RESUMO
Objective: The purpose of this study was to evaluate the prognosis of patients with anomalous left coronary artery originating from pulmonary artery with varying cardiac function after surgical correction. Methods: This was a single-center retrospective cohort study including 51 patients with anomalous left coronary artery originating from pulmonary artery, all of whom underwent surgery at our center. Results: All 5 deaths occurred in the pre-operative low cardiac function group (n = 39). After corrected by body surface area, parameters such as left coronary artery, right coronary artery, left atrial diameter, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and main pulmonary artery diameter, were lower in patients in the normal cardiac function group than in the low cardiac function group. The rate of collateral circulation formation was higher in the normal cardiac function group. The proportion of changes of T wave was higher in the low cardiac function group (P = 0.005), and the duration of vasoactive drugs (dopamine, milrinone, epinephrine, nitroglycerin.) was longer in the low cardiac function group. Left ventricular end-diastolic diameter, left ventricular end-systolic diameter, main pulmonary artery diameter, and left atrial diameter were smaller than those pre-operatively (P < 0.05). Left ventricular ejection fraction was higher than that pre-operatively (P = 0.003). The degree of mitral regurgitation in the low cardiac function group was reduced post-operatively (P < 0.001). Conclusion: There was a significant difference between the pre-operative baseline data of the low cardiac function group and the normal cardiac function group. After surgical repair, cardiac function gradually returned to normal in the low cardiac function group. The low cardiac function group required vasoactive drugs for a longer period of time. The left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left atrial diameter, and main pulmonary artery diameter decreased and gradually returned to normal after surgery. The degree of mitral regurgitation in the low cardiac function group was reduced after surgery.
RESUMO
Our objective was to investigate the protein level of phosphorylated N-methyl-D-aspartate (NMDA) receptor-1 at serine 897 (pNR1 S897) in both NMDA-induced brain damage and hypoxic-ischemic brain damage (HIBD), and to obtain further evidence that HIBD in the cortex is related to NMDA toxicity due to a change of the pNR1 S897 protein level. At postnatal day 7, male and female Sprague Dawley rats (13.12 ± 0.34 g) were randomly divided into normal control, phosphate-buffered saline (PBS) cerebral microinjection, HIBD, and NMDA cerebral microinjection groups. Immunofluorescence and Western blot (N = 10 rats per group) were used to examine the protein level of pNR1 S897. Immunofluorescence showed that control and PBS groups exhibited significant neuronal cytoplasmic staining for pNR1 S897 in the cortex. Both HIBD and NMDA-induced brain damage markedly decreased pNR1 S897 staining in the ipsilateral cortex, but not in the contralateral cortex. Western blot analysis showed that at 2 and 24 h after HIBD, the protein level of pNR1 S897 was not affected in the contralateral cortex (P > 0.05), whereas it was reduced in the ipsilateral cortex (P < 0.05). At 2 h after NMDA injection, the protein level of pNR1 S897 in the contralateral cortex was also not affected (P > 0.05). The levels in the ipsilateral cortex were decreased, but the change was not significant (P > 0.05). The similar reduction in the protein level of pNR1 S897 following both HIBD and NMDA-induced brain damage suggests that HIBD is to some extent related to NMDA toxicity possibly through NR1 phosphorylation of serine 897.