Sympathetic excitation

Mechanism of Action An herb that produces genital blood vessel dilation, improves nerve impulse transmission to genital area. Increases penile blood flow, central sympathetic excitation impulses to genital tissues. Therapeutic Effect Improves sexual vigor, affects impotence. 

The Class I agents decrease excitability, slow conduction velocity, inhibit diastoHc depolarization (decrease automaticity), and prolong the refractory period of cardiac tissues (1,2). These agents have anticholinergic effects that may contribute to the observed electrophysiologic effects. Heart rates may become faster by increasing phase 4 diastoHc depolarization in SA and AV nodal cells. This results from inhibition of the action of vagaHy released acetylcholine [S1-84-3] which, allows sympathetically released norepinephrine [51-41-2] (NE) to act on these stmctures (1,2). 

Studies of release of noradrenaline from sympathetic neurons provided the first convincing evidence that impulse (Ca +)-dependent release of any transmitter depended on vesicular exocytosis. Landmark studies carried out in the 1960s, using the perfused cat spleen preparation, showed that stimulation of the splenic nerve not only led to the detection of noradrenaline in the effluent perfusate but the vesicular enzyme, DpH, was also present. As mentioned above, this enzyme is found only within the noradrenaline storage vesicles and so its appearance along with noradrenaline indicated that both these factors were released from the vesicles. By contrast, there was no sign in the perfusate of any lactate dehydrogenase, an enzyme that is found only in the cell cytosol. The processes by which neuronal excitation increases transmitter release were described in Chapter 4. 

In addition to changes within the nerve, sympathetic afferents become able to activate sensory afferents via as yet poorly characterised a-adrenoceptors. These interactions between adjacent sensory and autonomic nerve axons and between ganglion cells result in excitation spreading between different nerve fibres. These peripheral ectopic impulses can cause spontaneous pain and prime the spinal cord to exhibit enhanced evoked responses to stimuli, which themselves have greater effects due to increased sensitivity of the peripheral nerves. 

This peripheral activity may be a rational basis for the use of systemic local anaesthetics in neuropathic states since ectopic activity in damaged nerves has been shown to be highly sensitive to systemic sodium channel blockers. This too is probably part of the basis for the analgesic effects of established effective anti-convulsants that block sodium channels such as carbamazepine, although central actions are important and may even predominate. The precise actions of excitability blockers therefore remains hazy as does any clear basis for the effectiveness of antidepressants and other adrenergic agents in the treatment of neuropathic pain as both central and peripheral actions, including sympathetic effects are possible. 

In spite of the excitement the race to transmutation had spurred in the worlds of chemistry and occult alchemy, the crash came in 1914. The prestige and identity transmutation efforts had conferred upon chemistry were called into question—by physicists. Criticism had already come heavily from physicists such as J. J. Thomson, who debunked some of the experiments following the announcement of the Chemical Society meeting in February 1913, as well as from Rutherford, Royds, and Robert John Strutt (Lord Rayleigh). Even sympathetic chemists such as Madame Curie had been unable to reproduce Ramsay s results. Ramsay s own student and research partner, Egerton, could not successfully repeat the experiments when he went to work in a lab in Berlin. 

Bolton TB, Aaronson PI, MacKenzie I 1988 Voltage-dependent calcium channel in intestinal and vascular smooth muscle cells. Ann NY Acad Sci 522 32 -2 Bolton TB, Prestwich SA, Zholos AV, Gordienko DV 1999 Excitation-contraction coupling in gastrointestinal and other smooth muscles. Annu Rev Physiol 61 85—115 Bramich NJ, Hirst GDS 1999 Sympathetic neuroeffector transmission in the rat anococcygeus muscle. J Physiol 516 101—115... 

Fear and excitement causes dilatation of the pupil as does adrenaline. Ergotoxine paralyses the sympathetic and causes constriction. 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

Sweat glands are also innervated by sympathetic fibers (wet palms due to excitement) however, these are exceptional as regards their neurotransmitter (ACh, p. 106). 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

SA node and A-V fibers become dominant. Activation of M2 receptors increases the potassium permeability and reduces cAMP levels, slowing the rate of depolarization and decreasing the excitability of SA node and A-V fiber cells. This results in marked bradycardia and a slowing of A-V conduction that can override the stimulation of the heart by catecholamines released during sympathetic stimulation. In fact, very high doses of a muscarinic agonist can produce lethal bradycardia and A-V block. Choline esters have relatively minor direct effects on ventricular function, but they can produce negative inotropy of the atria. 

Smooth muscle relaxation, central nervous system (CNS) excitation, and cardiac stimulation are the principal pharmacological effects observed in patients treated with theophylline. The action of theophylline on the respiratory system is easily seen in the asthmatic by the resolution of obstruction and improvement in pulmonary function. Other mechanisms that may contribute to the action of theophylline in asthma include antagonism of adenosine, inhibition of mediator release, increased sympathetic activity, alteration in immune cell function, and reduction in respiratory muscle fatigue. Theophylline also may exert an antiinflammatory effect through its ability to modulate inflammatory mediator release and immune cell function. 

Class II— sympathoplegic drugs that reduce heart responsiveness to sympathetic autonomic nervous system excitation molecules that reduce adrenergic stimulation of the heart, usually P-adrenergic blocking agents... 

Burning , etc are listed in Vol 1, p IX Calorimetric Tests for Explosives, Propel- Coefficient de self-excitation (CSE). Fr test for sympathetic detonation. See Vol 3, p C390-L... 

GAP TESTS. A general name for several tests used for determination of sympathetic detonation. They include Bur of Mines tests "Halved-Cartridge Method (Vol 1, p XIV), French "Coefficient de self-excitation ... 

Coefficient de self-excitation (Coefficient of Self-excitation Test), abbr CSE Aptitude a transmettre la detonation a distance (Capability to Transmit the Detonation at a Distance) Detonation par influence (Detonation by Influence) or Detonation sympatique (Sympathetic Detonation). See Ref 7, p 799 Ref 17, p 74 Ref 19, p 342 Ref 20, p 10 and Ref 23, pp D395-R to D405-L... 

Detonation by Influence or Sympathetic Detonation Tests (Transmission of Detonation at a Distance Test) (Aptitude a transmettre la detonation a distance, Essai or Coefficient de self-excitation, Essai, in Fr) (Detonationsiibertragung Probe ox Schlagweite Probe, in Ger) (Determinacion de la sensibilidad a la iniciacion por simp ana, in Span) (Distanxa di eaplosione persimpatia, prova, in Ital) include the following methods Booster Sensitivity Test(qy) b)Four-Cartridge Test]Sce PATR 2510(PB 1612 i(1958),p Ger 521... 

Conservative sentiment in England was also seriously disturbed, at this time, by the success of the American Revolution, and still more by the development of democratic spirit and the antichurch sentiment excited by the rise and progress of the French Revolution. As Priestley had favored the cause of the American colonists, so he was sympathetic with the ideals which dominated the rise and earlier development of the French revolutionary movement. The government party in England was aroused against Priestley, especially by his caustic reply to Edmund Burke s attack on the French Revolution in 1790. As Burke had been an outspoken advocate of the cause of the American colonists before the American Revolution, Priestley,... 

Fr) (Coefficient of Excitation Transmission of Detonation at a Distance or Ability to Transmit the Detonation at a Distance). This property known also as Sympathetic Detonation or as Detonation by Influence is detd in the US by the so - called gap test... 

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