Fig. 7 | Communications Biology

Fig. 7

From: Activation of oxytocin neurons in the paraventricular nucleus drives cardiac sympathetic nerve activation following myocardial infarction in rats

Fig. 7

Effect of atosiban (i.c.v.) and retosiban (i.v.) on cardiac sympathetic nerve activity following acute MI. a Changes in cardiac sympathetic nerve activity (% increase in cardiac SNA – of integrated area of the raw nerve signal) in SHAM rats treated with atosiban (4.5 µg in 5 µl i.c.v. n = 6) or retosiban (3 mg/kg, i.v. n = 6), or untreated MI rats (n = 6), or M -rats treated with atosiban (i.c.v. n = 6) or retosiban (3 mg kg−1, i.v. n = 8). There was a significant main effect of TIME (F(6, 90) = 10.96, P< 0.0001, two-way RM ANOVA), TREATMENT (F(2, 15) = 12.37, P= 0.0007, two-way RM ANOVA), and a significant TIME × TREATMENT interaction (F(12, 90) = 5.69, P< 0.0001, two-way RM ANOVA). *P< 0.05, ***P< 0.001 vs pre-MI (time zero), #P< 0.05, ###P< 0.001 vs MI + retosiban and vs MI + atosiban, Bonferroni’s post hoc test. All data are presented as mean ± SEM. b Representative transverse section of a heart slice stained with tetrazolium chloride (TTC) as a quantitative means of assessing of infarct size. The viable myocardium absorbs the TTC stain and forms a reddish pink pigment. In contrast, the infarcted myocardium remains unstained pale-white (encircled by blue dashed line)

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