Intraarterial mechanical thrombectomy for the treatment of postoperative cerebral infarction: a case report.

Perioperative ischemic stroke is an uncommon event associated with significant morbidity and mortality. The complexity of the surgical procedure and surgery induced hypercoagulable status also influence the incidence of stroke. The management of stroke involves a decision regarding the quickest suitable revascularization method. Endovascular mechanical thrombectomy, such as intra-arterial mechanical thrombectomy (IAMT), can restore vascular patency of the vessels, providing an alternative or synergistic method to restore blood flow. Although, there are no recommended treatment guidelines, IAMT is eligible to be a treatment of choice for perioperative ischemic stroke. We experienced a case of a patient who demonstrated hemiplegia and aphasia, the early symptom of acute ischemic stroke, in the post-anesthesia care unit and performed IAMT successfully. Thus we report the case with a review of the relevant literature.

CO2 relaxation of the rat lung parenchymal strip.

Evidence from liquid-filled rat lungs supported the presence of CO2-dependent, active relaxation of parenchyma under normoxia by unknown mechanisms (Emery et al., 2007). This response may improve matching of alveolar ventilation (V˙A) to perfusion (Q˙) by increasing compliance and V˙A in overperfused (high CO2) regions, and decrease V˙A in underperfused regions. Here, we have more directly studied CO2-dependent parenchymal relaxation and tested a hypothesized role for actin-myosin interaction in this effect. Lung parenchymal strips (∼1.5mm×1.5mm×15mm) from 16 rats were alternately exposed to normoxic hypocapnia ( [Formula: see text] ) or hypercapnia ( [Formula: see text] ). Seven specimens were used to construct length-tension curves, and nine were tested with and without the myosin blocker 2,3-butanedione monoxime (BDM). The results demonstrate substantial, reversible CO2-dependent changes in parenchyma strip recoil (up to 23%) and BDM eliminates this effect, supporting a potentially important role for parenchymal myosin in V˙A/Q˙ matching.

A comparative study of emergence agitation between sevoflurane and propofol anesthesia in adults after closed reduction of nasal bone fracture.

BACKGROUND: Emergence agitation is associated with increased morbidity and hospital costs. However, there have been few reports in the medical literature on the occurrence of emergence agitation in adults. The aim of this study was to compare emergence agitation between sevoflurane and propofol anesthesia in adults after closed reduction of nasal bone fracture. METHODS: Forty adults (ASA I-II, 20-60 yr) undergoing closed reduction of nasal bone fracture were randomly assigned to either sevoflurane or propofol group and anesthesia was maintained with sevoflurane or propofol. The bispectral index (BIS) was monitored and maintained within 40-60. At the end of surgery, patients were transported to the post anesthetic care unit (PACU) and agitation state scale was checked by Aono's four-point scale (AFPS). Emergence agitation was defined as and AFPS score of 3 or 4. Pain score were measured by numeric rating scale (NRS) on arrival and peak value at PACU. RESULTS: Nine (45.0%) patients in the sevoflurane group and 2 (10.0%) patients in the propofol group developed emergence agitation in the PACU (P = 0.031). There was no correlation between peak NRS and Aono's four-point scale. CONCLUSIONS: Propofol may decrease incidence of emergence agitation compared to sevoflurane in adults undergoing closed reduction of nasal bone fracture.

Transcriptomic configuration of mouse brain induced by adolescent exposure to 3,4-methylenedioxymethamphetamine.

The amphetamine derivative (+/-)-3,4-methylenedioxymethamphetamine (MDMA or ecstasy) is a synthetic amphetamine analogue used recreationally to obtain an enhanced affiliative emotional response. MDMA is a potent monoaminergic neurotoxin with the potential to damage brain serotonin and/or dopamine neurons. As the majority of MDMA users are young adults, the risk that users may expose the fetus to MDMA is a concern. However, the majority of studies on MDMA have investigated the effects on adult animals. Here, we investigated whether long-term exposure to MDMA, especially in adolescence, could induce comprehensive transcriptional changes in mouse brain. Transcriptomic analysis of mouse brain regions demonstrated significant gene expression changes in the cerebral cortex. Supervised analysis identified 1028 genes that were chronically dysregulated by long-term exposure to MDMA in adolescent mice. Functional categories most represented by this MDMA characteristic signature are intracellular molecular signaling pathways of neurotoxicity, such as, the MAPK signaling pathway, the Wnt signaling pathway, neuroactive ligand-receptor interaction, long-term potentiation, and the long-term depression signaling pathway. Although these resultant large-scale molecular changes remain to be studied associated with functional brain damage caused by MDMA, our observations delineate the possible neurotoxic effects of MDMA on brain function, and have therapeutic implications concerning neuro-pathological conditions associated with MDMA abuse.

Red blood cells prevent inhibition of hypoxic pulmonary vasoconstriction by nitrite in isolated, perfused rat lungs.

Nitrite reduction to nitric oxide (NO) may be potentiated by a nitrite reductase activity of deoxyHb and contribute to systemic hypoxic vasodilation. The effect of nitrite on the pulmonary circulation has not been well characterized. We explored the effect of nitrite on hypoxic pulmonary vasoconstriction (HPV) and the role of the red blood cell (RBC) in nitrite reduction and nitrite-mediated vasodilation. As to method, isolated rat lungs were perfused with buffer, or buffer with RBCs, and subjected to repeated hypoxic challenges, with or without nitrite. As a result, in buffer-perfused lungs, HPV was reduced at nitrite concentrations of 7 muM and above. Nitrite inhibition of HPV was prevented by excess free Hb and RBCs, suggesting that vasodilation was mediated by free NO. Nitrite-inhibition of HPV was not potentiated by mild acidosis (pH = 7.2) or xanthine oxidase activity. RBCs at 15% but not 1% hematocrit prevented inhibition of HPV by nitrite (maximum nitrite concentration of approximately 35 muM) independent of perfusate Po(2). Degradation of nitrite was accelerated by hypoxia in the presence of RBCs but not during buffer perfusion. In conclusion, low micromolar concentrations of nitrite inhibit HPV in buffer-perfused lungs and when RBC concentration is subphysiological. This effect is lost when RBC concentration approaches physiological levels, despite enhanced nitrite degradation in the presence of RBCs. These data suggest that, although deoxyHb may generate NO from nitrite, insufficient NO escapes the RBC to cause vasodilation in the pulmonary circulation under the dynamic conditions of blood flow through the lungs and that RBCs are net scavengers of NO.

Pulmonary vascular effects of red blood cells containing S-nitrosated hemoglobin.

The role of S-nitrosated hemoglobin (SNO-Hb) in the regulation of blood flow is a central and controversial question in cardiopulmonary physiology. In the present study, we investigate whether intact human red blood cells (RBCs) synthesized to contain high SNO-Hb levels are able to export nitric oxide bioactivity and vasodilate the pulmonary circulation, and whether SNO-Hb dependent vasodilation occurs secondary to an intrinsic oxygen-linked, allosteric function of Hb. RBCs containing supraphysiological concentrations (100-1,000x normal) of SNO-Hb (SNO-RBCs) were synthesized and added to isolated, perfused rat lungs during anoxic or normoxic ventilation, and during normoxic ventilation with pulmonary hypertension induced by the thromboxane mimetic U-46619. SNO-RBCs produced dose-dependent pulmonary vasodilation compared with control RBCs during conditions of both normoxic (U-46619) and hypoxic pulmonary vasoconstriction. These effects were associated with a simultaneous, rapid, and temperature-dependent loss of SNO from Hb. Both vasodilatory effects and the rate of SNO-Hb degradation were independent of oxygen tension and Hb oxygen saturation. Furthermore, these effects were not affected by inhibition of the RBC membrane band 3 protein (anion exchanger-1), a putative membrane facilitator of NO export from RBCs. Whereas these data support observations by multiple groups that synthesized SNO-Hb can vasodilate, this effect is not under intrinsic oxygen-dependent allosteric control, nor likely to be relevant in the pulmonary circulation at normal physiological concentrations.