxidants (i.e. ascorbate, α-tocopherol) by regenerating them from their radical form.In the present study, thioctic acid proved to protect against ischemia/reperfusion injury to Langendorff perfused Hearts. Hearts isolated from rats fed thioctic acid and subjected to ischemia exhibited better mechanical recovery (left ventricular developed pressure) after reperfusion and lower lactate dehydrogenase leakage. Thioctic acid supplementation also decreased the appearance of fluorescent lipid peroxidation products after ischemia/reperfusion, lowered the rate of 2,2′-azobis-(2,4-dimethylvaleron...
Katja Anttila - One of the best experts on this subject based on the ideXlab platform.
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hypoxia exposure and b type natriuretic peptide release from Langendorff Heart of rats
Acta Physiologica, 2017Co-Authors: Katja Anttila, Tomi Streng, Johanna Pispa, Minna Vainio, Mikko NikinmaaAbstract:Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B-type natriuretic peptide (BNP) from Langendorff Heart. Methods Rat Hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set-up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P < 0.001). Heart rate decreased when the oxygen concentration in the perfusate reached 9.1 ± 0.02 mg L−1 and continued to fall in lower oxygen concentrations (F = 14.8, P < 0.001). There was also a significant but inverse correlation between BNP and oxygen in the coronary flow (R2 = 0.27, P < 0.001). Conclusion In the spontaneously beating Langendorff rat Heart, a decreasing concentration of oxygen in the ingoing perfusion increased the secretion of BNP. The effect of oxygen was independent of mechanical stretch of the Heart as it occurred even when the Heart rate decreased but the pressure conditions remained constant. The difference in the oxygen capacitance of blood and Krebs–Henseleit solution appears to be a major factor affecting secretion of BNP, which is correlated with the oxygen tension of myocardial cells and affected both by the oxygen concentration and capacitance of solution perfusing the Heart and by the coronary flow.
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Hypoxia exposure and B-type natriuretic peptide release from Langendorff Heart of rats
Acta physiologica (Oxford England), 2016Co-Authors: Katja Anttila, Tomi Streng, Johanna Pispa, Minna Vainio, Mikko NikinmaaAbstract:Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B-type natriuretic peptide (BNP) from Langendorff Heart. Methods Rat Hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set-up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P
