Sialic acid accelerates the electrophoretic velocity of injured dorsal root ganglion neurons.

Peripheral nerve injury has been shown to result in ectopic spontaneous discharges on soma and injured sites of sensory neurons, thereby inducing neuropathic pain. With the increase of membrane proteins on soma and injured site neurons, the negatively charged sialic acids bind to the external domains of membrane proteins, resulting in an increase of this charge. We therefore speculate that the electrophoretic velocity of injured neurons may be faster than non-injured neurons. The present study established rat models of neuropathic pain via chronic constriction injury. Results of the cell electrophoresis test revealed that the electrophoretic velocity of injured neuronal cells was faster than that of non-injured (control) cells. We then treated cells with divalent cations of Ca(2+) and organic compounds with positive charges, polylysine to counteract the negatively charged sialic acids, or neuraminidase to specifically remove sialic acids from the membrane surface of injured neurons. All three treatments significantly reduced the electrophoretic velocity of injured neuronal cells. These findings suggest that enhanced sialic acids on injured neurons may accelerate the electrophoretic velocity of injured neurons.

[The relationship between lactate clearance rate and delayed encephalopathy after acute carbon monoxide poisoning].

OBJECTIVE: To study the relationship between lactate clearance rate (LCR) and prognosis after acute carbon monoxide poisoning in patients with delayed encephalopathy (DEACMP). METHODS: Data from 354 patients with acute severe carbon monoxide poisoning (ASCOP) were retrospectively analyzed. The patients were divided into hyperlactacidemia group (arterial lactic acid > 2 mmol/L, n=263) and low lactic acidosis group (arterial lactate ≤2 mmol/L, n=91) according to the blood lactic acid level at admission. Arterial blood (1 mL) was collected from all patients before and 6, 24, 72 hours after treatment at ambient air, and arterial blood lactic acid was determined, and LCR was calculated. The initial level of blood lactic acid and LCR at 6, 24, 72 hours were compared between two groups. At the same time, the patients with hyperlactacidemia were divided into high LCR group (LCR more than 10%, n=101) and low LCR group (LCR less than or equal to 10%, n=162) according to 6-hour LCR, and the incidence of DEACMP was compared between two groups. The relationship between LCR and the incidence of DEACMP was analyzed with Spearman linear correlation analysis. The risk factors associated with DEACMP were analyzed with logistic regression analysis. RESULTS: The initial level of blood lactic acid (2.73±0.57 mmol/L vs. 1.69±0.20 mmol/L, t=5.327, P=0.001) and LCR at 6, 24, 72 hours [6 hours: (9.0±2.4)% vs. (1.2±0.6)%, t=9.468, P=0.001; 24 hours: (8.6±3.7)% vs. (1.2±0.4)%, t=4.889, P=0.001; 72 hours: (14.0±3.9)% vs. (1.7±1.0)%, t=5.211, P=0.001] in hyperlactacidemia group were significantly higher than those in low lactic acidosis group. The initial level of blood lactic acid in high LCR group was significantly lower than that in low LCR group (2.41±0.23 mmol/L vs. 2.92±0.63 mmol/L, t=2.429, P=0.023), and LCR at 6 hours and 24 hours were significantly higher than those in low LCR group [6 hours: (11.0±1.2)% vs. (8.0±2.1)%, t=4.487, P=0.001; 24 hours: (12.2±3.0)% vs. (6.3±1.8)%, t=6.264, P=0.001]. But there was no difference in 72-hour LCR between high LCR group and low LCR group [(14.1±3.6)% vs. (13.9±4.1)%, t=0.182, P=0.857]. The incidence of DEACMP in high LCR group was significantly lower than that in low LCR group [15.8% (16/101) vs. 61.1% (99/162), χ(2)=51.814, P=0.001]. The blood LCR at early period (6, 24, 72 hours) in ASCOP patients with hyperlactacidemia was negatively correlated with the incidence of DEACMP (r1=-0.493, P1=0.011; r2=-0.408, P2=0.038; r3=-0.428, P3=0.029). Logistic regression analysis showed that LRC at 6 hours and 24 hours [odds ratio (OR) was 2.701, 1.070, P value was 0.035, 0.001], long-time coma (OR=1.537, P=0.068), contact carbon monoxide (CO) long time (OR=2.686, P=0.014), age (OR=1.464, P=0.017), acute carbon monoxide complications (OR=1.363, P=0.072) patients with ASCOP had an increased risk of DEACMP. CONCLUSIONS: LCR is helpful for the assess of DEACMP patients severity, for the treatment guide and for prognosis judgement.

[Effect of the pre-hospital systematic treatment on prognosis patients of with severe acute organophosphorus pesticide poisoning].

OBJECTIVE: To investigate if the duration from poisoning to treatment (no treatment period) is related to the prognosis of patients with severe acute organophosphorus pesticide poisoning (SAOPP). METHODS: One hundred and seventy-four patients with the pre-hospital systematic treatment served as the treatment group while 160 patients going to the hospital by themselves without treatment or rejecting gastrolavage served as the control group. Patients in both groups were treated by gastrolavage, pralidoxime chloride, atropine and other expectant treatment. The duration of no treatment period, death, and severe complication were observed. The time of disappearance of symptoms, the recovery time of acetyl cholinesterase (AChE), atropinization time, atropine dosage, pralidoxime chloride dosage, naloxone dosage, hospitalization days and other targets were also observed. RESULTS: The duration of no treatment period in treatment group [(1.2 +/- 0.3) h] was significantly shorter than that in control group [(2.8 +/- 0.5) h, (P < 0.01)]. The mortality rate in treatment group was 6.32% while that in control group 22.5% (P < 0.01). The incidence of respiratory failure, heart injury, brain injury, atropine poisoning, intermediate syndrome, liver injury in treatment group (12.64%, 5.75%, 8.62%, 1.72%, 4.60%, 5.17% respectively) were lower than those in control group (25.63%, 13.75%, 17.50%, 6.25%, 7.50%, 9.38% respectively, P < 0.05 or P < 0.01). The time of symptoms disappearance, the recovery time of AChE, atropinization time, atropine dosage, pralidoxime chloride dosage, naloxone dosage, hospitalization days in treatment group were significantly superior to those in control group (P < 0.05 or P < 0.01). CONCLUSION: The pre-hospital systematic treatment can improve the prognosis of the patients with SAOPP, which is worth popularizing and using.

[Pre-hospital systematic treatment for patients with severe acute organophosphorus pesticide poisoning].

OBJECTIVE: To evaluate the feasibility, safety and effectiveness of on-spot systematic treatment for the patients with severe acute organophosphorus pesticide poisoning (SAOPP). METHODS: Two hundred and twenty-three SAOPP patients were divided into two groups: pre-hospital treatment group (116 patients), in which rescue equipment and drugs were carried to the spot for the treatment of the patients; hospital treatment group (107 patients), in which the patients received emergency treatment after reaching the hospital. The pre-hospital group was sub-divided into group A and group B. In group A, gastric lavage was performed with aid of automatic lavage instrument, and in group B lavage was done by using suspending bucket. Antidotes including pralidoxime chloride and atropine were used simultaneously based on the patients' conditions. Cholinesterase (ChE) activity was dynamically monitored. When the symptoms disappeared, the length of atropinization, the total dosage of atropine and pralidoxime chloride, the recovery time of ChE, the mortality, hospital days, and the incidence of complications were analyzed. RESULTS: The therapeutic effect in pre-hospital group was better than that in in-patient group in terms of disappearance of the symptoms, length of atropinization, recovery time of ChE, the total dosage of atropine and pralidoxime chloride, hospital days, and the mortality rate in group A was markedly lower than in-patient group(P<0.05 or P<0.01). The incidence of respiratory failure, heart injury, brain injury, and atropine poisoning were also lower in pre-hospital group compared with in-patient group (all P<0.01). However, there were no significant differences in intermediate syndrome, relapse, liver injury (all P>0.05). On the other hand, there were no significant differences in mortality rate and hospital days between two subgroups of pre-hospital treatment group(P>0.05). CONCLUSION: Pre-hospital systematic treatment for SAOPP patients, due to its good effects, should be recommended as a safe and effective treatment strategy.