Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0151814 (
coronary occlusion
)
3,687
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The goal of the present study was to assess how genetic loss of microsomal prostaglandin E(2) synthase-1 (
mPGES-1
) affects acute cardiac ischemic damage after
coronary occlusion
in mice. Wild type (WT), heterozygous (
mPGES-1
(+/-)), and homozygous (
mPGES-1
(-/-)) knockout mice were subjected to left coronary artery occlusion. At 24h, myocardial infarct (MI) volume was measured histologically. Post-MI survival, plasma levels of creatine phosphokinase (CPK) and cardiac troponin-I, together with MI size, were similar in WT,
mPGES-1
(+/-) and
mPGES-1
(-/-) mice. In contrast, post-MI survival was reduced in
mPGES-1
(-/-) mice pretreated with I prostanoid receptor (IP) antagonist (12/16) compared with vehicle-treated controls (13/13
mPGES-1
(-/-)) together with increased CPK and cardiac troponin-I release. The deletion of
mPGES-1
in mice results in increased prostacyclin I(2) (PGI(2)) formation and marginal effects on the circulatory prostaglandin E(2) (PGE(2)) level. We conclude that loss of
mPGES-1
results in increased PGI(2) formation, and in contrast to inhibition of PGI(2), without worsening acute cardiac ischemic injury.
...
PMID:The effects of microsomal prostaglandin E synthase-1 deletion in acute cardiac ischemia in mice. 1952 23
The aim of the present study was to compare the effects of genetic
mPGES-1
loss and COX-2 inhibition on myocardial damage after
coronary occlusion
.
mPGES-1
(-/-) mice and their wild-type littermates were injected with vehicle or COX-2 inhibitor (celecoxib), and 30min later the left coronary artery was surgically occluded. At 24h, myocardial infarct (MI) volume was measured histologically. Post-MI survival was reduced in WT mice receiving celecoxib (12/20) compared with vehicle-treated controls (12/12) or the loss of
mPGES-1
(13/13) together with increased phosphokinase (CPK) and cardiac troponin-I release. Endogenous
mPGES-1
expression was unchanged by ischemia in WT mice and absent in
mPGES-1
(-/-) hearts. COX-2 expression was markedly increased at 24h after MI in WT hearts; this upregulation was largely attenuated in
mPGES-1
(-/-) mice. We conclude that loss of
mPGES-1
prevents the upregulation of COX-2 after myocardial infarct, and in contrast to inhibition of COX-2, does not increase ischemic myocardial damage.
...
PMID:Comparison of microsomal prostaglandin E synthase-1 deletion and COX-2 inhibition in acute cardiac ischemia in mice. 1955 11
