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Hypercapnic acidosis transiently weakens hypoxic pulmonary vasoconstriction in anesthetized pigs, without affecting the endogenous pulmonary nitric oxide production.

Nilsson, Manja C. A., 1966- (författare)
Uppsala universitet,Anestesiologi och intensivvård
Fredén, Filip (författare)
Uppsala universitet,Anestesiologi och intensivvård
Larsson, Anders (författare)
Uppsala universitet,Anestesiologi och intensivvård
visa fler...
Wiklund, Peter (författare)
Karolinska universitetssjukhus
Bergquist, Maria (författare)
Uppsala universitet,Institutionen för kirurgiska vetenskaper
Hambraeus-Jonzon, Kristina (författare)
Karolinska universitetssjukhus
visa färre...
 (creator_code:org_t)
2012-01-21
2012
Engelska.
Ingår i: Intensive Care Medicine. - : Springer Science and Business Media LLC. - 0342-4642 .- 1432-1238. ; 38:3, s. 509-517
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Purpose  Hypercapnic acidosis often occurs in critically ill patients and during protective mechanical ventilation; however, the effect of hypercapnic acidosis on endogenous nitric oxide (NO) production and hypoxic pulmonary vasoconstriction (HPV) presents conflicting results. The aim of this study is to test the hypothesis that hypercapnic acidosis augments HPV without changing endogenous NO production in both hyperoxic and hypoxic lung regions in pigs. Methods  Sixteen healthy anesthetized pigs were separately ventilated with hypoxic gas to the left lower lobe (LLL) and hyperoxic gas to the rest of the lung. Eight pigs received 10% carbon dioxide (CO2) inhalation to both lung regions (hypercapnia group), and eight pigs formed the control group. NO concentration in exhaled air (ENO), nitric oxide synthase (NOS) activity, cyclic guanosine monophosphate (cGMP) in lung tissue, and regional pulmonary blood flow were measured. Results  There were no differences between the groups for ENO, Ca2+-independent or Ca2+-dependent NOS activity, or cGMP in hypoxic or hyperoxic lung regions. Relative perfusion to LLL (Q LLL/Q T) was reduced similarly in both groups when LLL hypoxia was induced. During the first 90 min of hypercapnia, Q LLL/Q T increased from 6% (1%) [mean (standard deviation, SD)] to 9% (2%) (p < 0.01), and then decreased to the same level as the control group, where Q LLL/Q T remained unchanged. Cardiac output increased during hypercapnia (p < 0.01), resulting in increased oxygen delivery (p < 0.01), despite decreased PaO2 (p < 0.01). Conclusions  Hypercapnic acidosis does not potentiate HPV, but rather transiently weakens HPV, and does not affect endogenous NO production in either hypoxic or hyperoxic lung regions.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Anestesi och intensivvård (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Anesthesiology and Intensive Care (hsv//eng)

Nyckelord

Nitric oxide
hypercapnic acidosis
hypoxic pulmonary vasoconstriction
exhaled nitric oxide
cyclic guanosine monophosphate
pulmonary blood flow.
Anaesthesiology and Intensive Care
Anestesiologi och intensivvård

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