Ischaemic heart preconditioning in rats with adjuvant-induced arthritis.
BACKGROUND
Adjuvant-induced arthritis (AIA) in rats is a model of chronic systemic inflammation and a model of rheumatoidarthritis in humans.


OBJECTIVE
To investigate effectiveness of ischaemic preconditioning (IPC) in reducing the area of myocardial infarction in rats with AIA.


METHODS
The study was performed in vivo in male SPRD/Mol/Lod rats. Animals were assigned to the experimental group (n = 15) or the control group (n = 14). In the experimental group, AIA was induced by subcutaneous administration of 1 mLof Freund's complete adjuvant, and the experiment was performed after 14 days. In control (healthy) animals, no procedures were performed prior to the proper experiment. Animals were anaesthesized (by intraperitoneal administration of ketamineand xylazine) and put on a ventilator. Then, myocardial infarction was induced, preceded by IPC in some animals. To induceinfarction, left main coronary artery (LMCA) was occluded for 30 min, followed by 60 min of reperfusion. IPC protocol consisted of LMCA occlusion for 3 min, followed by 5 min of reperfusion and a second LMCA occlusion for 7 min. Weevaluated a percentage ratio of the infarct size to the risk area (IS/RA). Necrosis area was stained with tetrazolium, and thearea supplied by LMCA was determined using Evans blue. All areas were determined by planimetry. We used nonparametric Kruskal-Wallis rank ANOVA with multiple comparisons, and the results were shown as median values and 25th and 75th percentiles. P < 0.05 was considered statistically significant.


RESULTS
In the control group with IPC (n = 7), the IS/RA ratio of 25% (23-38) was significantly reduced compared to thecontrol group without IPC (n = 7) (58% [57-63], p < 0.05). In the AIA group with IPC (n = 7), the IS/RA ratio of 58% (51-65)did not differ significantly compared to the AIA group without IPC (n = 8) (65% [62-71]).


CONCLUSIONS
Our findings indicate that IPC in rats with AIA does not result in a significant reduction of myocardial necrosisarea induced by 30 min of ischaemia and 60 min of reperfusion. This effect might have been related to the presence ofchronic systemic inflammation. Absent or reduced benefits of IPC may be one reason for an increased cardiovascular risk inpatients with rheumatoid arthritis.
Department of General and Experimental Pathology, Medical University of Warsaw, Warsaw, Poland. gosiawojciech@yahoo.com.
Małgorzata
M
Wojciechowska
Mateusz
M
Wątroba
Grażyna
G
Ciużyńska
Mariusz
M
Bral
Dariusz
D
Szukiewicz
D000818:Animals; D000873:Anthracenes; D001169:Arthritis, Experimental / Q000150:complications / Q000628:therapy*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000150:complications / Q000628:therapy*; D005620:Freund's Adjuvant; D019157:Ischemic Preconditioning, Myocardial; D007958:Leukocyte Count; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley
C546739:AnOV compound; D000873:Anthracenes; D005620:Freund's Adjuvant