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Release and effects of catecholamines in myocardial ischemia

  • Chapter
Pathophysiology of Severe Ischemic Myocardial Injury

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 104))

Summary

Clinical and experimental studies suggest that in myocardial ischemia the sympathetic activity of the heart is closely related to the progression of cell injury and the incidence of malignant arrhythmias. Adrenergic stimulation of the ischemic myocardium is caused by increased local noradrenaline concentrations in the heart, while the plasma catecholamine levels are of minor relevance. In early ischemia, efferent sympathetic nerves are activated due to pain, anxiety, and fall in cardiac output or arterial blood pressure. However, excessive accumulation of noradrenaline is prevented since adenosine, formed in the ischemic myocardium, effectively suppresses the exocytosis of noradrenaline, and because released noradrenaline is rapidly removed as long as catecholamine re-uptake is functional.

With progression of ischemia to more than 10 minutes, however, the myocardium is no longer protected against excess catecholamine accumulation in the interstitial space since local metabolic release mechanisms become increasingly important. This release, which is independent from central sympathetic activity and from extracellular calcium, occurs in two steps: first, noradrenaline escapes from its intracellular storage vesicles and cumulates in the cytoplasma of the neuron. In a second, rate-limiting step, noradrenaline is transported accross the plasma membrane into the interstitial space, using the neuronal uptake carrier in reverse of its normal transport direction. The latter step requires increased intraneuronal sodium concentrations since noradrenaline leaves the nerve cell by a co-transport with the sodium ion.

Despite excessive interstitial noradrenaline concentrations, capable of rapidly desensitizing the ß-adrenergic receptor under normoxic conditions, myocardial ischemia induces a persistent 30% increase of ß-adrenergic receptor number.

The increased ß-receptor number causes enhanced sensitivity of the heart to catecholamines in the early phase of ischemia. In addition, the effector enzyme adenylatecyclase becomes temporarily supersensitive, followed by a rapid inactivation of the enzyme and its coupling protein Gs. In the αadrenergic system the receptor number at the cell surface is not consistently elevated and receptor-independent mechanisms lead to a self-potentiating sensitization of the post-receptor components of the α1-adrenergic system.

Evidence for the significance of adrenergic mechanisms in ischemiainduced myocardial injury is derived from studies with acute and chronic sympathetic denervation prior to ischemia and from interventions using antiadrenergic agents. It was concluded from these studies that local metabolic, rather than centrally induced noradrenaline release is critically involved in progressive ischemic cell damage and the occurrence of ventricullar fibrillation in early ischemia. As a consequence of local metabolic catecholamine release, extracellular noradrenaline reaches 100–1000 times the normal plasma concentration within 20 minutes of ischemia. The deleterious combination of these extremely high noradrenaline concentrations with at least a temporarily enhanced responsiveness of the tissue to catecholamines is thought to accelerate the propagation of the wavefront of irreversible cell damage in the ischemic myocardium. Moreover, the heterogeneous distribution of catecholamine excess within the heart is considered to promote malignant arrhythmias by unmasking and enhancing electrophysiological disturbances in early ischemia such as automaticity and inhomogeneities in conduction and refractoriness.

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  1. The Department of Cadiology, University of Heidelberg, Heidelberg, Germany

    Albert SchÖmig, Ruth Strasser & Gert Richardt

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    Hans Michael Piper

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SchÖmig, A., Strasser, R., Richardt, G. (1990). Release and effects of catecholamines in myocardial ischemia. In: Piper, H.M. (eds) Pathophysiology of Severe Ischemic Myocardial Injury. Developments in Cardiovascular Medicine, vol 104. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0475-0_19

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