Author/Editor     Giacomelli, Valentina Otja
Title     In vivo učinki aktinoporinov, izoliranih iz Actinae equinae
Translated title     In vivo effects of actinoporins, isolated from Actinia equina
Type     članek
Source     Med Razgl
Vol. and No.     Letnik 36, št. 4
Publication year     1997
Volume     str. 437-64
Language     slo
Abstract     The mechanism of action of the actinoporins, substances from the sea anemone Actinia equina, is by cationselective pore formation in the cellular membranes that consequently cause cell lysis. The aim of the present study cause cell lysis. The aim of the present study was to investigate the mechanism of the toxicity of actinoporin equinatoxin I. In in vivo experiments the measurements of ECG (lead l), respiratory activity and arterial blood pressure were taken, the hematological and biochemical analysis of the blood samples were performed. The tisue samples were taken for pathomorphologic examination. After application of equinatoxin l there was a fall in the arterial pressure. A prominent bradycardia was followed by the phase of the relative tahycardia. During the bradycardia the amplitude of P waves was diminished and the P-Q interval was prolonged. Eventually ventricular extrasistoly developed and P waves disappeared. The tahypnoe was followed by the breathing cessation. In a while the animal started to breath and terminated again. The experimental animals died due to the cardio-respiratory arrest. The blood samples revealed haemolysis and hyperkalemia, fall of hematokrit and rise in potassium plasma concentration for four times. Pathomorphological examination showed pulmonary edema with hemorrhages and early necrosis of cardiomyocytes. The lethality of actinoporins is due to cardiorespiratory arrest. Equinatoxin l differentiates from the other actinoporins in the special acivity on the excitability of the atrium, as the P waves in ECG disappeared. The induced hyperkalemia was not sufficient to explain the lethality of the toxin. Equinatoxin l induces acute necrosis of myocardium. Together with pulmonary edema this is the most important mechanism that leads to the death of experimental animals.
Summary     Aktinoporini, toksične beljakovine, izolirane iz morske vetrnice Actiniae equinae, oblikujejo selektivne pore za katione v celičnih membranah in s tem povzročijo citolizo. V nalogi sem rasikovala mehanizme toksičnosti aktinoporina ekvinatoksina l. Učinke ekvinatoksina l sem ugotavljala z merjenjem l. odvoda EKG, dihalnega volumna in arterijskega pritiska, z zasledovanjem hematoloških in biokemičnih spremembe krvi ter patohstoloških sprememb v tkivu srčne mišice in pljuč. Krvni tlak po vbizgu ekvinatoksina l pade na vrednost srednjega cirkulacijskega tlaka, nastopi tahipnoe in izrazita bradikardija, ki ji sledi obdobje relativne tahikardije. V času bradikardije je opaziti zmanjšanje amplitude valov P in podaljšanje intervala P-Q. Končno nastopi ventrikularna ekstrasistolija in valovi P izginejo. Po obdobju tahipnoe dihanje preneha, nato začne poskusna žival ponovno dihati, končno pa dihanje preneha. Poskusna žival pogine zaradi zastoja dihanja in delovanja srca. Analiza krvi je pokazala hemolizo in hiperkaliemijo, padec hematokrita in povečanje plazemske koncentracije kalija za štirikrat. Patomorfološki pregled je razkrila pljučni edem s krvavitvami, v srčni mičici pa zgodnjo nekrozo srčne mišičnine. Envinatoksin l za razliko od drugih aktinoporinov deluje na vzdraženost preddverov, saj po njegovem delovanju valovi P v EKG-zapisu izginejo. Hiperkaliemija kot vzrok smrti poskusne živali ni zadostna. Rezultati raziskave dovoljujejo sklep, da ekvinatoksin l povzroči akutno nekrozo srčne mišice, ki je poleg pljučnega edema v veliki meri odovorna za smrt poskusne živali.
Descriptors     SEA ANEMONES
CNIDARIAN VENOMS
ELECTROCARDIOGRAPHY
BLOOD PRESSURE
RATS, WISTAR
PLETHYSMOGRAPHY
AUTOPSY
HEMATOLOGIC TESTS
BLOOD CHEMICAL ANALYSIS
MYOCARDIUM
LUNG