(left ventricular pressure, LVP)

Transcription

1 Chinese Journal of Pathophysiology 2000,16 (6) : [ ] (2000) , 2, 1, 1, 3, 3 (11 ;21 ;31, ) [ ] : :, :,,(LVP) ( ) kpa,d p/ d t ( ) kpa/ s, LVP ( ) kpa,d p/ d t ( ) kpa/ s, P < 0101 ;,,,,LVP ( ) kpa,d p/ d t ( ) kpa/ s,, P < 0101:,,,,, ;,, [] ;, ;,;, [] R54212 [] A,,B 3 [1 ] : 1, ;2,Woodruff [2 ],,3 d,1,,, () B 3,Nancy () BALB/ c, 1820 g,, () 10 [ ] [ ] [ ] CMB ( ), ml, PFU ( ) B 3 Eagleye,, () 20,3 d () 14 d ( ), d,3 % 15 mg kg - 1 iv,,6 (left ventricular pressure, LVP) (d p/ d t), (Nihonkohden,RM , ), (),, 20 %,3 % () ( gx s),3 F, t B 3 2 d,5 d,3 d, 14 d,

2 492 3 d, 14 d Tab 1 The heart weight and body weight in BALB/ c mice ( gx s, n = 10) Group Heart weight (mg) Body weight (g) Heart weight/ body weight ( 10 2 ) Normal Virus direct damage # Immune damage P < 0105, vs normal group ; # P < 0105, vs immune damage group 2 Tab 2 Comparison between the hemodynamics in normal mice and myocarditis mice ( gx s, n = 10) Group Normal group Virus direct damage Immune damage LVP(kPa) d p/ d t (kpa/ s) P < 0101, vs normal group ; 3 3 P < 0101, vs virus di2 rect damage 2, LVP d p/ d t, LVP d p/ d t () 3 d,,, ( 1) ; 14 d,,,, (2) () 3 d,, (3) 14 d,,,,,, (4) (1,2 1) Fig 3 Electron microscopic characterization of myocardial CVB 3 infection in mice during virus damage stage. (EM ) The dilatation of mitochondria reveals at the time of first three days after injecting CVB 3 3 ( ), Klingel [3,4 ],(3 d ),,3 d Fig 4 Electron microscopic characterization of myocardial CVB 3 infection in mice during immune damage stage (EM ) There were the disruption of mitochondria and tenuous myocytes at the time of two weeks after injecting CVB 3 4 ( )

3 493, 10 d,,,3 d,,,,,, [ ], [1 ] Wolfgram LJ, Bciscl KW, Herskowitz A, et al. Variations LVP d p/ d t,, Hamrell [5 ] in the susceptibility to CVB 3 - induced myocarditis among different strains of mice[j ]. J Immunol, 1986, 136 : [2 ] Woodruff JF. Viral myocarditis [J ]. Am J Pathol, 1980,, 101 : , [3 ],,. A murine model of acute, myocarditis infected by coxsackie virus B 3 [ J ]. Chinese [6 ] Medical Journal, 1988, 101 :712., [4 ] Klingel K, Kandolf R. The role of enterovirus replication in,, ;, the development of acute and chronic heart muscle disease in different immunocompetent mouse strains[j ]. Scand J Infect Dis, 1993, Suppl 88 :7985. [5 ] Hamrell BB, Huber SA, Leslie KO. Reduced unloaded sar2 (- MHC),, comere shortening velocity and a shift to a slower myosin isodorm in acute murine Coxsackievirus myocarditis [ J ]., Circ Res, 1994, 75 : ,, [6 ],,,. B 3 [7 ],, [J ].,1998, 36 : (),, [7 ] Izumi T, Hanawa H, Saeki M, et al. Cardiac contractile,, proteins and autoimmune myocarditis [ J ]. Mol Cell Biochem, 1993, 119 :6771. Characteristics of morphology and left ventricular f unction in the mouse with myocarditis WAN Chao2min, WANG Zheng2rong, ZHOU Mi,DENGJian - jun, WU Tai2xiang, YU Hong2ji ( West China University of Medical Sciences, Chengdu , China) [ Abstract] AIM :To determine the relationship between microhistology and cardiac contractility in myocardi2 tis animal model. METHODS :Setting up myocarditis animal model by injecting Coxsackivevirus B 3 ( CVB 3 ) into mice, then observed myocardial morphological changes and measured left ventricular function of mice at the time of first three days and two weeks after injecting CVB 3. RESULTS :Subcellular structure (mitochondria) changed at the first three days after injecting CVB 3. The left ventricular pressure (LVP) and the rate of intraventricular pressure de2 velopment (d p/ d t) which is the index of reflecting cardiac contractility depressed in this stage ( ) kpa and ( ) kpa/ s, respectively. There were ( ) kpa and ( ) kpa/ s in normal mice, respectively ( P < 0. 01). Myocardial lesions were more severe during immune response stage - two weeks after inject2 ing CVB 3, including myocardial inflammation and necrosis. LVP was ( ) kpa and dp/ d t was (20915

4 ) kpa/ s in immune response stage. There was significant difference between mice with myocarditis at early stage and at immune response stage ( P < 0. 01). CONCL USIONS :The factor of causing the depression of cardiac contrac2 tility in early stage (virus - induced damage) is mainly change of subcellular structure. Mitochondria cannot provide energy as normal. There were more severe myocardial lesions in later stage (cell - mediated autoimmune response) than in early stage. The depression of cardiac contractility is a consequence of multifactor. [ MeSH] Myocardial diseases ; Mitochondria, Heart ; Ventricular function, left ; Animals, laboratory Chinese Journal of Pathophysiology 2000,16 (6) : 494 [ ] (2000) , (, ),,,,,,,, (,, ),,,,,,,,,,,,,,1 1, [ ] [ ] ,,,,,,,,,,,,,,, (534 )

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