The effect of acute stress exposure on ischemia and reperfusion injury in rat heart: Role of oxytocin

Figures & data

Figure 1.  Illustration of the experimental protocols. Hearts perfused in vitro in all groups were subjected to 30 min of ischemia followed by 60 min reperfusion. IR, in vitro and vehicle treatment in vivo; in vivo treatments: St, swim stress; OT, i.p. oxytocin injection; ATO, i.p. atosiban injection; NS, normal saline.

Table I.  Hemodynamic parameters.

		Baseline				End of ischemia				End of reperfusion
Group	n	HR (bpm)	LVDP (mmHg)	RPP (bpm × mmHg	CF (ml/min)	HR (bpm)	LVDP (mmHg)	RPP value (%, basal value)	CF (ml/min)	HR (bpm)	LVDP (mmHg)	RPP value (% basal value)	CF (ml/min)
IR	6	288 ± 15.7	90 ± 6.3	25920 ± 773.1	7 ± 0.49	235 ± 17.1	39 ± 4.6	57 ± 7.4^*	3.3 ± 0.36	246 ± 17.4	50.5 ± 3.1	47 ± 1.4^*	3 ± 0.32
St	8	252 ± 13.9	89.2 ± 7.8	22478 ± 1132	6.3 ± 0.5	212 ± 9.0	76 ± 7.7	57 ± 6.8^*	3.3 ± 0.22	213 ± 8.8	82 ± 2.5	52 ± 3.1^*	2.6 ± 0.26
St+OT	7	297 ± 12.0	73.0 ± 2	21681 ± 1206	6.5 ± 0.6	269 ± 9.5	66 ± 7.2	48 ± 5.4^*	3.2 ± 0.3	244 ± 16.5	61 ± 6	61 ± 6.9^*	2.6 ± 0.3
OT	5	256 ± 16.6	75 ± 2.9	19230 ± 1384	6 ± 0.5	218 ± 10.0	84 ± 20	58 ± 10^*	3.7 ± 0.73	211 ± 12.8	88.4 ± 2.9^†	75 ± 8.5^†	3.5 ± 0.55
St+ATO	9	274 ± 19.1	77 ± 3.6	21098 ± 1368	6 ± 0.47	225 ± 15.0	82 ± 8	49 ± 7.2^*	2 ± 0.36	204 ± 18.7	38+5.1^‡	27 ± 5.2^*^‡	3 ± 0.5
ATO	5	264 ± 26.8	78 ± 2.6	20631 ± 1890	6 ± 0.5	213 ± 21.0	76 ± 12	44 ± 3.7^*	3.3 ± 0.38	181 ± 14.0	74 ± 19	25 ± 6^*	2.7 ± 0.55

Note: ATO, atosiban; bpm, beats per minute; CF, coronary flow; HR, heart rate; IR, ischemia/reperfusion; LVDP, left ventricular developed pressure; n, number of rats; OT, oxytocin; RPP, rate pressure product; St, stress; repeated measures ANOVA was used for comparisons within groups.

^* P < 0.05 vs. baseline. One-way ANOVA was used for comparisons between and within groups.

^† P < 0.05 vs. IR group.

^‡ P < 0.05 vs. St group. Data are mean ± SEM.

Figure 2.  Myocardial area at risk (AAR/V%) and infarct size (IS/AAR%) in IR (n = 6), St (n = 8), St+ATO (n = 9), St+OT (n = 7), OT (n = 5), and ATO (n = 5) groups. St, stress; OT, oxytocin; ATO, atosiban; IR, ischemia–reperfusion. Data are presented as mean ± SEM. Two-way ANOVA: ^*P < 0.05 vs. IR group. ^#P < 0.001 vs. St group.

Figure 3.  Activity of creatine kinase MB (CK-MB) in coronary effluent at the end of reperfusion in IR (n = 6), St (n = 8), St+ATO (n = 9), St+OT (n = 7), OT (n = 5), and ATO (n = 5) groups. IR, ischemia–reperfusion; St, stress; OT, oxytocin; ATO, atosiban. Data are presented as mean ± SEM. Two-way ANOVA: ^*P < 0.05 vs. IR group. ^#P < 0.05 vs. St group.

Figure 4.  Activity of LDH in coronary effluent at the end of reperfusion in IR (n = 6), St (n = 8), St+ATO (n = 9), St+OT (n = 7), OT (n = 5), and ATO (n = 5) groups. IR, ischemia–reperfusion; St, stress; OT, oxytocin; ATO, atosiban. Data are presented as mean ± SEM. Two-way ANOVA: ^*P < 0.05 vs. IR group. ^#P < 0.01 vs. St group.