CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 6, November/December 2022 306 AFRICA In this study, DEGs were uploaded to the Search Tool for the Retrieval of Interacting Genes (STRING). STRING was used to construct a protein–protein interaction (PPI) network with a > 0.9 PPI score cut-off criterion. Comprehensive information on the PPIs of DEGs was downloaded. In addition, we ranked these DEGs according to the degree score calculated by the Cytoscape (http://www. cytoscape.org) plug-in cytoHubba.19 Statistical analysis The results are expressed as the mean ± SD of independent experiments. Statistical differences between the four groups were analysed using one-way analysis of variance with a Bonferroni post-test. The Bonferroni post-test was used to compare each grade separately and p < 0.05 was considered statistically significant. For comparisons of data between two groups, two-tailed, unpaired t-tests were applied. Prism 8 (GraphPad, La Jolla, CA) was used for statistical analyses. A p-value of < 0.05 was considered statistically significant. Results Haemodynamic effects of abrupt pressure overload Measured directly, there were statistically significant differences for LVSP and LVEDP between the sham-operated and aorticbanded animals (LVSP: 103.44 ± 9.30 vs 156.98 ± 7.21 mmHg, p < 0.01; LVEDP: 5.56 ± 1.80 vs 41.89 ± 6.79 mmHg, p < 0.01) over the five-minute period. In the VRP-pretreated (0.5 and 1 mg/kg) groups, the LVSPs significantly decreased (140.39 ± 6.83 mmHg in group 3, p < 0.01 and 132.73 ± 5.17 mmHg in group 4, p < 0.01) compared with that in the TAC group (156.98 ± 7.21 mmHg). The LVEDP also decreased (27.84 ± 3.82 mmHg in group 3, p < 0.01 and 18.96 ± 2.53 mmHg in group 4, p < 0.01) compared with that in the TAC group (41.89 ± 6.79 mmHg) (Fig. 1). Preventative effects of VRP on ventricular arrhythmias ECG analysis data were obtained from this research on the effects of (–) and (+) VRP (0.5 and 1 mg/kg, respectively) in our previously published experiment.20 Ventricular arrhythmias (including premature ventricular contraction and ventricular tachycardia) were generated in response to acute pressure overload; however, AVBs were not detected. Type I seconddegree AVBs and two-to-one second-degree AVBs were detected in two VRP-pretreated groups (groups 3 and 4). Compared with the control group, the incidence of ventricular arrhythmias was reduced by two doses of (+) VRP (0.5 and 1 mg/kg) pretreatment. The mean ventricular arrhythmia score (VAS) increased in the ## * * ## * * * * LVSP (mmHg) 200 150 100 50 0 Group 1 Group 2 Group 3 Group 4 ## * * ## * * * * LVEDP (mmHg) 60 40 20 0 Group 1 Group 2 Group 3 Group 4 Fig. 1. Elevated LV pressure in response to LV afterload increases (induced by TAC surgery) in each group. LVSP, left ventricular systolic pressure; LVEDP, left ventricular end-diastolic pressure; LVP, left ventricular pressure; TAC, transverse aortic constriction. A B ## ## * * ## * * * * VAS 5 4 3 2 1 0 Group 1 Group 2 Group 3 Group 4 Type I 2nd-degree AVB Two-to-one 2nd-degree AVB Number of rats 10 8 6 4 2 0 Group 1 Group 2 Group 3 Group 4 Fig. 2. Effects of VRP on VAS and number of rats in each group that presented with AVB. A: Effects of VRP (0.5 and 1 mg/kg) on VAS in response to increased LV afterload. B: Number of rats that presented with type I second-degree AVB and two-to-one second-degree AVB in the VRP-pretreated group. **p < 0.01 vs group 1, ##p < 0.01 vs group 2. VAS, ventricular arrhythmia score; AVB, atrioventricular block. VRP, verapamil; AVB, atrioventricular block. A B
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