FACTORS AFFECTING RENAL MICROVASCULAR BLOOD-FLOW IN RAT HYPERDYNAMIC BACTEREMIA

被引:6
作者
CRYER, HG
BLOOM, ITM
UNGER, LS
GARRISON, RN
机构
[1] UNIV LOUISVILLE, HLTH SCI CTR,SCH MED,CTR APPL MICROVASC RES, DEPT SURG, LOUISVILLE, KY 40202 USA
[2] UNIV LOUISVILLE, HUMANA HOSP, TRAUMA PROGRAM SURG, LOUISVILLE, KY 40292 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 264卷 / 06期
关键词
CHRONIC UNILATERAL HYDRONEPHROTIC KIDNEY; IN-VIVO VIDEOMICROSCOPY; ANGIOTENSIN-II BLOCKADE; ALPHA-ADRENERGIC BLOCKADE; LIVE ESCHERICHIA-COLI BACTEREMIA; PROSTAGLANDIN INHIBITION;
D O I
10.1152/ajpheart.1993.264.6.H1988
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
To determine whether angiotensin II and alpha-adrenergic activity contribute to the mechanism of impaired renal microvascular blood flow during hyperdynamic live Escherichia coli (E. coli) bacteremia, we used in vivo video microscopy in the chronic unilateral hydronephrotic kidney of decerebrate male Sprague-Dawley rats. Intravenous infusion of E. coli caused arteriolar constriction to 83 +/- 4% of baseline (BL) in cortical radial arteries (CRA), 82 +/- 3% of BL in afferent (AFF) arterioles, and decreased flow to 54 +/-9% of BL. Subsequent local inhibition of renal prostaglandin synthesis with mefenamate increased preglomerular arteriolar constriction to 55 +/- 6% of BL in CRA and 51 +/- 6% of BL in AFF arterioles and decreased renal microvascular blood flow to 26 +/- 8% of BL values in E. coli animals but had no effect on control animals. Subsequent local renal angiotensin II receptor blockade with saralasin acetate increased renal microvascular blood flow in E. coli animals to 64 +/- 9% of BL by dilating CRA to 78 +/- 5% of BL and AFF arterioles to 89 +/- 5% of BL. Phentolamine caused further dilation of CRA to 104 +/- 7% BL and AFF arterioles to 116 +/- 109% and increased flow to 99 +/- 8% of BL. Acetylcholine increased diameters further to 110 +/- 3% of BL in CRA and 136 +/- 12% of BL in AFF arterioles. These data indicate that in our chronic hydronephrotic kidney model during E. coli bacteremia, renal microvascular tone is due to increased angiotensin II and alpha-adrenergic activity and some other, as yet, undefined factor.
引用
收藏
页码:H1988 / H1997
页数:10
相关论文
共 30 条
[1]  
ADAMS HR, 1983, CIRC SHOCK, V10, P215
[2]   AN OPTICAL DOPPLER INTRAVITAL VELOCIMETER [J].
BORDERS, JL ;
GRANGER, HJ .
MICROVASCULAR RESEARCH, 1984, 27 (01) :117-127
[3]  
BUHRLE CP, 1986, LAB INVEST, V54, P462
[4]   CONTROL OF THE RENAL MICROVASCULATURE BY VASOACTIVE PEPTIDES [J].
CARMINES, PK ;
FLEMING, JT .
FASEB JOURNAL, 1990, 4 (15) :3300-3309
[5]  
CRYER HM, 1988, CIRC SHOCK, V26, P71
[6]   PROSTAGLANDINS AND NONSTEROIDAL ANTIINFLAMMATORY DRUGS - EFFECTS ON RENAL HEMODYNAMICS [J].
DIBONA, GF .
AMERICAN JOURNAL OF MEDICINE, 1986, 80 (1A) :12-21
[7]  
EDWARDS RM, 1988, NEWS PHYSIOL SCI, V3, P216
[8]   CALCIUM-ANTAGONISTS PREFERENTIALLY DILATE PREGLOMERULAR VESSELS OF HYDRONEPHROTIC KIDNEY [J].
FLEMING, JT ;
PAREKH, N ;
STEINHAUSEN, M .
AMERICAN JOURNAL OF PHYSIOLOGY, 1987, 253 (06) :F1157-F1163
[9]   LIMITATIONS OF THERMODILUTION CARDIAC-OUTPUT MEASUREMENTS IN THE RAT [J].
HAYES, BE ;
WILL, JA ;
ZARNSTORFF, WC ;
BISGARD, GE .
AMERICAN JOURNAL OF PHYSIOLOGY, 1984, 246 (06) :H754-H760
[10]   DISSOCIATION OF SYSTEMIC AND RENAL EFFECTS IN ENDOTOXEMIA - PROSTAGLANDIN INHIBITION UNCOVERS AN IMPORTANT ROLE OF RENAL NERVES [J].
HENRICH, WL ;
HAMASAKI, Y ;
SAID, SI ;
CAMPBELL, WB ;
CRONIN, RE .
JOURNAL OF CLINICAL INVESTIGATION, 1982, 69 (03) :691-699