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Inhaled Nitric Oxid...
Inhaled Nitric Oxide Therapy : Non-response and Rebound Response
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- Chen, Luni, 1962- (author)
- Uppsala universitet,Institutionen för medicinska vetenskaper
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Weitzberg, Eddie (opponent)
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(creator_code:org_t)
- ISBN 9155454755
- Uppsala : Acta Universitatis Upsaliensis, 2002
- English 58 s.
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Series: Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, 0282-7476 ; 1201
- Related links:
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https://urn.kb.se/re...
Abstract
Subject headings
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- Therapeutic inhaled nitric oxide (INO) has proved beneficial in patients with pulmonary hypertension. However, around 30-40% of the patients are non-responders to this therapy, and a life-threatening rebound response may occur during attempts to withdraw INO. This thesis investigated the link between vasoconstrictors and non- and rebound responses in piglets subjected to acute lung injury by exposure to endotoxin or oleic acid (OA). We found that INO had strong effect in mainly ET-1 related, endotoxin-induced pulmonary hypertension, and there was a rebound response after INO withdrawal. Thus, the weaker the response to INO, the greater the rebound. Neither response nor rebound was seen in oleic acid-induced, mainly prostaglandin related pulmonary hypertension. INO decreased expression of the ET-A receptor, and this might be another signal transduction pathway whereby INO relieves pulmonary vasoconstriction besides increasing c-GMP. Thus INO might have better effect in pulmonary vasoconstriction that is mainly mediated by ET-1 than when other vasoconstrictors are involved in the vascular reaction. Increased production and/or release of vasoconstrictor peptide endothelin-1 (ET-1) during INO, and release of prostaglandin TXA2 and PGF2α after INO withdrawal, were more important causes of the rebound, than a decreasing endogenous NO production during INO. The latter mechanism has been proposed in previous studies. An increase in prostaglandins after INO withdrawal is possibly secondary to the increase in ET-1 during INO. Combination of INO with the COX inhibitor diclofenac blocked the rebound reaction. These findings may open the way for new therapeutic modalities.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Anestesi och intensivvård (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Anesthesiology and Intensive Care (hsv//eng)
Keyword
- Anaesthesiology and intensive care
- nitric oxide inhalation
- rebound response
- non-response
- endothelin-1
- COX inhibitor
- prostaglandin
- ARDS
- endotoxin
- oleic acid
- Anestesiologi och intensivvård
- Anaesthetics and intensive care
- Anestesiologi och intensivvård
- Clinical Physiology
- klinisk fysiologi
Publication and Content Type
- vet (subject category)
- dok (subject category)
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