PROLONGED LEUKOCYTE TRANSIT-TIME IN CORONARY MICROCIRCULATION OF ENDOTOXEMIC PIGS

被引:40
作者
GODDARD, CM [1 ]
ALLARD, MF [1 ]
HOGG, JC [1 ]
HERBERTSON, MJ [1 ]
WALLEY, KR [1 ]
机构
[1] UNIV BRITISH COLUMBIA, ST PAULS HOSP, PULM RES LAB, VANCOUVER, BC V6Z 1Y6, CANADA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1995年 / 269卷 / 04期
关键词
SEPSIS; CAPILLARY TRANSIT TIME; MORPHOMETRY;
D O I
10.1152/ajpheart.1995.269.4.H1389
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We quantified the timing and extent of leukocyte retention by the coronary microcirculation in a pig model of hyperdynamic sepsis in three ways. First, the transmyocardial leukocyte gradient was determined as coronary blood flow (calibrated ultrasonic flow probe) multiplied by the difference between leukocyte count's in the aorta and coronary sinus. Measurements were taken at 1-min intervals for 30 min and then at S-min intervals for 45 min in anesthetized pigs exposed to either endotoxin (50 mu g/kg iv over 30 min) (n = 7) or vehicle (n = 7). Second, postmortem morphometric analysis was used to quantitate the number and location of retained myocardial leukocytes. Finally, myocardial capillary transit time of leukocytes was calculated from the above measures. In the endotoxin group 2.1 +/- 0.8 x 10(9) leukocytes/100 g wet wt were retained in the coronary circulation, primarily in capillaries. This resulted in 111 +/- 37 (P < 0.05) times as many leukocytes in the coronary microcirculation than predicted from the arterial leukocyte concentration. Myocardial capillary transit time of leukocytes was prolonged to 39.1 +/- 20.6 s (P < 0.05) in the endotoxin group versus 5.0 +/- 1.4 s in the control group. We conclude that, after endotoxin infusion in a pig model of hyperdynamic sepsis, myocardial leukocyte transit is slowed, leading to the retention of large numbers of leukocytes in the coronary microcirculation.
引用
收藏
页码:H1389 / H1397
页数:9
相关论文
共 38 条
  • [1] REGIONAL MYOCARDIAL CAPILLARY ERYTHROCYTE TRANSIT-TIME IN THE NORMAL RESTING HEART
    ALLARD, MF
    KAMIMURA, CT
    ENGLISH, DR
    HENNING, SL
    WIGGS, BR
    [J]. CIRCULATION RESEARCH, 1993, 72 (01) : 187 - 193
  • [2] POLYMORPHONUCLEAR NEUTROPHIL CONTRIBUTION TO INDUCED TOLERANCE TO BACTERIAL LIPOPOLYSACCHARIDE
    BARROSOARANDA, J
    SCHMIDSCHONBEIN, GW
    ZWEIFACH, BW
    MATHISON, JC
    [J]. CIRCULATION RESEARCH, 1991, 69 (05) : 1196 - 1206
  • [3] BENGTSSON A, 1993, CIRC SHOCK, V39, P83
  • [4] THE RELEASE OF LEUKOCYTES AND PLATELETS FROM THE PULMONARY CIRCULATION BY EPINEPHRINE
    BIERMAN, HR
    KELLY, KH
    CORDES, FL
    BYRON, RL
    POLHEMUS, JA
    RAPPOPORT, S
    [J]. BLOOD, 1952, 7 (07) : 683 - 692
  • [5] NITRIC-OXIDE PRODUCTION WITHIN CARDIAC MYOCYTES REDUCES THEIR CONTRACTILITY IN ENDOTOXEMIA
    BRADY, AJB
    POOLEWILSON, PA
    HARDING, SE
    WARREN, JB
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (06): : H1963 - H1966
  • [6] BRIGHAM KL, 1986, AM REV RESPIR DIS, V133, P913
  • [7] SAMPLING DESIGNS FOR STEREOLOGY
    CRUZORIVE, LM
    WEIBEL, ER
    [J]. JOURNAL OF MICROSCOPY, 1981, 122 (JUN) : 235 - 257
  • [8] THE CORONARY CIRCULATION IN HUMAN SEPTIC SHOCK
    CUNNION, RE
    SCHAER, GL
    PARKER, MM
    NATANSON, C
    PARRILLO, JE
    [J]. CIRCULATION, 1986, 73 (04) : 637 - 644
  • [9] DAHINDEN C, 1983, J IMMUNOL, V130, P857
  • [10] COMPARISON OF NEUTROPHIL AND CAPILLARY DIAMETERS AND THEIR RELATION TO NEUTROPHIL SEQUESTRATION IN THE LUNG
    DOERSCHUK, CM
    BEYERS, N
    COXSON, HO
    WIGGS, B
    HOGG, JC
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 1993, 74 (06) : 3040 - 3045