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No significant differences were observed in the body temperatures of animals in the S group, VF-C group and VF-I group at each time point (Table 1). At a MAP > 90 mmHg, the heart rates of the animals in the VF-C group and VF-I group after ROSC were significantly higher than those in the S group. The heart rates in the two groups of animals reached their peak 1 h after ROSC and then decreased over time. At 6 h after ROSC, these values remained significantly higher than those in the S group.
Item Baseline ROSC immediate ROSC 30 min ROSC 1 h ROSC 2 h ROSC 4 h ROSC 6 h Sham operation 35.97 ± 1.11 36.30 ± 0.67 36.48 ± 0.33 36.55 ± 0.42 36.75 ± 0.33 36.58 ± 0.64 36.67 ± 0.52 VF control 35.65 ± 1.36 35.91 ± 1.17 36.55 ± 1.63 36.54 ± 1.69 36.85 ± 2.03 36.58 ± 2.50 36.49 ± 2.46 654-1 group 36.75 ± 1.54 36.11 ± 1.36 35.98 ± 1.85 36.29 ± 1.88 35.90 ± 1.97 35.91 ± 2.21 35.40 ± 2.48 Note. The unit is degrees Celsius. ROCS, recovery of spontaneous circulation. Table 1. Comparison of the body temperatures of the three groups of animals at different time points
At 0.5 h after ROSC, the VF-I group began to receive 654-1 intravenously, and the infusion lasted approximately 1.5 h. The heart rates of animals in the VF-I group were significantly higher than those in the VF-C group at 1 h after ROSC (0.5 h after medication); the heart rates then decreased starting 2 h after ROSC. From baseline until 6 h after ROSC, the heart rates in the VF-I group did not significantly differ from those in the VF-C group (Figure 1).
Figure 1. Comparison of the heart rates in the three groups of animals at different time points. The yellow curve represents the S group, the blue curve represents the VF-C group, and the red curve represents the VF-I group, *P < 0.05. The heart rates in the post-ROSC VF-C group and the VF-I group were significantly higher than those in the S group, reaching a peak at 1 h after ROSC. These rates remained significantly higher than those in the S group at 6 h after ROSC. The VF-I group began to receive 654-1 at 0.5 h after ROSC, and the infusion time was approximately 1.5 h. The heart rates in the VF-I group were significantly higher than those in the VF-C group at ROSC 1 h (0.5 h after medication). From 2 h after ROSC (1.5 h after medication) to 6 h after ROSC, the heart rates in the VF-I group did not significantly differ from those in the VF-C group. ROSC, return of spontaneous circulation; CPR, cardiopulmonary resuscitation.
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No significant difference was observed in Pv-aCO2 and lactic acid levels among the S groups, VF-C group and VF-I group at baseline and immediately after ROSC. However, at various time points after ROSC, the levels of Pv-aCO2 and lactic acid in the VF-C group were significantly higher than those in the S group. Pv-aCO2 peaked at 1 h after ROSC, then slowly decreased until 6 h after ROSC but remained significantly higher than that in the S group. Lactic acid peaked at 0.5 h after ROSC. Although it decreased significantly afterward, it remained significantly higher than that in the S group at 6 h after ROSC.
The Pv-aCO2 level in the VF-I group decreased rapidly at 0.5 h after ROSC after 654-1 administration and was significantly lower than that in the VF-C group at 1 h ROSC. It was also significantly lower than that in the VF-C group at each subsequent time point. No significant difference was observed with respect to that in the S group. After initiation of the 654-1 intervention, the blood lactic acid level also changed rapidly. At 1 h after ROSC and various time points thereafter, the indicators in the VF-I group were significantly lower than those in the VF-C group.
The cardiac ejection capacity of experimental animals significantly decreased after ROSC. The cardiac index (CI) in the VF-C group and VF-I group was significantly lower than that in the S group, and this effect persisted until 6 h after ROSC. However, the VF-I group began to receive 654-1 0.5 h after ROSC, and the CI was significantly higher than that in the VF-C group at each subsequent time point, although it remained lower than that in the sham operation group.
The small vessel resistance (SVR) of experimental animals in the VF-C group and VF-I group after ROSC was significantly higher than that in the S group. The SVR level in the VF-C group peaked 1 h post-ROSC, then slowly decreased, and remained significantly higher than that in the S group 6 h after ROSC. The SVR in the VF-I group did not differ from that in the VF-C group at the time of ROSC until 0.5 h afterward, but after administration of 654-1 at 0.5 h, the SVR level was significantly lower than that in the VF-C group; the SVR level was not significantly different from that in the S group at 6 h after ROSC (Figure 2).
Figure 2. Comparison of lactic acid levels, Pv-aCO2, CI and SVR indicators at different time points in the three groups of animals. The yellow curve represents the S group, the blue curve represents the VF-C group, and the red curve represents the VF-I group, *P < 0.05. At various time points after ROSC, the levels of Pv-aCO2 and LAC in the VF-C group were significantly higher than those in the S group, then slowly decreased thereafter. These levels remained significantly higher than those in the S group at 6 h ROSC. After administration of 654-1, the blood lactic acid level and Pv-aCO2 were significantly lower than those in the VF-C group. The ejection capacity of the heart after ROSC was significantly diminished and remained significantly lower than that in the S group 6 h after ROSC. After administration of 654-1, the CI at each time point was significantly higher than that in the VF-C group but remained lower than that in the S group, whereas the SVR level was significantly lower than that in the VF-C group. No difference with respect to the S group was observed at 6 h ROSC. CPR, cardiopulmonary resuscitation; ROSC, return of spontaneous circulation; CI, cardiac index; SVR, small vessel resistance; LAC, Lactic acid.
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At baseline, the visceral microcirculation monitoring parameters in the three groups of experimental animals, including MFI, TVD, PPV and PVD, showed no significant differences. Although the experimental animals maintained a MAP > 90 mmHg after ROSC, no significant difference was observed with respect to the S group values, although the microcirculation indices after ROSC remained significantly lower than those in the S group until 6 h after ROSC.
After the 654-1 intervention at 0.5 h after ROSC, the MFI, TVD, PPV and PVD in the VF-I group were significantly higher than those in the VF-C group at all subsequent time points, although they remained significantly lower than those in the S group at 6 h post-ROSC (Figure 3).
Figure 3. Comparison of microcirculation indices of the three groups of animals at different time points. The yellow curve represents the S group, the blue curve represents the VF-C group, and the red curve represents the VF-I group, compare VF-C and the VF-I group, *P < 0.05. After ROSC, the experimental animals maintained a MAP > 90 mmHg; however, the microcirculation indices (MFI, TVD, PPV and PVD) in the experimental group were significantly lower than those in the S group at ROSC and for 6 h thereafter. The MFI, TVD, PPV, and PVD after 654-1 intervention were significantly higer than those in the VF-C group at all subsequent time points, but remained significantly lower than those in the S group at 6 h after ROSC. MFI, microcirculation flow index; TVD, total vessel density. PPV, perfusion pressure of valve; PVD, perfusion vessel density; CPR, cardiopulmonary resuscitation; ROSC, return of spontaneous circulation.
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No significant differences were observed in TNF-α among the three groups of animals at baseline, and its level increased significantly after CPR. The level in the VF-C group remained significantly higher than that in the S group until 6 h after ROSC. The level in the VF-I group was higher than that in the S group at 1 h, 2 h, and 4 h after ROSC, but was significantly lower than that in the VF-C group. At 6 h after ROSC, no significant difference was observed with respect to the S group.
The SDC-1 of the three groups of animals showed no significant differences at baseline, and its level increased significantly after CPR. The VF-C group level peaked at 4 h after ROSC, then decreased thereafter, but remained significantly higher than that in the S group after 6 h. No significant difference was observed between the VF-I group and VF-C group at 1 h ROCS, and the level was significantly lower than that in the VF-C group at each subsequent time point. No significant difference was observed at 6 h after ROSC with respect to the S group (Figure 4).
Figure 4. Comparison of TNF-α and SDC-1 levels in the three groups of animals at different time points. The yellow curve represents the S group, the blue curve represents the VF-C group, and the red curve represents the VF-I group, *P < 0.05. No significant difference was observed in the levels of TNF-α and SDC-1 in the three groups at baseline, and the levels significantly increased after ROSC. The VF-C group level was significantly higher than that in the S group at 6 h after ROSC. The levels of the two indicators were significantly lower than those in the VF-C group at simultaneous time points, and no significant difference with respect to the S group was observed at 6 h after ROSC. CPR, cardiopulmonary resuscitation; ROSC, return of spontaneous circulation.
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At 6 h post-ROSC, the levels of TNF-α and SDC-1 in the myocardial tissue of the VF-C group were significantly higher than those in the S group and the VF-I group, whereas the TNF-α level in the VF-I group did not significantly differ from that in the S group. Although the SDC-1 level in the VF-I group was higher than that in the S group, it was significantly lower than that in the VF-C group (Figure 5).
Figure 5. Comparison of TNF-α and SDC-1 levels in myocardial tissues of the three groups of animals 6 h after ROSC. The green bar represents the S group, the red bar represents the VF-C group, and the blue bar represents the VF-I group. *Significant difference with respect to the S group, #significant difference with respect to the VF-C group. At 6 h post-ROSC, the levels of TNF-α and SDC-1 in the myocardial tissue of the VF-C group were significantly higher than those in the S group. No significant difference was observed in TNF-α levels between the VF-I group and the S group. The SDC-1 level was higher than that in the S group but significantly lower than that in the VF-C group. ROSC, recovery of spontaneous circulation.
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Under a light microscope, the myocardial myofilaments of samples from the VF-I group appeared to be arranged neatly, whereas those in the VF-C group samples were disordered. Under an electron microscope, the myocardial muscle fibers of samples from the VF-I group appeared mildly damaged, with relatively complete and neatly arranged myofilament structures, whereas those in the VF-C group were severely damaged, showing a damaged, broken and disordered myofilament structure (Figure 6).
Figure 6. Electron microscopy and histopathological (H&E-stained samples) light microscopy of myocardial tissue from the VF-I group and the VF-C group. Pictures of the VF-I group: 0.5 μm transmission electron microscopy (A); 2 μm transmission electron microscopy (B); 400× magnification of histopathologic (H&E-stained) samples (C). Pictures of the VF-C group: 0.5 μm transmission electron microscopy (D); 3 µm transmission electron microscopy (E); 400× magnification of histopathologic (H&E-stained) samples (F). The results of electron microscopy and light microscopy of histopathologic (H&E-stained) tissue samples revealed that the myocardial myofilament structure in the VF-I group was nearly complete and neatly arranged, and showed minimal muscle fiber damage; in contrast, the myocardial fibers in the VF-C group were severely damaged, as indicated by myofilament structures with clear damage and disordered arrangement.
Influence of Microcirculatory Dysfunction on Myocardial Injury after Cardiopulmonary Resuscitation
doi: 10.3967/bes2022.044
- Received Date: 2021-10-25
- Accepted Date: 2022-01-27
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Key words:
- Cardiopulmonary resuscitation /
- Post-cardiac arrest syndrome /
- Microcirculation dysfunction /
- Myocardial injury /
- Anisodamine hydrobromide (654-1)
Abstract:
Citation: | YANG Jun, DONG Gui Juan, WANG Hong Wei, ZHAO Xin, WANG Fu Jun, ZHANG Jian, GUO Shu Bin. Influence of Microcirculatory Dysfunction on Myocardial Injury after Cardiopulmonary Resuscitation[J]. Biomedical and Environmental Sciences, 2022, 35(4): 334-344. doi: 10.3967/bes2022.044 |