In the early 1980s, Dr. Masquelier discovered that OPCs are capable of mitigating “any illness generated by free radicals.” At the time, this was a breakthrough invention for which the French professor was even granted a U.S. Patent. In it, Masquelier described the use of OPCs in “preventing and fighting the harmful biological effects of free radicals in the organism of warm blooded animals and more especially human beings, namely cerebral involution, hypoxia following atherosclerosis, cardiac or cerebral in farction, tumour promotion, inflammation, ischaemia, alterations of the synovial liquid, collagen degradation, among others.”
What makes the Heart tick
The heart contracts and relaxes under the continuous influence of two “opposing” nervous sytstems: the Sympathetic (activation) and Parasympathetic (relaxing) impulses. An imbalance between these two systems plays a key role in the onset of a heart attack. Contrary to what many people believe, it is not the activating impulse but the weakness or absence of the relaxing impulse that is associated with heart attacks ! When the relaxing impulse is weak, the stress impulse gets the upper hand, even when you’re not “stressed out” or involved in heavy exercise or physical work. The relaxing impulse is the dominant one. The balanced interplay between the two impulses forms the basis of a healthy life. In heart patients, however, the relaxing impulse is chronically defective and weak.
The Rapid Messengers cGMP and cAMP
The nervous impulses that orchestrate the functioning of the heart use so called “rapid messengers” as chemical intermediates that are designed to transfer their instructions from the brain to the cells of the heart muscle. The lengthy names of these messengers have been abbreviated to “cGMP” and its antagonist “cAMP.” cGMP transmits the messages of the Parasympathetic (relaxing) nervous impulse in the cells of the heart muscle, while cAMP does the same for the Sympathetic (activation) impulse. As explained by Dr. Knut Sroka on his website, the Sympathetic impulse stimulates activity, performance and energy consumption, whereas the Parasympathetic impulse commands relaxation, regeneration, economy, cell protection and “homeostasis.” In its concern for “homeostasis,” the relaxing impulse ensures that the functioning of the cells remains balanced and does not get out of control. This is the essential impulse which we must at all times maintain and support.
Another crucial Substance: Nitric Oxide
Normally, cAMP and cGMP keep each other in check. An increase in one activates an increase in the other, so that the nervous impulses are transmitted to the heart muscle in a balanced rythm. Relaxation counters activation, even when the activation has reached the level of severe stress. But there is another tiny little substance that plays a key role in all this. It’s name is nitric oxide or simply “NO.” NO is involved in a large number of cardiovascular processes, such as preventing blood clots and regulating the contraction and dilation of the blood vessel. NO also passes into the heart muscle where it stimulates the formation cGMP, the relaxing impulse’s rapid messenger. In case of a weakening of the strength of the relaxing nervous impulse, cGMP will still be formed under the influence of NO, provided of course that there is a sufficient amount of it. But, what if a weakening of the Parasympathetic – relaxing – nervous impulse is accompanied by a reduced level of NO ? Then, the metabolism in the cells of the heart muscle will break down, it will shift to fermentation to produce energy. The result of fermentation is an acidification of the muscle, which is experienced as angina pectoris. Unless reversed, this dreaded cascade may eventually produce a heart attack, which is a breakdown of the heart muscle.
The Glycocalix and NO
The inner lining of the vascular wall consists of endothelial cells. At the luminal side of this sheet of cells, where it is in contact with the blood, it is coated with a thin film that, simply put, is made of sugar and protein. The film’s name is glycocalix. It is the glycocalix that facilitates the production of NO by the endothelial cells. Other than this, the glycocalix functions as a messenger system that transforms mechanical forces – the physical pressure of the blood on the vascular wall ‒ into chemical signals that are transmitted to all the constituent parts of the endothelium and the extracellular matrix in which it is embedded. This intricate signaling-system is geared toward keeping the vascular structure organized and have it function to the best of its capacity. When the glycocalix is damaged, the vascular wall will experience a lack of information – signals ‒ that it needs to maintain the dynamic cooperation of its active components.
Oxidative Stress impairs the Production of NO
What is important specifically with respect to the functioning of the heart muscle, is that, when the glycocalix is compromised, less NO will be produced by the endothelium. This will create a shortage of NO in the heart muscle, which, in case of a weakened relaxing nervous impulse, will result in a shortage of cGMP. The heart will be in trouble. So, the important question is: How can the glycocalix be damaged ? One of the causes is an overload of sugar in the blood, which may quite easily occur in diabetic patients, but also in apparently healthy people who have a habit of consuming excess amounts of carbohydrates (bread, potatoes, pasta, rice, and … sugar). The main culprit, as you may have guessed, is the free radical, which is very capable of damaging the glycocalix. Indirectly, this leads to a decrease in NO production. Other than this, free radicals also directly react with NO and destroy it by way of NO’s enforced oxidation.
Free Radicals = Oxidative Stress
Molecules function, communicate and attract or reject each other by way of the negatively charged particles that orbit their positively charged nuclei. A free radical is a chemical “gangster” who steals electrons from the outer orbit of any molecule it encounters. The theft is called “oxidation.” But, as you know, not all oxidation is theft. Without it, we would die immediately. Oxidation is harmful when, as in theft, it takes place “against the will” of the oxidized substance. The only way to protect vital substances from being robbed of their electrons is to have sufficient amounts of molecules around that have plenty of “spare” electrons that can be donated to still a free radical’s unstoppable thirst for electrons. In the human body certain enzymes and nutrients act as electron-donators. They are called anti-oxidants, not because they stop oxidation, but because they sacrifice their electrons to protect fellow-substances from being robbed. When our anti-oxidative forces are being overwhelmed or exhausted, because they have to deal with an excess of free radicals, we speak of oxidative stress.
OPCs interrupt the deadly cascade
Let’s return to the beginning of this article. According to professor Masquelier, OPCs prevent and fight the harmful biological effects of free radicals in the human organism. In the cascade of the numerous events that lead to a heart attack, OPCs are of vital importance as anti-oxidants. More in general, OPCs’ numerous ways of assisting in the maintainance of the integrity and constancy of the endothelium, the inner lining of the vascular wall, has been unequivocally established in clinical research that began in the late 1940s with Masquelier’s earliest discovery that OPCs enhance vascular health. An intact endothelium will be able to produce sufficient amounts of NO, which, in case of a weakening of the Parasympathetic – relaxing ‒ nervous impulse, will be able to maintain a sufficient level of the latter’s relaxing messenger, cGMP. As a result, the metabolism of the cells of the heart muscle will continue doing what they were designed for: contract and relax. In the broadest of terms, OPCs will assist in help in withering an attack of the muscle that keeps the blood flowing to every nook and cranny of your body to deliver oxygen and nutrients to ALL the cells of your body.