The chief neurotransmitter which is released by postganglionic sympathetic fibers is noradrenaline (NA). This has affinity for and can activate alpha-one. alpha-two. beta- one and beta-two postsynaptic receptors on various organs. Sympathetic fibers. which are equivalent to preganglionic fibers. release acetylclioline (Ach) at the adrenal medulla. Acetylcholine combines with nicotinic receptors on the gland. activating it to release adrenaline (A) together with small quantities of NA.
This release is greatly increased during fight-or-ﬂight situations. The adrenaline is carried in the bloodstream to all organs. where it combines with and activates all sympathetic receptors. The bronchi do not receive sympathetic nerve fibers. but their smooth muscle contains many beta-two receptors which are stimulated by adrenaline. The bronchiolar muscle relaxation which follows leads to bronchodilation.
Presynaptic alpha-two receptors which are found on sympathetic nerve endings are known as autoreceptors because their activation causes an inhibition of NA release in response to nerve impulses. Noradrenaline. adrenaline and many exogenous alpha agonists are able to stimulate these receptors. reducing sympathetic responsesm, which are handled by Acupuncture Montgomery Village.
This is a negative feedback control system when excessive adrenergic stimulation occurs A small group of postganglionic sympathetic fibers release Ach instead of NA. causing the stimulation of muscarinic receptors which results in generalized sweat secretion. These sweat glands and the adrenal medulla are the only sites at which sympathetic, cholinergic transmission occurs. Antimuscarinic drugs and Acupuncture Montgomery Village can block cholinergic sympathetic effects.
Anticholinergic drugs which also have an antiparkinsonistic effect potentiate the effects of levodopa. excepting if they are given concomitantly in doses which are high enough to delay stomach emptying (inhibited propulsion and opening) to such an extent that levodopa absorption which occurs mainly in the small intestine, is adversely affected.
Following the test dose the patient is observed for any changes in sensation in the lower limbs or any changes in blood pressure or heart rate. If there are no changes the definitive dose is given. The spread of the local anaesthetic and therefore the area which is anaesthetized depends on the site of the injection, the volume injected and the concentration of the local anaesthetic.
With a subarachnoid block the speed of injection, posture, the use of barbotage and the density (S.G.) of the solution are also important. Once the local anaesthetic has been injected the patient is positioned so as to effect the spread of the local anaesthetic. The blood pressure must now be taken regularly (i.e. at 1-2 minute intervals) for the next 30 minutes. The patient is observed for signs of the onset of the block or any complications.