title: Changes of local brain tissue oxygen pressure after vasopressin during spontaneous circulation.
abstract: BACKGROUND
  Brain tissue oxygen pressure (PbtO2) correlates to cerebral blood flow (CBF) during spontaneous circulation, with one important regulator being nitric oxide (NO). Although it is established that arginine vasopressin (AVP) improves CBF and global cerebral oxygenation during cardiopulmonary resuscitation, it is unknown whether similar beneficial effects are present during spontaneous circulation. The purpose of this study was to investigate the effects of AVP with and without pre-treatment with the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on local brain tissue oxygenation in a beating heart model.
  
  
  METHODS
  Following approval of the Animal Investigational Committee, nine healthy piglets underwent general anaesthesia, and were instrumented with a probe in the cerebral cortex to measure PbtO2. Each animal was assigned to receive AVP (0.4 U . kg(-1)), and after a wash-out period, L-NAME (25 mg x kg(-1) over 20 min) followed by AVP (0.4 U x kg(-1)). After each AVP administration, nitroglycerine (25 microg x kg(-1) over 1 min) as a NO donor was infused to test the vascular reactivity independently from NOS inhibition.
  
  
  RESULTS
  Three minutes after administration of AVP, PbtO2 increased significantly (P < .05; mean +/- SEM, 31 +/- 11 versus 43 +/- 14 mm Hg, +39%), compared with baseline. After pre-treatment with L-NAME, the changes of PbtO2 after AVP were not significant (32 +/- 11 versus 28 +/- 10, -13%) when compared with the baseline.
  
  
  CONCLUSIONS
  In this beating heart porcine model, local brain tissue oxygenation was improved after AVP alone, but not after inhibition of NO synthesis with L-NAME.
authors.affiliation: Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Campus Kiel, Germany. e.cavus@t-online.de
authors.forename: E
authors.initials: E
authors.lastname: Cavus
authors.forename: V
authors.initials: V
authors.lastname: Dörges
authors.forename: H
authors.initials: H
authors.lastname: Wagner-Berger
authors.forename: K-H
authors.initials: KH
authors.lastname: Stadlbauer
authors.forename: M
authors.initials: M
authors.lastname: Steinfath
authors.forename: V
authors.initials: V
authors.lastname: Wenzel
authors.forename: B
authors.initials: B
authors.lastname: Bein
authors.forename: J
authors.initials: J
authors.lastname: Scholz
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D001921:Brain / Q000098:blood supply* / Q000187:drug effects* / Q000502:physiology; D002536:Cerebral Arteries / Q000187:drug effects* / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D004347:Drug Interactions / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006323:Heart Arrest / Q000150:complications / Q000503:physiopathology; D000860:Hypoxia / Q000188:drug therapy / Q000517:prevention & control; D020925:Hypoxia-Ischemia, Brain / Q000188:drug therapy / Q000517:prevention & control; D008297:Male; D023421:Models, Animal; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects* / Q000502:physiology; D034421:Sus scrofa; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D004791:Enzyme Inhibitors; D018696:Neuroprotective Agents; D020030:Nitric Oxide Donors; D014665:Vasodilator Agents; D001127:Arginine Vasopressin; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester