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CARDIOVASCULAR ACTIONS OF THE VENOM FROM THE IRUKANDJI ( CARUKIA BARNESI ) JELLYFISH: EFFECTS IN HUMAN, RAT AND GUINEA‐PIG TISSUES IN VITRO AND IN PIGS IN VITRO
Author(s) -
Winkel Kenneth D,
Tibballs James,
Molenaar Peter,
Lambert Gavin,
Coles Peter,
RossSmith Mark,
Wiltshire Carolyn,
Fenner Peter J,
Gershwin LisaAnn,
Hawdon Gabrielle M,
Wright Christine E,
Angus James A
Publication year - 2005
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2005.04258.x
Subject(s) - tetrodotoxin , cardiotoxin , inotrope , guinea pig , atropine , prazosin , contraction (grammar) , mesenteries , medicine , endocrinology , propranolol , pharmacology , chemistry , anesthesia , anatomy , antagonist , receptor , skeletal muscle
SUMMARY 1. We have investigated the cardiovascular pharmacology of the crude venom extract (CVE) from the potentially lethal, very small carybdeid jellyfish Carukia barnesi , in rat, guinea‐pig and human isolated tissues and anaesthetized piglets. 2. In rat and guinea‐pig isolated right atria, CVE (0.1–10 µg/mL) caused tachycardia in the presence of atropine (1 µmol/L), a response almost completely abolished by pretreatment with tetrodotoxin (TTX; 0.1 µmol/L). In paced left atria from guinea‐pig or rat, CVE (0.1–3 µg/mL) caused a positive inotropic response in the presence of atropine (1 µmol/L). 3. In rat mesenteric small arteries, CVE (0.1–30 µg/mL) caused concentration‐dependent contractions that were unaffected by 0.1 µmol/L TTX, 0.3 µmol/L prazosin or 0.1 µmol/L ω‐conotoxin GVIA. 4. Neither the rat right atria tachycardic response nor the contraction of rat mesenteric arteries to CVE were affected by the presence of box jellyfish ( Chironex fleckeri ) antivenom (92.6 units/mL). 5. In human isolated driven right atrial trabeculae muscle strips, CVE (10 µg/mL) tended to cause an initial fall, followed by a more sustained increase, in contractile force. In the presence of atropine (1 µmol/L), CVE only caused a positive inotropic response. In separate experiments in the presence of propranolol (0.2 µmol/L), the negative inotropic effect of CVE was enhanced, whereas the positive inotropic response was markedly decreased. 6. In anaesthetized piglets, CVE (67 µg/kg, i.v.) caused sustained tachycardia and systemic and pulmonary hypertension. Venous blood samples demonstrated a marked elevation in circulating levels of noradrenaline and adrenaline. 7. We conclude that C. barnesi venom may contain a neural sodium channel activator (blocked by TTX) that, in isolated atrial tissue (and in vivo ), causes the release of transmitter (and circulating) catecholamines. The venom may also contain a ‘direct’ vasoconstrictor component. These observations explain, at least in part, the clinical features of the potentially deadly Irukandji syndrome.