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Related post: It is diminished by depression of the muscle, produced by cold or excessive heat; by fatigue (Fig. 22); or by muscular depressants, such as potassium or ether. (If the veratrin action is weak, cold increases the Contracture, probably by adding its own contracture to that of the veratrin. Sollmann.) FIG. 22. Effect of fatigue on veratrin curve: a., normal veratrin tracing; b, after partial fatigue; \^ natural size. Double Peak Curve. A careful inspection of veratrin-curves generally reveals two contractions (Fig. 21) : a primary contraction (a), which occurs with the normal rapidity, .but is somewhat higher than normal, and which tends to relax quickly; and a secondary contraction (b), which occurs more slowly and lasts longer. The two contractions are more or less fused (v. Bezold), but the form varies with conditions (Mostinski, 1904). Overend, 1889, attributed this phenomenon to the different contraction velocity of the white and red muscle fibers. Cervello and Weiss, 1899, showed, however, that uniform muscles exhibit the same phenomenon. Boltazzi, 1901, suggested that the veratrin curve is due to the fusion of two contrac- tions; the first peak representing the normal contraction of the fibrils, and the further portion of the curve the contraction of the sarcoplasmic substance, which he assumes has the properties of smooth muscle. According to this the veratrin action would con- sist essentially in raising the excitability of the sarcoplasmic substance above the threshold. There is, however, no direct evidence that the sarcoplasm has contractile functions (Mueller, 1908); and the modern theories of muscle contraction render this very improbable. Woebbecke, 1913, has modified the theory somewhat. He believes that muscle has two distinct functions, but that these are not specifically connected with the histologic constituents. Verzar and Felter, 1914, attribute the action to increased sensitiveness to normal stimuli. Veratrin acts directly on the muscle substance, for the effects occur after curare (Prevost, 1867), and in the nerve-free end of the sartorius muscle. When a muscle is immersed in a dilute solution, a single stimulus produces at first a normal contraction, then fibrillary twitching (Lamm, 1912). The excitability of curarized muscle to direct electric stimulation is not increased; it is diminished by large doses Buy Flavoxate Hcl (Boehm, 1913). Large doses of veratrin, however, paralyze the motor endings without previous stimulation. Spontaneous Contraction of Muscle. The immersion of a muscle in veratrin causes a slowly developing contracture, even in the absence of spontaneous stimulation. High concentrations paralyze all forms of muscle completely (Koellicker, 1856). 430 MANUAL OF PHARMACOLOGY Other Substances Producing Veratrin Effects. The prolonged contracture which is so characteristic of veratrin, is by no means confined to this alkaloid, but is also pro- duced by Digitalin, Helleborein, Muscarin, Strychnin; by aldehyds (Verzar and Felter, 1915), etc., by cold, and by very strong electric stimulation. This wide occurrence signifies that the phenomenon is of fundamental physiologic importance. These measures also prolong the contraction of cardiac and smooth muscles. The Action of Glycerin on Muscle. The muscles of frogs poisoned with glycerin respond to single stimuli by prolonged contraction, the curve having a superficial resemblance to that of veratrin, but being rather more irregular. The glycerin contrac- tion is, however, a true tetanus, due to greater irritability of the muscle substance; the action-current of each contraction sufficing to start another contraction. The phe- nomenon occurs also after curarization (Santesson, 1903). Nerve Trunks. Direct application of veratrin lessens their excitability (Boehm, 1913). Circulation. The effects are complex. Those on excised hearts resemble aconite and digitalis (slowing with increased systole). In intact animals, stimulation of the vagus center (Fig. 23) predominates at first (marked slowing); later, the fall of pressure from vasomotor paralysis becomes prominent. FlG. 23. Cevadin (Veratrin) on Blood pressure; showing the stimulation of the vagus center. Intravenous injection of 0.02 mg. per Kg. into anesthetized dog; artificial respiration. Mammalian Circulation. Small doses sometimes cause primary quickening of the heart. With larger doses (0.025-0.05 mg. per Kg.) there is sudden and marked slowing with corresponding fall of blood pressure (Bezold and Hirt, 1874; Lissauer, 1887; Pilcher and Sollmann, 1915). The slowing is greatest soon after the injection, often with marked arythmia or Flavoxate Hcl 100 Mg temporary arrest. This acute effect is due to stimulation of the vagus center (see, however, under Veratrum), for section of the vagi largely abolishes it, and stimulation of the vagus trunk does not produce further slowing (Busquet, 1907). With divided vagi, large doses may cause primary quickening and gene-ally moderate rise of blood pressure (Bezold; Pilcher and Sollmann). The fall of blood pres- sure is mainly due to the slowing, although some fall may occur independently (Lissauer). The vasomotor center is moderately stimulated by the respiratory embarrassment, even when the vagi are cut. The stimulation does not occur if artificial respiration is maintained (Pilcher and Sollmann, 1915). Reflex stimulation causes vasoconstriction. VERATRIN (CEVADIN) 431 Late Effects. The acute effect soon passes off. The heart then beats with a steady, moderately slowed rate. This slowing is not removed by atropin and is therefore cardiac. The blood pressure falls progressively, occasionally interrupted by spasmodic rise from central vasomotor stimulation. The strength of the heart is not impaired, for it reacts well to compression of the aorta, and beats efficiently just before death. The fall must therefore be vasomotor; and accordingly, sciatic stimulation or asphyxia fails to raise the pressure (Lissauer, 1887). The vagus remains excitable. The cerebral vessels are constricted (Dixon and Halliburton, 1910). The isolated mammalian heart (Hedbom-Langendorff) shows a primary slowing from stimulation of the peripheral vagus mechanism; then irregularity, and finally paralysis of the cardiac muscle. The tone is increased. Frog's Heart. The effects resemble aconite and digitalis. They involve mainly the ventricle and consist in slowing (no further slowing on vagus stimulation; Busquet, 1907); prolonged systole and increased tonus; sudden change in the rate to one-half; "peristaltic" contractions; and final median standstill. High concentrations cause prompt systolic standstill, with continued shortening. The auricles continue much longer. The same effects occur on the excised and perfused heart (Lissauer, 1887; Boehm, 1913).
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