Avtor/Urednik		Burjak, Mateja
Naslov		Vpliv famotidina in kloropiramina na ishemično okvaro pri izoliranem podganjem srcu
Prevedeni naslov		The influence of famotidine and chloropyramine on ischemic rat hearts
Tip		članek
Vir		Med Razgl
Vol. in št.		Letnik 36, št. 2
Leto izdaje		1997
Obseg		str. 227-43
Jezik		slo
Abstrakt		In the present study the effects of either H2 antagonist chloropyramine or H2 antagonist famotidine were investigated in isolated Langendorff's rat hearts. Ischemia lasted 60 minutes. Perfusion with either 10 micromol chloropyramine or 10 micromol famotidine was initiated 10 minutes before ischemia and lasted till the end of the experiments. Registered were left ventricular pressure, heart rate, Q, coronary flow and ECG. The temperature in the left ventricle was kept at 38.5 +- 0.5 degreeC. The extent of myocardial damage was assessed by the release rate of the enzyme lactate dehydrogenase. In control experiments chloropyramine had negative chronotropic effect and increased Q. Its additon decreased the coronary flow during reperfusion, caused bradicardia and did not influence the lactate dehydrogenase release. In control experiments famotidine had positive inotropic and positive chronotropic effects and decreased Q. In control experiments famotidine increased the coronary flow. During reperfusion famotidine induced tachycardia and fibrillation. Famotidine did not influence the lactate dehydrogenase release during reperfusion. Results of our experiments indicate that in the rat heart additionaly to H1 receptors also H2 receptors might exist and that both of them could be involved in the myocardial damage induced by ischaemia and reperfusion.
Izvleček		Pri našem delu smo preiskovali učinke antagonista histaminskih receptorjev H1 kloropiramina in antagonista histaminskih receptorjev H2 famotidina na ishemično okvaro pri podganjem srcu, izoliranem po Langendorffu. Srca smo izpostavili ishemiji, ki je trajala 60 minut. Skozi srca je tekla Riner-Locke raztopina z 10 mikromol kloropiramina oz.10 mikromol famotidina 10 minut pred pričetkom ishemije do konca poskusov. Beležili smo pritisk v levem prekatu, frekvenco utripov srca, količnik Q, pretok v srčnih žilah in elektrokardiogram. Temperatura v levem prekatu je bila 38,5 +- 0,5 stopinj C. Obsežnost poškodbe srčnih celic smo ocenjevali s hitrostjo sprogžanja encima laktatne dehidrogenaze. Kloropir min je v kontrolnih poskusih učinkoval negativno kronotropno in je zvišal vrednost količnika Q. Ob reperfuziji je zmanjšal pretok v srčnih žilah, pod njegovim vplivom se je pojavila v reperfuziji bradikardija. Kloropiramin ni vplival na hitrost sproščanja laktatne dehidrogenaze v reperfuziji. Famotidin je v kontrolnih poskusih učinkoval pozitivno inotropno ter pozitivno kronotropno in je znižal količnik Q. Pretok v srčnih žilah se je v kontrolnih poskusih pod vplivom famotidina povečal. Ob reperfuziji sta se v posk sih z ishemijo pod vplivom famotidina pojavili tahikardija in fibrilacija: Famotidin ni vplival na hitrost sproščanja laktatne dehidrogenaze v reperfuziji. Rezultati naših poskusov kažejo, da so v podganjem srcu poleg histaminskih receptorjev H1 verjetno prisotni tudi receptorji H2 in da lahko oboji sodelujejo pri poškodbi, ki nastane zaradi ishemije in reperfuzije.
Deskriptorji		MYOCARDIAL ISCHEMIA FAMOTIDINE HISTAMINE ANTAGONISTS RATS MYOCARDIAL CONTRACTION HEART RATE BLOOD PRESSURE ELECTROCARDIOGRAPHY LACTATE DEHYDROGENASE