Linked Life Data

1284561

Source:http://linkedlifedata.com/resource/pubmed/id/1284561

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1993-6-9
pubmed:abstractText
Prostaglandins participate in the regulation of blood pressure in normotensive and hypertensive subjects; vascular tone is subject to the continuous relaxing influence of endogenous vasodilating prostaglandins. Prostaglandin I2 (PGI2; prostacyclin), probably the most important physiological modulator of vascular tone, decreases blood pressure together with a concomitant increase in cardiac output and a reduction in systemic vascular resistance secondary to peripheral vasodilation. In addition, vasodilation within the splanchnic, pulmonary and coronary vascular beds has been observed, with increased blood flow through the mesenteric, renal and coronary vascular beds. These changes in regional blood flow have been associated with the inhibition, by PGI2, of the vasoconstrictor response to sympathetic nervous stimulation and pressor hormones [noradrenaline (norepinephrine), angiotensin II]. However, other prostaglandins, such as prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha), induce coronary vasoconstriction and have different effects on pulmonary artery blood pressure because of their effect on pulmonary vascular resistance. Nonsteroidal anti-inflammatory drugs (NSAIDs; e.g. indomethacin) have been reported to induce hypertension parallel to a fall in cardiac output, suggesting that the underlying mechanism is an increase in systemic vascular resistance. In animal models these agents reduced regional blood flow in the ischaemic myocardium, with a corresponding increase in infarct size. Ibuprofen, which inhibits prostaglandin synthesis to a lesser extent than indomethacin, did not exert systemic or coronary haemodynamic effects. NSAIDs also provide protection in shock models but may exacerbate haemodynamic derangements and decrease survival in acute hypovolaemic hypotension. To what extent do NSAIDs and opioids influence cardiovascular status during the postoperative course and analgesic therapy? Continuous infusion of NSAIDs for analgesia had no major haemodynamic effects. Also, there were insignificant changes in indices of left heart function (cardiac output, stroke volume) and the systemic circulation (mean arterial pressure, systemic vascular resistance) following intravenous ketorolac injections, whereas cardiac output and mean arterial pressure decreased after administration of morphine. The pulmonary circulation was unaffected by ketorolac administration, whereas morphine administration induced an increase in pulmonary vascular resistance. Indices of right and left cardiac work were decreased by morphine. Thus, ketorolac produces fewer haemodynamic effects than morphine, although it is possible that some of the effects of morphine may result from morphine-induced histamine release. NSAIDs may be seen as a worthwhile gain with respect to morphine in clinical situations when hypotension is disadvantageous or when reduction in afterload is not a specific therapeutic aim.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0012-6667
pubmed:author
pubmed:issnType
Print
pubmed:volume
44 Suppl 5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
42-51
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Cardiovascular risks and benefits of perioperative nonsteroidal anti-inflammatory drug treatment.
pubmed:affiliation
Department of Anaesthesiology, Flemish Free University, Brussels Medical Centre, Belgium.
pubmed:publicationType
Journal Article, Review