What is a negative and positive inotropic effect? These are efferent pathways that go to the heart from the centers of the brain and together with them are the third level of regulation.
Discovery history
The influence that the vagus nerves have on the heart was first discovered by the brothers G. and E. Weber in 1845. They found that as a result of electrical stimulation of these nerves, there is a decrease in the strength and frequency of heart contractions, that is, an inotropic and chronotropic effect is observed. At the same time, the excitability of the heart muscle decreases (batmotropic negative effect) and, along with it, the speed with which excitation moves through the myocardium and the conduction system (dromotropic negative effect).
For the first time he showed how the irritation of the sympathetic nerve affects the heart, I. F. Zion in 1867, and then studied it in more detail by I. P. Pavlov in 1887. The sympathetic nerve affects the same areas of cardiac activity as the vagus, but in the opposite direction. It manifests itself in stronger contraction of the atrial ventricles, increased heart rate, increased cardiac excitability and faster conduction of excitation (positiveinotropic effect, chronotropic, bathmotropic and dromotropic effects).
Innervation of the heart
The heart is an organ that is quite strongly innervated. An impressive number of receptors located in the walls of its chambers and in the epicardium give reason to consider it a reflexogenic zone. The most important in the field of sensitive formations of this organ are two types of mechanoreceptor populations, which are located mostly in the left ventricle and atria: A-receptors that respond to changes in the tension of the heart wall, and B-receptors that are excited during its passive stretching.
In turn, the afferent fibers associated with these receptors are among the vagus nerves. The free sensory endings of the nerves located under the endocardium are the terminals of the centripetal fibers that make up the sympathetic nerves. It is generally accepted that these structures are directly involved in the development of pain syndrome, radiating segmentally, which characterizes attacks of coronary disease. The inotropic effect is of interest to many.
Efferent innervation
Efferent innervation occurs due to both divisions of the ANS. The sympathetic preanglionic neurons involved are located in the gray matter in the upper three thoracic segments in the spinal cord, namely the lateral horns. In turn, preanglionic fibers move to the neurons of the sympathetic ganglion (superior thoracic). The fibers are postganglionic together with parasympatheticvagus nerve create the upper, middle and lower nerves of the heart.
The entire organ is permeated by sympathetic fibers, while they innervate not only the myocardium, but also the components of the conduction system. The parasympathetic preanglionic neurons involved in the cardiac innervation of the body are located in the medulla oblongata. The axons related to them move among the vagus nerves. After the vagus nerve enters the chest cavity, branches that are included in the nerves of the heart depart from it.
Derivatives of the vagus nerve, which run among the cardiac nerves, are parasympathetic preganglionic fibers. Excitation from them passes to intramural neurons, and then, first of all, to the components of the conduction system. The influences that are mediated by the right vagus nerve are mainly addressed by the cells of the sinoatrial node, and the left - by the atrioventricular node. The vagus nerves cannot directly affect the ventricles of the heart. The inotropic effect of cardiac glycosides is based on this.
Intramural neurons
Intramural neurons are also located in the heart in large numbers, and they can be located both singly and assembled in the ganglion. The main number of these cells is located next to the sinoatrial and atrioventricular nodes, forming, together with efferent fibers located in the interatrial septum, the intracardiac plexus of nerves. It contains all the elements that are needed in order to close the local reflex arcs. It is for thisFor this reason, the intramural nervous cardiac apparatus is referred in some cases to the metasympathetic system. What else is interesting about the inotropic effect?
Features of the influence of nerves
While the autonomic nerves innervate the tissue of the pacemakers, they can influence their excitability and thus cause changes in the frequency of generation of action potentials and heart contractions (chronotropic effect). Also, the influence of nerves can change the rate of electrotonic transmission of excitation, and hence the duration of the phases of the heart cycle (dromotropic effects).
Since the action of mediators in the composition of the autonomic nervous system contains a change in energy metabolism and the level of cyclic nucleotides, in general, autonomic nerves can affect the strength of heart contractions, that is, an inotropic effect. Under the influence of neurotransmitters in laboratory conditions, the effect of changing the value of the excitation threshold of cardiomyocytes, which is designated as bathmotropic, was achieved.
All of these pathways by which the nervous system influences myocardial contractility and cardiac pumping are of course of paramount importance, but are secondary to the myogenic mechanisms that modulate the influences. Where is the negative inotropic effect?
The vagus nerve and its effects
As a result of stimulation of the vagus nerve, a chronotropic negative effect appears, and against its background - a negative inotropic effect (drugs will be discussed below) anddromotropic. There are constant tonic effects of the bulbar nuclei on the heart: if it is bilaterally cut, the heart rate increases from one and a half to two and a half times. If the irritation is strong and prolonged, then the influence of the vagus nerves weakens over time or even stops. This is called the "escape effect" of the heart from the corresponding influence.
Separation of the mediator
When the vagus nerve is stimulated, the chronotropic negative effect is associated with inhibition (or slowdown) of impulse generation in the pacemaker of the sinus node. At the endings of the vagus nerve, when it is irritated, a mediator, acetylcholine, is released. Its interaction with muscarinic-sensitive cardiac receptors increases the permeability of the surface of the cell membrane of pacemakers for potassium ions. As a result, membrane hyperpolarization appears, slowing down or suppressing the development of slow spontaneous diastolic depolarization, as a result of which the membrane potential reaches a critical level later, which affects the slowing of the heart rate. With strong stimulation of the vagus nerve, suppression of diastolic depolarization occurs, hyperpolarization of pacemakers appears, and the heart stops completely.
During vagal influences, the amplitude and duration of the action potential of atrial cardiomyocytes decreases. When the vagus nerve is excited, the atrial stimulation threshold rises, automation is suppressed and conductionatrioventricular node slows down.
Electrical fiber stimulation
Electrical stimulation of the fibers that originate from the stellate ganglion results in an acceleration of the heart rate and an increase in myocardial contractions. In addition, the inotropic effect (positive) is associated with an increase in the permeability of the cardiomyocyte membrane for calcium ions. If the incoming calcium current increases, the level of electromechanical coupling expands, resulting in an increase in myocardial contractility.
Inotropics
Inotropic drugs are drugs that increase myocardial contractility. The most famous are cardiac glycosides ("Digoxin"). In addition, there are non-glycoside inotropic drugs. They are used only in acute heart failure or when there is severe decompensation in patients with chronic heart failure. The main non-glycoside inotropic drugs are: Dobutamine, Dopamine, Norepinephrine, Adrenaline. So, the inotropic effect in the activity of the heart is a change in the force with which it contracts.
