Cardiovascular failure produced by a peptide from the venom of the Southern Pacific rattlesnake, Crotalus viridis helleri
| Autor: | R C Schaeffer, Richard W. Carlson, Findlay E. Russell, Max Harry Weil, T.R. Pattabhiraman |
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| Rok vydání: | 1979 |
| Předmět: |
Time Factors
Venom Vascular permeability Peptide Pharmacology Toxicology Lethal Dose 50 Hypoproteinemia Crotalid Venoms medicine Animals Respiratory system chemistry.chemical_classification biology Respiration Hemodynamics Crotalus Blood Proteins Carbon Dioxide Hydrogen-Ion Concentration biology.organism_classification medicine.disease Hemoconcentration Hemolysis Rats chemistry Cardiovascular Diseases Immunology Lactates Peptides |
| Zdroj: | Toxicon. 17:447-453 |
| ISSN: | 0041-0101 |
| DOI: | 10.1016/0041-0101(79)90278-2 |
| Popis: | R. C. Schaeffer, Jr. , T. R. Pattabhiraman , R. W. Carlson , F. E. Russell and M. H. Weil . Cardiovascular failure produced by a peptide from the venom of the Southern Pacific rattlesnake, Crotalus viridis helleri . Toxicon 17 , 447–453, 1979.—Hemodynamic, metabolic and respiratory effects of a 30 min i.v. infusion of crude venom (1·4 mg/kg) and three venom components (Peptide I, 0·5 mg/kg; Protein I, 1·2 mg/kg, Protein II, 3·4 mg/kg) were studied in 24 sedated rats (270–309 g). Venom shock, characterized by hypotension, lactacidemia, hemoconcentration, hypoproteinemia and death was observed in animals given the crude venom or Peptide I. Just prior to death, respiratory distress was observed in most animals that died. Hemolysis and hematuria were observed in the animals given Protein I or Protein II. These data suggest that the increase in vascular permeability to protein and red blood cells induced by the crude venom can, for the most part, be attributed to the peptide. In addition, Protein I and Protein II appear to account for the hemolytic activity. The toxic effects of the venom components appear to be synergistic. |
| Databáze: | OpenAIRE |
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