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Factors affecting renal microvascular blood flow in rat hyperdynamic bacteremia
H G Cryer1, I T Bloom, L S Unger
1Department of Surgery, University of California, Los Angeles 90024.
The American Journal of Physiology
|June 1, 1993
Summary
During E. coli bacteremia, angiotensin II and alpha-adrenergic activity constrict renal microvasculature. Blocking these pathways restored normal blood flow, indicating their key roles in sepsis-induced kidney injury.
Area of Science:
- Nephrology
- Sepsis Pathophysiology
- Renal Microcirculation
Background:
- Sepsis-induced kidney injury involves impaired renal microvascular blood flow.
- The roles of angiotensin II and alpha-adrenergic activity in this impairment are not fully understood.
Purpose of the Study:
- To investigate the contribution of angiotensin II and alpha-adrenergic activity to renal microvascular dysfunction during hyperdynamic Escherichia coli (E. coli) bacteremia.
Main Methods:
- Utilized in vivo video microscopy in a rat model of chronic unilateral hydronephrotic kidney.
- Administered intravenous E. coli, followed by local inhibition of prostaglandin synthesis, angiotensin II receptor blockade, and alpha-adrenergic blockade.
Main Results:
- E. coli infusion caused significant arteriolar constriction and reduced renal blood flow.
- Inhibition of prostaglandin synthesis exacerbated constriction.
- Angiotensin II receptor blockade and phentolamine (alpha-adrenergic blocker) reversed constriction and restored blood flow.
- Acetylcholine further increased vessel diameters.
Conclusions:
- Renal microvascular tone during E. coli bacteremia is mediated by increased angiotensin II and alpha-adrenergic activity.
- An additional, unidentified factor also contributes to vasoconstriction.