Blood catecholamine

Cardiovascular adverse effects are minimal with pancuronium. Ganglion blockade does not occur. Shght dose-dependent rises in heart rate, blood pressure, and cardiac output are common (5), but are often masked by the actions of other co-administered agents, such as fentanyl or halothane, which cause bradycardia or hypotension. These adverse effects of pancuronium are thus often beneficial and can be deliberately harnessed. Several mechanisms contribute vagal blockade via selective blockade of cardiac muscarinic receptors (6), release of noradrenaline from adrenergic nerve endings (7), increased blood catecholamine concentrations (8), inhibition of neuronal catecholamine reuptake (9-11), and direct effects on myocardial contractility (12). These have been reviewed (13-15). 

Cardan E, Nana A, Domokos M. Blood catecholamine changes after pancuronium bromide administration. Xth Congress of the Scandinavian Society of Anesthesiologists. Lund 1971 57. 

Figure 2 indicates the unequivocal rise in blood catecholamines obtained in normal subjects within the very first minutes after intravenous glucagon injection. This effect is very transitory. In fact, table I shows that, 5 and 15 min after the glucagon injection, there is no detectable change in the catecholamines blood level in the normal subjects as well as in the hypertensive patients. On the contrary, in the two cases of pheochromocytoma, a rise in blood adrenaline and noradrenaline has been obtained. The values reached in case I.F. are particularely high in this particular case, the catecholamines blood response is completely normalized six weeks after the removal of the tumor. 

The results here reported demonstrate the existence of a stimulation of the adrenergic system after an intravenous injection of glucagon in man. The increase in peripheral blood catecholamines, in normal men or in hypertensive subjects, is transitory, reaching its maximum during the first minutes after the injection. Afte... 

Piaacidil has a short half-life and most human studies were carried out ia slow-release formulatioas. The reductioa ia blood pressure produced by piaacidil is accompanied by tachycardia and fluid retention. Plasma catecholamines and renin activity are iacreased. Other side effects are headache, di22iaess, and asthenia. 

Besides behavior and blood pressure, catecholamine neurons also have important roles in other brain functions. Regulation of neuroendocrine function is a well-known action of catecholamines for example, DA agonists reduce semm prolactin concentration, especially in conditions of hypersecretion. Ingestive behavior can be modulated by brain catecholamines, and some appetite-suppressing dmgs are beheved to act via catecholaminergic influences. Catecholamines also participate in regulation of body temperature. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

At low doses, ketamine may result in impairment of attention, learning ability, and memory, and at high doses it has been associated with delirium, amnesia, impaired motor function, hypertension, depression, and respiratory depression (Krystal et al. 1994). Another mechanism of action appears to be a blocking of the reuptake of catecholamines. This effect leads to an increase in heart rate and blood pressure (Reich and Silvay 1989). 

As the rate-limiting enzyme, tyrosine hydroxylase is regulated in a variety of ways. The most important mechanism involves feedback inhibition by the catecholamines, which compete with the enzyme for the pteridine cofactor. Catecholamines cannot cross the blood-brain barrier hence, in the brain they must be synthesized locally. In certain central nervous system diseases (eg, Parkinson s disease), there is a local deficiency of dopamine synthesis. L-Dopa, the precursor of dopamine, readily crosses the blood-brain barrier and so is an important agent in the treatment of Parkinson s disease. 

In stroke patients presenting to the ED, the first goal of treatment is immediate cardiac and respiratory stabilization. The systemic blood pressure is most often elevated in the setting of an acute stroke as the result of a catecholamine surge, and if the patient is hypotensive, the clinician should consider a concomitant cardiac process, such as myocardial infarction (MI), congestive heart failure (CHF), or pulmonary embolism (PE). 

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. 

Fenn, R. J., Siggia, S., and Curran, D. J., Liquid chromatography detector based on single and twin electrode thin-layer electrochemistry application to the determination of catecholamines in blood plasma, Anal. Client., 50, 1067,1978. 

Robertson, D., Frolich, J., Carr, R., Watson, J., FFollifield, J., Shand, D., and Oates, J., Effects of caffeine on plasma renin activity, catecholamines, and blood pressure, New England Journal of Medicine, 298, 181, 1978. 

As previously mentioned, the cells of the adrenal medulla are considered modified sympathetic postganglionic neurons. Instead of a neurotransmitter, these cells release hormones into the blood. Approximately 20% of the hormonal output of the adrenal medulla is norepinephrine. The remaining 80% is epinephrine (EPI). Unlike true postganglionic neurons in the sympathetic system, the adrenal medulla contains an enzyme that methylates norepinephrine to form epinephrine. The synthesis of epinephrine, also known as adrenalin, is enhanced under conditions of stress. These two hormones released by the adrenal medulla are collectively referred to as the catecholamines. 

Because catecholamines travel in the blood, organs and tissues throughout the body are exposed to them. Therefore, they are capable of stimulating tissues that are not directly innervated by sympathetic nerve fibers, hepato-cytes, and adipose tissue, in particular. As a result, the catecholamines have a much wider breadth of activity compared to norepinephrine released from sympathetic nerves. 

Amine hormones include the thyroid hormones and the catecholamines. The thyroid hormones tend to be biologically similar to the steroid hormones. They are mainly insoluble in the blood and are transported predominantly (>99%) bound to proteins. As such, these hormones have longer half-lives (triiodothyronine, t3, = 24 h thyroxine, T4, = 7 days). Furthermore, thyroid hormones cross cell membranes to bind with intracellular receptors and may be administered orally (e.g., synthryoid). In contrast to steroid hormones, however, thyroid hormones have the unique property of being stored extra-cellularly in the thyroid gland as part of the thyroglobulin molecule. 

The catecholamines are biologically similar to protein/peptide hormones. These hormones are soluble in the blood and are transported in an unbound form. Therefore, the catecholamines have a relatively short half-life. Because these hormones do not cross cell membranes, they bind to receptors on the membrane surface. Finally, the catecholamines are stored intracellu-larly in secretory granules for future use. 

Sympathetic nerves are distributed to most vascular beds. They are most abundant in the renal, gastrointestinal, splenic, and cutaneous circulations. Recall that these tissues receive an abundant blood flow, more than is necessary simply to maintain metabolism. Therefore, when blood is needed by other parts of the body, such as working skeletal muscles, sympathetic vasoconstrictor activity reduces flow to the tissues receiving excess blood so that it may be redirected to the muscles. Interestingly, there is no sympathetic innervation to cerebral blood vessels. In fact, these vessels do not have a.j-adrenergic receptors, so they cannot be affected by circulating catecholamines. No physiological circumstance exists in which blood should be directed away from the brain. 

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