Increased basal tone and hyperresponsiveness to acetylcholine and ergonovine in spasm related coronary arteries in patients with variant angina: basal coronary artery tone in patients with variant angina

In patients with variant angina, previous data have been inconclusive as to whether basal coronary artery tone is elevated at the spastic and non-spastic sites. Thus, the purpose of this study was to assess the basa coronary artery tone and the responsiveness to acetylcholine (Ach) and ergonovine (Erg) in patients with variant angina. We compared the basal coronary artery tone and the constrictive responses to Ach and Erg between 31 patients (Group 1) with variant angina in whom spasm was provoked by the low doses of Ach (intracoronary 20 micrograms) or Erg(intravenous 50 micrograms) and 35 patients (Group 2) provoked by higher doses of Ach (intracoronary 100 micrograms) or Erg (intravenous cumulative dose of 350 micrograms), and 26 control subjects. Patients with variant angina in whom spasm was provoked by low doses of Ach or Erg, had a higher incidence of mixed disease, multi-vessel spasm and higher disease activity. The basal coronary artery tone at the spastic and nonspastic sites of spasm related artery was significantly more elevated in Group 1 than that in Group 2 (44+/- 17 vs 14 +/- 11% and 26 +/- 14 vs 16 +/- 10% respectively, P< 0.05), but not in the nonspasm related artery, The magnitudes of vasoconstrictive responses to Ach and Erg at the nonspastic sites were also greater in Group 1 than those in Group 2 and the control groups (Ach; 40 +/- 20 vs 26+/- 11, 27 +/- 12%: Erg; 37 +/- 18 vs 12 +/- 8, 13 +/- 10% respectively, P< 0.05). However, the basal coronary artery tone was not elevated at the spastic and nonspastic sites in Group 2 compared to the in control subjects. These findings suggest that the basal coronary artery tone is increased in patients with variant angina with higher disease activity at the spastic sites and nonspastic sites of the spasm-related artery, and this may be related to the occurrence of coronary artery spasm.

Rigidez del musculo masetero e inducción anestésica en la cirugía del estrabismo / Masseter muscle rigidity and anesthetic induction in strabisms surgery

La aparición de la rigidez del músculo masetero con la consiguiente dificultad para realizar la intubación endotraqueal y la hipertemia maligna, (desorden farmacogenético de alta mortalidad) están relacionados con la administración de ciertos agentes anestésicos y de relajantes musculares, especialmente usados en la inducción de la anestesia general. En nuestro trabajo utilizamos como agente de inducción anestésica el tiopental sódico y la succinilcolina; no se observa la aparición de dichas complicaciones en niños tratados con cirugía correctora del estrabismo

Açöes espasmogênicas do extrato etanólico bruto de Himatanthus phagedaenica (Mart.) Woodson, em íleo isolado de cobaia / Spasmogenic action of the crude ethanosic estract of Himatanthus phagedaenica (Mart) Woodson in guinea pig isolated ileum

O extrato bruto do lenho de Himatanthus phagedaenica (Mart.) Woodson foi submetido a triagem farmacológica na tentativa de obter evidências sobre seu uso popular. Das açöes apresentadas pelo extrato, foram estudadas aquelas espasmogênicas, sobre a musculatura lisa intestinal de íleo isolado de cobaia. O efeito contrátil do extrato, nesta preparaçäo, näo foi abolido pela atropina e hexametônio, além de näo ser potenciado pela eserina. O mecanismo de açäo proposto para a contraçäo produzida neste tipo de músculo, pelo extrato estanólico bruto de H. phagedanica foi o de aumentar o efluxo de Ca2ñ através dos canais de Ca2+ voltagem-dependentes. O antagonismo exercido pelo verapamil sobre estas contraçöes, forneceu evidências a favor desta hipótese

Lack tolerance of morphine induced spasm of Guinea pig sphincter of Oddi

To determine whether guinea pigs chronically exposed to morphine would develop tolerance to the morphine-induced contraction of the sphincterof Oddi (SO), adult male guinea pigs were implanted with morphine pellets (100 mg morphine). The effect of increasing IV doses of morphine on the SO was assessed by determining the duration of which saline perfusate stopped flowing into the duodenum of morphine-treated guinea pigs (MTGP) vs monimplanted animals (non-MTGP). Isolated bovine and guinea pigs SO were also challenged with morphine. Int the in vivo experiments the spasmogenic response of the SO from MTGP to morphine was greater than of SO from non-MTGP. However, morphine had no effect on isolated SO. These results indicate that chronic morphine exposure does not results in tolerance of the SO to the spasmogenic effects of morphine. On the contrary, chronic morphine even sensitized the SO to morphine, in addition, the in vitro data indicated that morphine does not act directly on the smooth muscle of SO to cause spasmogenic effect