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Objective:To study the role of myocardial work parameters in early identification of myocardial injury in neonatal asphyxia.Methods:From July 2020 to December 2021, neonates diagnosed with mild neonatal asphyxia admitted to the Department of Neonatology of our hospital within 24 h after birth were prospectively enrolled into the asphyxia group. Neonates without asphyxia during the same period were selected as the control group and matched with the asphyxia group for gender, gestational age and birth weight at a ratio of 1:1~1:2. The asphyxia group was subgrouped into preterm asphyxia group and term asphyxia group. All neonates received echocardiography within 24 h after birth. Multiple parameters were measured including M-mode, two-dimensional image, Doppler image, global longitudinal strain (GLS) and myocardial work parameters [global work index (GWI), global constructive work (GCW), global wasted work (GWW), global work efficiency (GWE)]. The level of serum N-terminal pro brain natriuretic peptide (NT-proBNP) was recorded in the asphyxia group. The data were compared between the asphyxia group and the control group. Correlations between myocardial work parameters and other parameters were analyzed.Results:A total of 33 cases were in the asphyxia group and 43 cases were in the control group. The preterm asphyxia group (18 cases) showed significantly lower GWI and GCW than the preterm control group (18 cases) [GWI: (702±153) mmHg vs. (879±205) mmHg, GCW: (1 016±221) mmHg vs. (1 200±271) mmHg] ( P<0.05). No differences existed in GLS, GWW and GWE. The term asphyxia group (15 cases) showed significantly lower GWW than the term control group (25 cases) [45.0 (30.0, 65.0) mmHg vs. 71.0 (35.5,85.5) mmHg] ( P<0.05). No differences existed in GLS, GWI, GCW and GWE. GWI was negatively correlated with serum NT-proBNP level ( r=-0.327, P<0.05). Conclusions:GWI and GCW may indicate myocardial injury in preterm neonates with mild asphyxia.
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Objective To explore the expressions of autophagy-related gene Beclin-1 and LC3 in adriamycin induced eardiomyopathy rats,to prnve that autophagy might take part in the development of adriamycin induced eardiomyopathy in rats,so as to provide experimental and theoretical evidence for preventing and treating adriamycin induced cardiomyopathy.Methods Forty-five male SD rats were randomly divided into 3 groups,control groups,ADR group and ADR+3-MA group.The model of adriamycin induced cardiomyopathy rats was established.The tissue sample taken from the left ventricle wall was checked for the morphons of autophagosome by electron microscope. The expressions of Beelin-1 and LC3 of myocardium were detected.Results The morphons of autophagosome in ADR group was significantly increased compared with that in control and ADR +3-MA groups. The expression of Beclin-1 in myocardium of ADR group was significantly inereased compared with that in control and ADR +3-MA groups (P < 0.05).The level of LC3 in myocardium of ADR group was significantly increased compared with that in control and ADR+3-MA groups (P < 0.05).Conclusions Autophagy plays an important role in adriamycin induced cardiomyopathy.
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Aim To determine whether pranlukast (ONO-1078), a cysteinyl leukotriene receptor antagonist, possesses therapeutic effect when administered after focal cerebral ischemia in mice. Methods Persistent focal cerebral ischemia was induced by middle cerebral artery occlusion. Pranlukast and edaravone, a positive control drug, were ip injected 1, 6 and 24 h after ischemia. The neurological deficits were evaluated by neurological scores and inclined plane test 24 and 48 h after the surgery. Forty-eight h later, the brain slices were prepared for measurements of infarct volume and the ratio of ischemic/non-ischemic hemispheres. Brain sections were cut and examined for neuron densities in different regions of the brain. The effects of pranlukast and edaravone were evaluated by the changes of these variables. Results Pranlukast (0.1 and 0.2 mg?kg -1) and edaravone (3 and 10 mg?kg -1) significantly reduced the neurological deficits, infarct volume (maximally 82.3%), ratio of ischemic/non-ischemic hemispheres, and attenuated the reduction of neuron densities in hippocampal CA1 region, cortex and striatum. Conclusion Pranlukast possesses therapeutic effect on ischemic insults when administered after ischemia as effective as edravone, indicating a therapeutic potential in the treatment of ischemic stroke.
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AIM:To confirm the action of the light transmission method in evaluating focal ischemic cerebral infarction on persistent focal cerebral ischemia in mice. METHODS:Persistent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Bederson's neurological scores, climbing board and hanging test were performed 24 h after ischemia, and infarct volume, brain hemisphere area, neuron density of cortex and subcortex were measured with computer-assisted imaging. Pranlukast ( 0.1 mg?kg -1) or nimodipine ( 0.4 mg?kg -1) were injected ip once daily for 3 days and to 1 h before MCAO assess the neuroprotective effect. RESULTS:The infarct volumes measured by light transmission closely correlated with that measured by TTC staining and neuron densities. The infarct volumes measured by light transmission well correlated with the neurological scores measured by integrated graded approach, too. Both pranlukast and nimodipine significantly attenuated infarct volumes and the ratio of ischemic/non-ischemic hemispheres, and reduced neurological deficits and neuron death. CONCLUSION:Light transmission and integrated graded approach can be used not only for qualitative analysis of focal cerebral ischemia, but also for evaluating the neuroprotective effect of drugs.