Adrenaline, heart rate

Halogenated hydrocarbons depress cardiac contractility, decrease heart rate, and inhibit conductivity in the cardiac conducting system. The cardiac-toxicity of these compounds is related to the number of halogen atoms it increases first as the number of halogen atoms increases, but decreases after achieving the maximum toxicity when four halogen atoms are present. Some of these compounds, e.g., chloroform, carbon tetrachloride, and trichloroethylene, sensitize the heart to catecholamines (adrenaline and noradrenaline) and thus increase the risk of cardiac arrhythmia. 

Hi-receptors in the adrenal medulla stimulates the release of the two catecholamines noradrenaline and adrenaline as well as enkephalins. In the heart, histamine produces negative inotropic effects via Hr receptor stimulation, but these are normally masked by the positive effects of H2-receptor stimulation on heart rate and force of contraction. Histamine Hi-receptors are widely distributed in human brain and highest densities are found in neocortex, hippocampus, nucleus accumbens, thalamus and posterior hypothalamus where they predominantly excite neuronal activity. Histamine Hrreceptor stimulation can also activate peripheral sensory nerve endings leading to itching and a surrounding vasodilatation ( flare ) due to an axonal reflex and the consequent release of peptide neurotransmitters from collateral nerve endings. 

If a series of related chemicals, say noradrenaline, adrenaline, methyladrenaline and isoprenaline, are studied on a range of test responses (e.g. blood pressure, heart rate, pupil size, intestinal motility, etc.) and retain exactly the same order of potency in each test system, then it is likely that there is only one type of receptor for all four of these catecholamines. On the other hand, if, as Ahlquist first found in the 1940s, these compounds give a distinct order of potency in some of the tests, but the reverse (or just a different) order in others, then there must be more than one type of receptor for these agonists. 

If one set of these responses can be blocked (antagonised) by a drug that does not affect the other responses (e.g. propranolol blocks the increase in heart rate produced by adrenaline, but not the dilation of the pupil evoked by adrenaline) then this is good evidence that adrenoceptors in the pupil are not the same as those in the heart. 

Figure 9. Blood pressure and heart rate under the influence of clonidine before and after spinalization in a cat. Spinalization was done between the two parts of the figure. Adrenaline (Adr.) and clonidine (Clonidin) were given i.v. (14).

Many years later. Sir James Black identified fhe beta adrenergic receptor in heart muscle. Adrenaline increases heart rate by activating the beta adrenergic receptor in this organ. Within a decade. Black and his colleagues had synthesized a molecule known as propranolol, marketed as Inderal. 

Adrenaline, which turns on both receptors, increases heart rate via the beta-1 receptor and dilates airways by the beta-2 receptors. Propranolol, which is a nonspecihc blocker of both beta-1 and beta-2 receptors, decreases heart rate and lowers blood pressure, beta-1 receptor action, but can constrict airways in the lung, beta-2 receptor action, and that is not so good. 

Adrenaline is the main hormone released from the adrenal medulla. The glandular cells in this structure correspond to the second, postganglionic neuron of the sympathetic nervous system. Furthermore, adrenaline can be found in chromaffin cells in various tissues. For the better understanding of the function of noradrenaline it is important to realize that this substance, as a neuronal transmitter, affects only the innervated target structure, that is it acts mainly locally. Among these effects are the activation of the musculus dilatator to widen the pupillae in response to a reduced light intensity, an increase in heart rate as a response to a blood pressure drop due to a reduction of the peripheral resistance or constriction... 

Epinephrine, commonly referred to as adrenaline, is an amine secreted in increased amounts during times of stress (Figure 15.21). Adrenaline increases the heart rate and blood pressure, releases sugar stored in the liver, and constricts blood vessels. It is sometimes administered to people in shock or during periods of acute asthma attacks. 

Patient remains drowsy but conscious. Respiratory depression is marked and predictable. There is slight fall in blood pressure. Heart rate often decreases but myocardium is not sensitized to adrenaline. 

Heart Direct effects on the heart are determined largely by receptors. Adrenaline increases the heart rate, force of myocardial contraction and cardiac output which is associated with increased metabolism by the myocardium, increased oxygen consumption and thus decreasing cardiac efficiency. 

Enflurane produces a dose-related decrease in systemic arterial blood pressure secondary to reductions in cardiac output and systemic vascular resistance. There is evidence that cardiac output is partially maintained by a compensatory increase in heart rate. This effect seems dependent on a degree of hypercardia and does not occur during controlled ventilation. Enflurane and halothane depress myocardial contractility to a similar extent and less than isoflurane. Enflurane does not sensitise the heart to the effects of catecholamines to any significant extent and adrenaline (epinephrine) may be given subcutaneously for control of bleeding. 

There is a risk of inducing uterine contractions if adrenaline is used in late pregnancy. Increased oxygen demand resulting from increases in heart rate and myocardial contractility may outstrip the myocardial oxygen supply and predispose to ischaemia. 

ADRENAL MEDULLA HORMONES. Adrenaline (epinephrine) and its immediate biological precursor noradrenaline (norepinephrine, levartei-nol) are the principal hormones of the adult adrenal medulla. See Fig.l. Some of the physiological effects produced by adrenaline arc contraction of the dilator muscle of the pupil of the eye (mydriasis), relaxation of the smooth muscle of the bronchi constriction of most small blood vessels dilation of some blood vessels, notably those in skeletal muscle increase in heart rate and force of ventricular conlraction relaxation of the smooth muscle of the intestinal tract and either contraction or relaxation, or both, of uterine smooth muscle. Electrical stimulation of appropriate sympathetic (adrenergic) nerves can produce all the aforementioned effects with exception of vasodilation in skeletal muscle. 

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