Wild Honey

Introduction

Honey is a most remarkable substance. Revered by the ancients, it can be enjoyed today in exactly the condition in which it was discovered many thousands of years ago. It is the only sweatening material that requires no manipulation or processing to render it ready to eat. The first known written passages dealing with honey have been dated about 4000 years ago, and honey has been treasured ever since. An extensive essay on the history of honey is available (Crane, 1975). As will become evident, honey is an exceedingly variable and complex material, and we are far from knowing all about it (White, 1992).

Several studies on the honey bee products, including honey as the most familiar product, started a long time ago. Most of these studies have focused on their potential health benefits for human, but the influence of these products on the cardiovascular system needs more investigations. However, Rakha et al. (2003) studied the effect and mechanism of action of wild honey on the electrical activity of the heart. Chemical analysis of the wild honey was also performed to establish the relationship between the honey constituents and its mode of action.

The results of the study revealed that wild honey has both negative chronotropic and dromotropic effects as well as positive inotropic effect on the isolated toads’hearts. Besides, substantial quantities of calcium, potassium, chlorine, sodium and magnesium were also estimated in wild honey. The conclusion emerged that effects of wild honey on the heart activity may be due to its direct action on the myocardium. Moreover, minerals in wild honey play a prime role in its cardiac activity.

A number of synthetic catecholamines have been developed for the treatment of cardiovascular disorders and conditions such as asthma and nasal congestion because of their ability to activate alpha- and beta-receptors, especially in the cardiovascular system. However, high circulating concentrations of epinephrine and norepinephrine and high doses of synthetic catecholamines such as isoproterenol may induce toxic effects on the heart, including myocardial necrosis. Because the oxidation of catecholamines may result in the formation of aminochromes and oxygen free radicals, oxidative stress may play a significant role in catecholamine-induced cardiotoxicity (Klaassen and Watkins, 1999).

Sympathetic stimulation or the presence of catecholamines is known to encourage arrhythmia formation. Experimentally induced arrhythmia may be substantially reduced by the thoracic sympathectomy and cardiac denervation, while stellate ganglion stimulation increases sensetivity to arrhythmias. Furthermore, there is a close association between palpitation, tachycardia and arrhythmia in patients with phaeochromocytoma, which is a tumor of the adrenal gland that secretes large amounts of epinephrine and norepinephrine. Paradoxically, however, at times of extreme stress or emotion vagal activity can predominate, leading to bradycardia rather than tachycardia (Brown and Kozlowski, 1997).

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