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Left ventricular asynchrony: an indicator of regional myocardial dysfunction.

American heart journal

Ehring T, Heusch G.
PMID: 2239657
Am Heart J. 1990 Nov;120(5):1047-57. doi: 10.1016/0002-8703(90)90116-f.

There is a marked heterogeneity of myocardial wall thickening within the left ventricle and among different individuals. It is therefore difficult to detect regional myocardial dysfunction from absolute values of systolic wall thickening. We tested whether the extent of...

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Ehring T, Heusch G. Left ventricular asynchrony: an indicator of regional myocardial dysfunction. Am Heart J. 1990;120(5):1047-57doi: 10.1016/0002-8703(90)90116-f.
Ehring, T., & Heusch, G. (1990). Left ventricular asynchrony: an indicator of regional myocardial dysfunction. American heart journal, 120(5), 1047-57. https://doi.org/10.1016/0002-8703(90)90116-f
Ehring, T, and Heusch, G. "Left ventricular asynchrony: an indicator of regional myocardial dysfunction." American heart journal vol. 120,5 (1990): 1047-57. doi: https://doi.org/10.1016/0002-8703(90)90116-f
Ehring T, Heusch G. Left ventricular asynchrony: an indicator of regional myocardial dysfunction. Am Heart J. 1990 Nov;120(5):1047-57. doi: 10.1016/0002-8703(90)90116-f. PMID: 2239657.
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No impairment of sympathetic neurotransmission in stunned myocardium.

Basic research in cardiology

Schulz R, Frehen D, Heusch G.
PMID: 1965400
Basic Res Cardiol. 1990;85:267-80. doi: 10.1007/978-3-662-11038-6_22.

Reversibly injured myocardium after short periods of ischemia is characterized by a prolonged depression of contractile function which can, however, be enhanced by inotropic interventions. Thus, a lack of inotropic stimulation due to ischemic damage of cardiac sympathetic nerves...

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Schulz R, Frehen D, Heusch G. No impairment of sympathetic neurotransmission in stunned myocardium. Basic Res Cardiol. 1990;85:267-80doi: 10.1007/978-3-662-11038-6_22.
Schulz, R., Frehen, D., & Heusch, G. (1990). No impairment of sympathetic neurotransmission in stunned myocardium. Basic research in cardiology, 85267-80. https://doi.org/10.1007/978-3-662-11038-6_22
Schulz, R, et al. "No impairment of sympathetic neurotransmission in stunned myocardium." Basic research in cardiology vol. 85 (1990): 267-80. doi: https://doi.org/10.1007/978-3-662-11038-6_22
Schulz R, Frehen D, Heusch G. No impairment of sympathetic neurotransmission in stunned myocardium. Basic Res Cardiol. 1990;85:267-80. doi: 10.1007/978-3-662-11038-6_22. PMID: 1965400.
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Consequences of regional inotropic stimulation of ischemic myocardium on regional myocardial blood flow and function in anesthetized swine.

Circulation research

Schulz R, Miyazaki S, Miller M, Thaulow E, Heusch G, Ross J, Guth BD.
PMID: 2720914
Circ Res. 1989 Jun;64(6):1116-26. doi: 10.1161/01.res.64.6.1116.

Determination of the effect of inotropic stimulation on regionally ischemic and hypokinetic myocardium is complicated when intravenous administration of the inotropic agent also causes stimulation of nonischemic adjacent and distant regions, thereby altering global ventricular hemodynamics. To obviate such...

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Schulz R, Miyazaki S, Miller M, et al. Consequences of regional inotropic stimulation of ischemic myocardium on regional myocardial blood flow and function in anesthetized swine. Circ Res. 1989;64(6):1116-26doi: 10.1161/01.res.64.6.1116.
Schulz, R., Miyazaki, S., Miller, M., Thaulow, E., Heusch, G., Ross, J., & Guth, B. D. (1989). Consequences of regional inotropic stimulation of ischemic myocardium on regional myocardial blood flow and function in anesthetized swine. Circulation research, 64(6), 1116-26. https://doi.org/10.1161/01.res.64.6.1116
Schulz, R, et al. "Consequences of regional inotropic stimulation of ischemic myocardium on regional myocardial blood flow and function in anesthetized swine." Circulation research vol. 64,6 (1989): 1116-26. doi: https://doi.org/10.1161/01.res.64.6.1116
Schulz R, Miyazaki S, Miller M, Thaulow E, Heusch G, Ross J, Guth BD. Consequences of regional inotropic stimulation of ischemic myocardium on regional myocardial blood flow and function in anesthetized swine. Circ Res. 1989 Jun;64(6):1116-26. doi: 10.1161/01.res.64.6.1116. PMID: 2720914.
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Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels.

Basic research in cardiology

Deussen A, Busch P, Schipke J, Thämer V, Heusch G.
PMID: 1965398
Basic Res Cardiol. 1990;85:193-206. doi: 10.1007/978-3-662-11038-6_16.

Increases in the activity of efferent cardiac sympathetic nerves by 35 +/- 9% were induced by 60 s bilateral occlusion of the common carotid arteries (BCO) in anesthetized dogs. Under control conditions the reflex rise in sympathetic nerve activity...

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Deussen A, Busch P, Schipke J, et al. Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels. Basic Res Cardiol. 1990;85:193-206doi: 10.1007/978-3-662-11038-6_16.
Deussen, A., Busch, P., Schipke, J., Thämer, V., & Heusch, G. (1990). Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels. Basic research in cardiology, 85193-206. https://doi.org/10.1007/978-3-662-11038-6_16
Deussen, A, et al. "Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels." Basic research in cardiology vol. 85 (1990): 193-206. doi: https://doi.org/10.1007/978-3-662-11038-6_16
Deussen A, Busch P, Schipke J, Thämer V, Heusch G. Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels. Basic Res Cardiol. 1990;85:193-206. doi: 10.1007/978-3-662-11038-6_16. PMID: 1965398.
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The power-duration product--evaluation of a new reference system for cardiopulmonary exercise testing.

European journal of applied physiology and occupational physiology

Breuer HW, Pfeiffer U, Worth H, Heusch G.
PMID: 1396633
Eur J Appl Physiol Occup Physiol. 1992;65(2):118-23. doi: 10.1007/BF00705067.

The aim of this study was to assess the discriminatory power of the new reference system, power-duration product (PDP), for the analysis of haemodynamic and metabolic variables derived from cardiopulmonary exercise tests. The PDP was calculated as the cumulative...

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Breuer HW, Pfeiffer U, Worth H, et al. The power-duration product--evaluation of a new reference system for cardiopulmonary exercise testing. Eur J Appl Physiol Occup Physiol. 1992;65(2):118-23doi: 10.1007/BF00705067.
Breuer, H. W., Pfeiffer, U., Worth, H., & Heusch, G. (1992). The power-duration product--evaluation of a new reference system for cardiopulmonary exercise testing. European journal of applied physiology and occupational physiology, 65(2), 118-23. https://doi.org/10.1007/BF00705067
Breuer, H W, et al. "The power-duration product--evaluation of a new reference system for cardiopulmonary exercise testing." European journal of applied physiology and occupational physiology vol. 65,2 (1992): 118-23. doi: https://doi.org/10.1007/BF00705067
Breuer HW, Pfeiffer U, Worth H, Heusch G. The power-duration product--evaluation of a new reference system for cardiopulmonary exercise testing. Eur J Appl Physiol Occup Physiol. 1992;65(2):118-23. doi: 10.1007/BF00705067. PMID: 1396633.
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Recruitment of an inotropic reserve in moderately ischemic myocardium at the expense of metabolic recovery. A model of short-term hibernation.

Circulation research

Schulz R, Guth BD, Pieper K, Martin C, Heusch G.
PMID: 1576742
Circ Res. 1992 Jun;70(6):1282-95. doi: 10.1161/01.res.70.6.1282.

The regional, functional as well as metabolic consequences of inotropic stimulation on myocardium subjected to prolonged moderate ischemia were investigated. In 35 enflurane-anesthetized swine the left anterior descending coronary artery was cannulated and perfused at constant flow. The vein...

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Schulz R, Guth BD, Pieper K, et al. Recruitment of an inotropic reserve in moderately ischemic myocardium at the expense of metabolic recovery. A model of short-term hibernation. Circ Res. 1992;70(6):1282-95doi: 10.1161/01.res.70.6.1282.
Schulz, R., Guth, B. D., Pieper, K., Martin, C., & Heusch, G. (1992). Recruitment of an inotropic reserve in moderately ischemic myocardium at the expense of metabolic recovery. A model of short-term hibernation. Circulation research, 70(6), 1282-95. https://doi.org/10.1161/01.res.70.6.1282
Schulz, R, et al. "Recruitment of an inotropic reserve in moderately ischemic myocardium at the expense of metabolic recovery. A model of short-term hibernation." Circulation research vol. 70,6 (1992): 1282-95. doi: https://doi.org/10.1161/01.res.70.6.1282
Schulz R, Guth BD, Pieper K, Martin C, Heusch G. Recruitment of an inotropic reserve in moderately ischemic myocardium at the expense of metabolic recovery. A model of short-term hibernation. Circ Res. 1992 Jun;70(6):1282-95. doi: 10.1161/01.res.70.6.1282. PMID: 1576742.
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Alpha 2-adrenergic coronary constriction in ischemic myocardium during exercise.

Basic research in cardiology

Seitelberger R, Guth BD, Heusch G, Ross J.
PMID: 1982609
Basic Res Cardiol. 1990;85:207-17. doi: 10.1007/978-3-662-11038-6_17.

The effect of either selective alpha 1- or alpha 2-adrenoceptor blockade on ischemic myocardial blood flow and function was examined in beta-blocked dogs trained to run on a motor-driven treadmill. The animals were instrumented with sonomicrometers for the assessment...

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Seitelberger R, Guth BD, Heusch G, et al. Alpha 2-adrenergic coronary constriction in ischemic myocardium during exercise. Basic Res Cardiol. 1990;85:207-17doi: 10.1007/978-3-662-11038-6_17.
Seitelberger, R., Guth, B. D., Heusch, G., & Ross, J. (1990). Alpha 2-adrenergic coronary constriction in ischemic myocardium during exercise. Basic research in cardiology, 85207-17. https://doi.org/10.1007/978-3-662-11038-6_17
Seitelberger, R, et al. "Alpha 2-adrenergic coronary constriction in ischemic myocardium during exercise." Basic research in cardiology vol. 85 (1990): 207-17. doi: https://doi.org/10.1007/978-3-662-11038-6_17
Seitelberger R, Guth BD, Heusch G, Ross J. Alpha 2-adrenergic coronary constriction in ischemic myocardium during exercise. Basic Res Cardiol. 1990;85:207-17. doi: 10.1007/978-3-662-11038-6_17. PMID: 1982609.
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Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo.

Journal of cardiovascular pharmacology

Heusch G, Deussen A, Schipke J, Thämer V.
PMID: 6209507
J Cardiovasc Pharmacol. 1984 Sep-Oct;6(5):961-8. doi: 10.1097/00005344-198409000-00034.

The role of alpha-adrenoceptor subtypes mediating vasoconstriction of large epicardial and small resistive coronary arteries was investigated in 26 open-chest dogs. The left circumflex coronary artery was perfused at a constant pressure. Large vessel vasomotion was determined by measurement...

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Heusch G, Deussen A, Schipke J, et al. Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo. J Cardiovasc Pharmacol. 1984;6(5):961-8doi: 10.1097/00005344-198409000-00034.
Heusch, G., Deussen, A., Schipke, J., & Thämer, V. (1984). Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo. Journal of cardiovascular pharmacology, 6(5), 961-8. https://doi.org/10.1097/00005344-198409000-00034
Heusch, G, et al. "Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo." Journal of cardiovascular pharmacology vol. 6,5 (1984): 961-8. doi: https://doi.org/10.1097/00005344-198409000-00034
Heusch G, Deussen A, Schipke J, Thämer V. Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo. J Cardiovasc Pharmacol. 1984 Sep-Oct;6(5):961-8. doi: 10.1097/00005344-198409000-00034. PMID: 6209507.
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Quinidine attenuates sympathetically induced poststenotic myocardial ischemia.

Journal of cardiovascular pharmacology

Schipke J, Schulz R, Tölle T, Heusch G, Thämer V.
PMID: 2450230
J Cardiovasc Pharmacol. 1987 Dec;10(6):622-6. doi: 10.1097/00005344-198712000-00003.

Beside its antiarrhythmic properties, which in particular are used for the treatment of atrial fibrillation, quinidine is known to have alpha-adrenoceptor blocking properties. On the other hand, atrial fibrillation is reported to cause activation of the sympathetic nervous system...

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Schipke J, Schulz R, Tölle T, et al. Quinidine attenuates sympathetically induced poststenotic myocardial ischemia. J Cardiovasc Pharmacol. 1987;10(6):622-6doi: 10.1097/00005344-198712000-00003.
Schipke, J., Schulz, R., Tölle, T., Heusch, G., & Thämer, V. (1987). Quinidine attenuates sympathetically induced poststenotic myocardial ischemia. Journal of cardiovascular pharmacology, 10(6), 622-6. https://doi.org/10.1097/00005344-198712000-00003
Schipke, J, et al. "Quinidine attenuates sympathetically induced poststenotic myocardial ischemia." Journal of cardiovascular pharmacology vol. 10,6 (1987): 622-6. doi: https://doi.org/10.1097/00005344-198712000-00003
Schipke J, Schulz R, Tölle T, Heusch G, Thämer V. Quinidine attenuates sympathetically induced poststenotic myocardial ischemia. J Cardiovasc Pharmacol. 1987 Dec;10(6):622-6. doi: 10.1097/00005344-198712000-00003. PMID: 2450230.
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Pharmacological mechanisms to attenuate sympathetically induced myocardial ischemia.

Cardiovascular drugs and therapy

Schulz R, Guth BD, Heusch G.
PMID: 2487523
Cardiovasc Drugs Ther. 1989 Mar;3(1):43-56. doi: 10.1007/BF01881528.

Distal to a coronary stenosis, resting myocardial blood flow and function can be maintained by a compensatory dilation of the poststenotic vascular bed and an increased collateral blood flow from adjacent coronary vessels. Under this condition, electrical stimulation of...

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Schulz R, Guth BD, Heusch G. Pharmacological mechanisms to attenuate sympathetically induced myocardial ischemia. Cardiovasc Drugs Ther. 1989;3(1):43-56doi: 10.1007/BF01881528.
Schulz, R., Guth, B. D., & Heusch, G. (1989). Pharmacological mechanisms to attenuate sympathetically induced myocardial ischemia. Cardiovascular drugs and therapy, 3(1), 43-56. https://doi.org/10.1007/BF01881528
Schulz, R, et al. "Pharmacological mechanisms to attenuate sympathetically induced myocardial ischemia." Cardiovascular drugs and therapy vol. 3,1 (1989): 43-56. doi: https://doi.org/10.1007/BF01881528
Schulz R, Guth BD, Heusch G. Pharmacological mechanisms to attenuate sympathetically induced myocardial ischemia. Cardiovasc Drugs Ther. 1989 Mar;3(1):43-56. doi: 10.1007/BF01881528. PMID: 2487523.
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Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs.

Basic research in cardiology

Schulz R, Janssen F, Guth BD, Heusch G.
PMID: 1786034
Basic Res Cardiol. 1991 Nov-Dec;86(6):534-43. doi: 10.1007/BF02190703.

The "Gregg phenomenon" implies that myocardial function and oxygen consumption (MVO2) increase when coronary perfusion is enhanced within or above the autoregulatory range. We have recently demonstrated that the "Gregg phenomenon" has no significance for regional myocardial function and...

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Schulz R, Janssen F, Guth BD, et al. Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs. Basic Res Cardiol. 1991;86(6):534-43doi: 10.1007/BF02190703.
Schulz, R., Janssen, F., Guth, B. D., & Heusch, G. (1991). Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs. Basic research in cardiology, 86(6), 534-43. https://doi.org/10.1007/BF02190703
Schulz, R, et al. "Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs." Basic research in cardiology vol. 86,6 (1991): 534-43. doi: https://doi.org/10.1007/BF02190703
Schulz R, Janssen F, Guth BD, Heusch G. Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs. Basic Res Cardiol. 1991 Nov-Dec;86(6):534-43. doi: 10.1007/BF02190703. PMID: 1786034.
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Adenosine, dipyridamole and isosorbide dinitrate are ineffective to prevent the sympathetic initiation of poststenotic myocardial ischemia.

Arzneimittel-Forschung

Heusch G, Deussen A, Schipke J, Thämer V.
PMID: 3768070
Arzneimittelforschung. 1986 Jul;36(7):1045-8.

An activation of cardiac sympathetic nerves increases coronary vascular resistance distal to severe stenoses and induces ischemia of the dependent myocardium. The selective alpha 2-adrenoceptor antagonist rauwolscine and the calcium antagonist nifedipine prevent both poststenotic vasoconstriction and ischemia. To...

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Heusch G, Deussen A, Schipke J, et al. Adenosine, dipyridamole and isosorbide dinitrate are ineffective to prevent the sympathetic initiation of poststenotic myocardial ischemia. Arzneimittelforschung. 1986;36(7):1045-8
Heusch, G., Deussen, A., Schipke, J., & Thämer, V. (1986). Adenosine, dipyridamole and isosorbide dinitrate are ineffective to prevent the sympathetic initiation of poststenotic myocardial ischemia. Arzneimittel-Forschung, 36(7), 1045-8.
Heusch, G, et al. "Adenosine, dipyridamole and isosorbide dinitrate are ineffective to prevent the sympathetic initiation of poststenotic myocardial ischemia." Arzneimittel-Forschung vol. 36,7 (1986): 1045-8.
Heusch G, Deussen A, Schipke J, Thämer V. Adenosine, dipyridamole and isosorbide dinitrate are ineffective to prevent the sympathetic initiation of poststenotic myocardial ischemia. Arzneimittelforschung. 1986 Jul;36(7):1045-8. PMID: 3768070.
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Showing 1 to 12 of 638 entries