Winkel, Kenneth D;
Tibballs, James;
Molenaar, Peter;
Lambert, Gavin;
Coles, Peter;
Ross‐Smith, Mark;
Wiltshire, Carolyn;
Fenner, Peter J;
Gershwin, Lisa‐Ann;
Hawdon, Gabrielle M;
Wright, Christine E;
Angus, James A
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
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Medientyp:
E-Artikel
Titel:
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
Beteiligte:
Winkel, Kenneth D;
Tibballs, James;
Molenaar, Peter;
Lambert, Gavin;
Coles, Peter;
Ross‐Smith, Mark;
Wiltshire, Carolyn;
Fenner, Peter J;
Gershwin, Lisa‐Ann;
Hawdon, Gabrielle M;
Wright, Christine E;
Angus, James A
Erschienen:
Wiley, 2005
Erschienen in:Clinical and Experimental Pharmacology and Physiology
Beschreibung:
<jats:title>SUMMARY</jats:title><jats:p>1. We have investigated the cardiovascular pharmacology of the crude venom extract (CVE) from the potentially lethal, very small carybdeid jellyfish <jats:italic>Carukia barnesi</jats:italic>, in rat, guinea‐pig and human isolated tissues and anaesthetized piglets.</jats:p><jats:p>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).</jats:p><jats:p>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.</jats:p><jats:p>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 (<jats:italic>Chironex fleckeri</jats:italic>) antivenom (92.6 units/mL).</jats:p><jats:p>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.</jats:p><jats:p>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.</jats:p><jats:p>7. We conclude that <jats:italic>C. barnesi</jats:italic> venom may contain a neural sodium channel activator (blocked by TTX) that, in isolated atrial tissue (and <jats:italic>in vivo</jats:italic>), 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.</jats:p>