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  <leader>02433nab a2200253 i 4500</leader>
  <controlfield tag="001">publ31965</controlfield>
  <controlfield tag="005">20250317093645.0</controlfield>
  <controlfield tag="008">250317s1994    hu      o     000   eng d</controlfield>
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   <subfield code="a">1073-2322</subfield>
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  <datafield tag="024" ind1="7" ind2=" ">
   <subfield code="a">10.1097/00024382-199412000-00005</subfield>
   <subfield code="2">doi</subfield>
  </datafield>
  <datafield tag="024" ind1="7" ind2=" ">
   <subfield code="a">1320997</subfield>
   <subfield code="2">mtmt</subfield>
  </datafield>
  <datafield tag="040" ind1=" " ind2=" ">
   <subfield code="a">SZTE Publicatio Repozitórium</subfield>
   <subfield code="b">hun</subfield>
  </datafield>
  <datafield tag="041" ind1=" " ind2=" ">
   <subfield code="a">eng</subfield>
  </datafield>
  <datafield tag="100" ind1="1" ind2=" ">
   <subfield code="a">Kaszaki József</subfield>
  </datafield>
  <datafield tag="245" ind1="1" ind2="0">
   <subfield code="a">Role of histamine in the intestinal flow response following mesenteric ischemia</subfield>
   <subfield code="h">[elektronikus dokumentum] /</subfield>
   <subfield code="c"> Kaszaki József</subfield>
  </datafield>
  <datafield tag="260" ind1=" " ind2=" ">
   <subfield code="c">1994</subfield>
  </datafield>
  <datafield tag="300" ind1=" " ind2=" ">
   <subfield code="a">413-420</subfield>
  </datafield>
  <datafield tag="490" ind1="0" ind2=" ">
   <subfield code="a">SHOCK</subfield>
   <subfield code="v">2 No. 6</subfield>
  </datafield>
  <datafield tag="520" ind1="3" ind2=" ">
   <subfield code="a">Sudden reperfusion of the gut following prolonged ischemia can itself have more deleterious consequences than the ischemia alone. Studies of vasodilator factors influencing the increased flow on reperfusion are therefore of importance. In the present study, a possible role of histamine in the postischemic flow response was examined after a period of total segmental ischemia. The artery supplying the terminal ileum was occluded in anesthetized dogs. Ischemia of 30 min duration was followed by a 30 min reperfusion period (control postischemic flow response), and the arterial blood flow to the segment was measured. After the control postischemic flow response, one of the following drugs was administered intravenously: histamine H-1- or H-2-blockers (tripelennamine, .5 mg/kg, cimetidine, 10 mg/kg, ranitidine, 2 mg/kg), cromolyn (a mast cell stabilizer, 25 mg/kg), and aminoguanidine (a diamine oxidase blocker, 50 mg/kg). The 30 min ischemia-30 min reperfusion cycle was then repeated (test postischemic flow response). A 30 min mesenteric ischemia-reperfusion period is reproducible once without a significant change in its hemodynamic parameters. The duration and volume of the postischemic flow response were significantly decreased by cimetidine, ranitidine, or cromolyn, and were increased by aminoguanidine. Tripelennamine did not affect the postischemic vasodilatator response. At the onset of reperfusion, a release of endogenous histamine occurs from the gut, originating mainly from mast cells. It is proposed that histamine participates in the postischemic flow response through the H-2-receptors.</subfield>
  </datafield>
  <datafield tag="650" ind1=" " ind2="4">
   <subfield code="a">Klinikai orvostan</subfield>
  </datafield>
  <datafield tag="700" ind1="0" ind2="1">
   <subfield code="a">Boros Mihály</subfield>
   <subfield code="e">aut</subfield>
  </datafield>
  <datafield tag="700" ind1="0" ind2="1">
   <subfield code="a">Szabó Andrea</subfield>
   <subfield code="e">aut</subfield>
  </datafield>
  <datafield tag="700" ind1="0" ind2="1">
   <subfield code="a">Nagy Sándor</subfield>
   <subfield code="e">aut</subfield>
  </datafield>
  <datafield tag="856" ind1="4" ind2="0">
   <subfield code="u">http://publicatio.bibl.u-szeged.hu/31965/1/aok_klny_54_94.pdf</subfield>
   <subfield code="z">Dokumentum-elérés </subfield>
  </datafield>
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