Effects of the venom of the yellow scorpion (Leiurus quinquestriatus) on the isolated work-performing guinea pig heart

Grupp, I L; Grupp, Günter; Gueron, M; Adolph, Robert J.; Fowler, Noble O.

doi:10.1016/0041-0101(80)90004-5

Cited by 11 publications

(1 citation statement)

References 26 publications

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“…On another work, several authors have reported a role for altered Ca 2+ influx in LQQ scorpion venom eliciting pathological changes in different systems such as skeletal (45) and cardiac muscles (9,20). Additionally, several scorpion venoms have been known to affect Ca 2+ release from sarcoplasmic reticulum in skeletal and cardiac muscles by binding to ryanodine receptors that regulate intracellular free Ca 2+ concentration, and whose elevation triggers a cascade of events culminating in muscle contraction (11,39).…”

Section: Introductionmentioning

confidence: 99%

The effects of a sodium and a calcium channel blocker on lethality of mice injected with the yellow scorpion (Leiurus quinquestriatus) venom

Al-Shanawani¹,

Fatani²,

El-Sayed³

2005

J. Venom. Anim. Toxins incl. Trop. Dis

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Scorpion venom toxins generally produce similar effects by mainly acting on sodium channels, and to a lesser extent, on potassium, calcium, and chloride channels. This leads to increased release of neurotransmitters and mediators, resulting in a cascade of pathological events, involving the central nervous system, the autonomic nervous system, the cardiovascular and the respiratory system, eventually leading to death. The objective of this paper was to discover whether a sodium channel blocker, lidocaine, or a calcium channel blocker, verapamil, would prolong the survival of mice injected with the venom from the common yellow scorpion Leiurus quinquestriatus quinquestriatus (LQQ). For this purpose, mice were divided into 2 groups, each injected with a different venom dose (250 or 300 µg.kg-1, s.c.). Subgroups (n=10) from each group were given venom alone; different doses of lidocaine (4, 10, 15, or 20 mg.kg-1); or several doses of verapamil (0.01, 0.03, 0.1, 0.3, or 1 mg.kg-1). All doses of lidocaine and verapamil were intravenously administered 3 minutes before, 1, 5, and 15 minutes after venom injection. Percent surviving after 24 hours was recorded in addition to the time of death. In general, lidocaine significantly prolonged survival at the dose of 10 mg.kg-1 (P<0.05 and P<0.01, versus low and high dose of venom, respectively) or 15 mg.kg-1 (P<0.01 and P<0.001, versus low and high dose of venom, respectively; Covariance Wilcoxon survival statistics), especially when injected before the venom or in the early stages of envenomation. On the other hand, in all doses administered, verapamil was either toxic or showed non-significant results. Lidocaine, the sodium channel blocker, appears to play an important role in the protection from lethality of mice injected with LQQ venom, and significantly prolonged the survival time of mice whether injected before or in the early stages of envenomation

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Section: Introductionmentioning

confidence: 99%

The effects of a sodium and a calcium channel blocker on lethality of mice injected with the yellow scorpion (Leiurus quinquestriatus) venom

Al-Shanawani¹,

Fatani²,

El-Sayed³

2005

J. Venom. Anim. Toxins incl. Trop. Dis

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Selective updates on mechanisms of action of positive inotropic agents

Grupp

1987

Mol Cell Biochem

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Several extensive reviews concerning the actions of new positive inotropic agents in the treatment of congestive heart failure, often with reference to their mechanism of action, have recently been published. Each of them has presented specific points of view. This review will place special emphasis on the significance of intracellular sodium activity for the modulation of myocardial inotropy; the continuing importance, after a 200 year history, of the use of cardiac glycosides as strong inotropic agents; the emerging significance of the phosphoinositide (PIP2) pathway to provide additional second messengers for the modulation and regulation of cardiac inotropy; the contribution of the alpha 1-adrenergic system to cardiac inotropy; the increasing awareness of the significant involvement of adenosine and its antagonists in cardiac function; and the increasing realization that myocardial tissues are not homogeneous, i.e., that in many species the atrial and ventricular tissues are using different, even opposite mechanisms in the generation of their functional responses.

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