Attention to pulmonary arteriovenous fistula in a case of transient hypoxemia and cerebral infarction during pregnancy: a case report and literature review.

BACKGROUND: Pulmonary arteriovenous fistula is rare during pregnancy. Pulmonary arteriovenous fistula presents no pulmonary symptoms in most patients but can be exacerbated by pregnancy. If not diagnosed and treated promptly, pulmonary arteriovenous fistula can lead to respiratory failure, stroke, spontaneous hemothorax, or other fatal complications. CASE PRESENTATION: A 29-year-old healthy pregnant woman presented with a transient drop in blood oxygen level of unknown cause during a routine examination at 34 weeks of gestation and during a cesarean section at 38 weeks of pregnancy. The patient's oxygen saturation quickly returned to normal and was not further investigated. On day 3 postpartum, the patient suddenly displayed slurred speech and right limb myasthenia. A head magnetic resonance imaging revealed cerebral infarction in the left basal ganglia. Subsequent computed tomography pulmonary arteriography revealed bilateral pulmonary arteriovenous fistula, which was likely the cause of cerebral infarction. The patient was transferred to the Department of Thoracic Surgery after one month of treatment and successfully underwent percutaneous embolization of pulmonary arteriovenous fistula. CONCLUSION: Pulmonary arteriovenous fistula should not be neglected if a pregnant woman presents with transient hypoxemia and cerebral infarction. A transient decrease in pulse oxygen saturation that cannot be explained by common clinical causes can be an early warning sign of the disease. Early diagnosis and multidisciplinary management could improve the prognosis.

PHLDA1 promotes sevoflurane-induced pyroptosis of neuronal cells in developing rats through TRAF6-mediated activation of Rac1.

Sevoflurane anesthesia induces neurocognitive impairment and pyroptosis in the developing brain. Pleckstrin homology-like domain, family A, member 1 (PHLDA1) was involved in neuronal apoptosis, oxidative stress and inflammation during ischemic stroke. The role of PHLDA1 in sevoflurane-induced pyroptosis in developing rats was investigated. Firstly, neonatal rats at day 7 was exposed to 2.0% sevoflurane for 6 h to induce neurotoxicity. Pathological analysis showed that sevoflurane anesthesia induced hippocampal injury and reduced the number of neurons. The expression of PHLDA1 was elevated in hippocampus of sevoflurane-treated rats. Secondly, sevoflurane anesthesia-treated neonatal rats were injected with adeno-associated virus serotype (AAV) to mediate knockdown of PHLDA1. Injection with AAV-shPHLDA1 ameliorated sevoflurane-induced hippocampal injury and neurocognitive impairment in rats. Moreover, knockdown of PHLDA1 increased the number of neurons in sevoflurane-treated rats. Silence of PHLDA1 suppressed neuronal apoptosis, and inhibited pyroptosis in sevoflurane-treated rats. Thirdly, PHLDA1 was also elevated in sevoflurane-treated primary neuronal cells. Loss of PHLDA1 also enhanced cell viability and suppressed pyroptosis of sevoflurane-treated primary neuronal cells. Lastly, silence of PHLDA1 reduced protein expression of TRAF6 and p-Rac1 in sevoflurane-treated rats and neuronal cells. Over-expression of TRAF6 attenuated PHLDA1 silence-induced increase of cell viability and decreased pyroptosis in neuronal cells. In conclusion, loss of PHLDA1 protected against sevoflurane-induced pyroptosis in developing rats through inhibition of TRAF6-mediated activation of Rac1.

[Effect of Penehyclidine hydrochloride in systemic inflammatory response syndrome caused by cardiopulmonary bypass].

OBJECTIVE: To investigate whether Penehyclidine hydrochloride has effect on the inflammatory process and leukocytes in cardiac surgery patients undergoing cardiopulmonary bypass. METHODS: 40 rheumatic heart disease patients undergoing CPB were randomly divided into Penehyclidine hydrochloride (P) group and control (C) group (20 patients in each group). In group P, intravenous drip of 0.01 mg/kg of Penehyclidine hydrochloride injection was given before anesthesia, and 0. 015 mg/kg of Penehyclidine hydrochloride was added into initial volume of CPB. While in control group, 0.9% NaCl solution was given instead of injection as a placebo. Blood samples were taken before anesthesia (T0), 30 min after CPB (T1), 10 min after aortic off-clamping (T2) and 2 hours when CPB was over (T3). Interleukin-6 (IL-6), tumornecross alpha (TNF-alpha) levels were detected by ELISA. The morbility of pneumonia and SIRS caused by CPB was also evaluated. RESULTS: At T2 and T3, the IL-6 level was higher than T0 and T1 both in group C and group P (P < 0.05). At T2 and T3, the IL-6 level in group C was higher than that of group P (P < 0.05). The TNF-alpha level at T3 was lower than at T1 and T2 in group P (P < 0.05). There was no significant difference between group P and group C at each time point (P > 0.05). The morbility of pneumonia and SIRS was higher in group C (P < 0.05). CONCLUSION: Penehyclidine hydrochloride can decrease the levels of proinflamnlatory cytokines in plasma and therefore attenuate the morbility of pneumonia and SIRS caused by CPB.