title: Effects of norepinephrine on kidney in a swine model of cardiopulmonary resuscitation.
abstract: BACKGROUND
  The aim of this study was to study the effects of norepinephrine (NE)-induced hypertension (HT) on renal biochemistry, enzymology, and morphology after restoration of spontaneous circulation (ROSC) by cardiopulmonary resuscitation (CPR) in swine.
  
  
  METHODS
  After 4 minutes of ventricular fibrillation, standard CPR was carried out. The survivors were then divided into 2 groups. The HT group (n = 5) received 0.4 to 1.0 μg kg⁻¹ min⁻¹ of NE continuously to maintain the mean arterial pressure (MAP) at 130% of the baseline (ie, MAP before ventricular fibrillation). The normal pressure (NP) group (n = 5) received 0.2 to 0.5 μg kg⁻¹ min⁻¹ NE continuously to maintain MAP at the baseline level. Hemodynamic status and oxygen metabolism were monitored, and blood urea nitrogen and creatinine were measured in blood samples obtained at baseline and at 10 minutes, 2 and 4 hours after ROSC. At 24 hours after ROSC, the animals were killed and the kidney was removed to determine Na⁺-K⁺-ATPase and Ca²⁺-ATPase activities and histologic changes under a light and electron microscopy.
  
  
  RESULTS
  mean arterial pressure, cardiac output, and coronary perfusion pressure were significantly higher (P < .01), whereas the oxygen extraction ratio was lower in the HT group than in the NP group (P < .05). Blood urea nitrogen and creatinine increased in the NP group but did not change in the HT group. Renal ATP enzyme activity was significantly higher in the HT group than the NP group (Na⁺-K⁺-ATP enzyme: 4.024 ± 0.740 U versus 3.190 ± 0.789 U, Ca²⁺-ATP enzyme: 3.615 ± 0.668 versus 2.630 ± 0.816; both P < .05). The HT group showed less cellular edema, necrosis, and fewer damaged mitochondria compared with the NP group.
  
  
  CONCLUSIONS
  These data suggest that inducing HT by NE helps to maintain stable hemodynamic status and oxygen metabolism and may protect the kidney in terms of biochemistry, enzymology, and histology after CPR.
authors.affiliation: Emergency Department of Beijing Chaoyang Hospital affiliated as Capital Medical University, Beijing, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Han
authors.forename: Chun-Sheng
authors.initials: CS
authors.lastname: Li
authors.forename: Zhi-Yu
authors.initials: ZY
authors.lastname: Su
authors.forename: Yi
authors.initials: Y
authors.lastname: Lu
authors.forename: Sheng-Qi
authors.initials: SQ
authors.lastname: Wang
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001806:Blood Urea Nitrogen; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002302:Cardiac Output / Q000502:physiology; D016887:Cardiopulmonary Resuscitation; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013552:Swine; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D003404:Creatinine; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D009638:Norepinephrine