Key result
Pharmacologic agents such as cobra-venom factor reduce myocardial ischemic injury in laboratory animals by preventing the effects of the complement system.
Pharmacologic agents targeting the complement and kallikrein systems, such as cobra-venom factor, may reduce myocardial ischemic injury in experimental models.
Supports complement inhibition in experimental ischemia; leaves open translation to human cardioprotection.
Pharmacologic InterventionsA number of pharmacologic agents reduce myocardial ischemic injury in the laboratory animal, and some have been used in limited numbers of patients. The activation of the complement system via its alternate pathway, a shift that characterizes ischemic tissue, releases leukotactic factors and increases capillary permeability, leading to interstitial edema. As a result, the microvasculature is compressed, further diminishing blood flow to the ischemic area.18, 233 , 234 Cobra-venom factor, a protein that enzymatically cleaves C3 and prevents the effects of the complement system, reduces myocardial injury.196,197 Similarly, the kallikrein system enhances leukotactic activity, capillary permeability, interstitial edema and proteolytic activity. . . .
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Hillis et al. (1977) conducted a review in Myocardial Ischemia. Pharmacologic agents (e.g., Cobra-venom factor) was evaluated. Pharmacologic agents such as cobra-venom factor reduce myocardial ischemic injury in laboratory animals by preventing the effects of the complement system.
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