title: Effects of increased intra-abdominal pressure and volume expansion on renal function in the rat.
abstract: BACKGROUND
  The effects of increased intra-abdominal pressure (IAP) and volume expansion on renal function in the rat were studied to gain more knowledge of the oliguria seen during laparoscopic procedures and to reduce the detrimental renal effects of IAP.
  
  
  METHODS
  IAP was elevated to 5 or 10 mmHg by insufflation of CO(2) and maintained for 2 h in anaesthetized and mechanically ventilated rats. Rats with normal IAP served as controls. An angiotensin II receptor I antagonist, candesartan, was given as a bolus injection and a 5% volume expansion was achieved by i.v. saline infusion. An angiotensin-converting enzyme (ACE) inhibitor was also given. Renal parameters were the glomerular filtration rate (GFR), urine production, the urinary concentrations of sodium and potassium and the osmolality in the urine. The arterial acid-base balance and blood pressure were also monitored.
  
  
  RESULTS
  The GFR deteriorated by 70% during pneumoperitoneum (PP) of 10 mmHg. There was a dramatic drop in sodium excretion (88-97%). With candesartan and elevated IAP, there was a drop in mean arterial pressure (from 90 to 55 mmHg) and the negative renal effects were very pronounced. Renal function was better preserved during elevated IAP in combination with volume expansion.
  
  
  CONCLUSIONS
  Capnoperitoneum suppresses renal function, especially in combination with angiotensin II receptor 1 blockade and ACE inhibition. Volume expansion reduces the deleterious effects of PP on renal function during elevated IAP. The results suggest that patients should not be given pharmaceuticals blocking the renin-angiotensin-aldosterone system prior to procedures that may increase IAP. It may be beneficial, however, to reduce angiotensin II tension by volume expansion.
authors.affiliation: Division of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
authors.forename: Pernilla
authors.initials: P
authors.lastname: Lindström
authors.forename: Jonas
authors.initials: J
authors.lastname: Wadström
authors.forename: Anna
authors.initials: A
authors.lastname: Ollerstam
authors.forename: Cecilia
authors.initials: C
authors.lastname: Johnsson
authors.forename: A Erik G
authors.initials: AE
authors.lastname: Persson
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds; D002216:Captopril / Q000494:pharmacology; D004195:Disease Models, Animal; D007668:Kidney / Q000187:drug effects* / Q000503:physiopathology*; D008297:Male; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects*; D011312:Pressure; D051381:Rats; D011919:Rats, Inbred Strains; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology*; D013777:Tetrazoles / Q000494:pharmacology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; D002216:Captopril; C081643:candesartan