Alveolarwal Hemorrhage 8/18 Acuteinfarction 11/20 Organizing Infarction 14/38 Organized Infarction 7/11 Table1 Histologicalfindingsofinfarction Background Lesions Totaly6cases Recanalization0:1:2 Ret.Fib.0:1:2: Alv.Fib.0:1:2 BM Dil.0:1:2 BM Dis.0:1:2 Bypass0:1:2 Encapsulation Recanalization0:1:2 Ret.Fib.0:1:2 Alv.Fib.0:1:2 BM Dil.0:1:2 BM Dis.0:1:2 Bypass0:1:2 Encapsulation Recanalization0:1:2 Ret.Fib.0:1:2 Alv.Fib.0:1:2 BM Dil.0:1:2 BM Dis.0:1:2 Bypass0:1:2 3:1:3:1 Mildfibrosis Thrombus Recanalization Bypass 4:1:5:1 2 2 3 3 1(10%):5(45%):5(45%) 0:2(18%):9(82%) 4(36%):5(46%):2(18%) 0:0:11(100%) 0:0:11(100%) 0:5(45%):6(55%) 6:1:7:0 Reticulosis13(93%) Colagenosis1(7%) 0:12(86%):2(14%) 0:0:14(100%) 3(21%):9(65%):2(14%) 0:0:14(100%) 0:0:14(100%) 0:4(29%):10(71%) 3:2:2:0 Elastoreticulosis7 0:4(58%):3(42%) 0:2(29%):5(71%) 0:4(57%):3(43%) 0:1(14%):6(86%) 0:1(14%):6(86%) 0:5(71%):2(29%) Abb.N:Numbers,A:M:V:U:Arterial,mixed,andvenousinfarctionsand unknowncause,ret.fib.:dilatationofreticulinfibersofthealveolarwal, Alv.Fib.:Fibrosisofthealveolarwal,BM:Basementmembrane,BM Dil.: DilatationbetweenbothsidesofepithelialBM,BM Dis.:DisruptionofBM betweenepithelialandendothelial,bypass:communicationbetweensys temicandpulmonarycirculation.
Fig.1 Histologicalfeaturesofacinar-sizedalveolarwalhemorrhage(a d).approximatelythesameareas andthesamemagnification( 200)wereselected.a.Thealveolarwalwasfiledwithbloodandshowed markeddilatation,he.b.lossofalveolarepithelia(arrow)wasnotedinmultipleareasonthealveolar wal,immunostainingforkeratin.c.endotheliaofthealveolarcapilary(arrow)showeddiscontinuous stainingandthecapilaryluminawererathercolapsed.bloodislocatedinthealveolarwaloutsideofthe capilarylumina,immunostainingforendothelium.d.markeddilatationbetweentheepithelialbasement membranes(bm,outsidebrownline,betweenthethinarrows)wasnoted.insomeplaces,theendothelial BM showedcolapsebutnodisruption(thickarrow)andwideseparationfrom epithelialbm wasalso noted.
Fig.2 Microscopicfeaturesofacuteinfarction(a d)usingthesamemagnification( 200).a.Alveolarlu minawerefiledwithbloodandthealveolarwalbecameunclearwithoutstainedepithelialandendothe lialnucleiwhichindicatesnecrosisordropout,he.b.thealveolarwalshowedmarkedcolagenous thickening(blackarrow)andmarkedexpansionintothealveolarlumenofreticulinfibers(whitearrows. suspectedepithelialbm),silverstaining.c.alveolarepithelialbm showedmildtomarkedoutsideexpan sion(thinarrow)buttheendothelialbm wascolapsedandwidelyseparatedfrom theepithelialbm (thickarrows).thesefeatureswerethesameasthoseshowninfig.1d,immunostainingfortypeiv colagen.d.thereweremanycommunications(thickarrows)betweenalveolarcapilariesandcapilaries oftheinterlobularsepta(locatedinthecenteroffig.2d,betweenthethinarrows),immunostainingfor typeiv colagen.
Fig.3 Histologicalfeaturesoforganizedinfarction.a.Sublobularsized(about1cm)infarctionwassurroundedbytwo-layeredfibroustissues,HE,panoramaticview.b.Theouterlayeroffibroustissues(box attheleftsideoffig.3a)showedsevereelastosis(blackfibers)withcolapseandlossofthelung structure.mostirregularshapedtinylumina(arrow)meannewlyformedbloodvessels,evg, 40.c.The innerlayeroffibroustissues(boxatthebotom sideoffig.3a)showedintraluminalorganization(brown fibrosisinthealveoli)andnewlyformedsmalbloodvessels(arrow).therightsideshowsnewlyformed organizationintoinfarctionandtheleftsideshowsunorganizedinfarction,evg, 200.d.Theinnerlayer offibroustissuesisnearlythesameasinfig.3c,showedcolagenosis(arrowhead)andrecentextension ofnewlyformingreticulinfiberintothefrontofinfarction(arrow).therightsideshowsnewlyformedorganizationintoinfarction,thecentershowsnewlyformingreticulosis,andtheleftsideshowsunorganizedinfarction,silverstaining. 200.