Feasibility of enlarging the ventral space by using a drill under spinal endoscopy in the treatment of severe free lumbar disc herniation / 中国骨伤

OBJECTIVE@#To evaluate the clinical efficacy of spinal endoscopy in the treatment of severe free lumbar disc herniation and explore the feasibility and application of microscopic drills to expand ventral space.@*METHODS@#Thirty patients with severe free lumbar intervertebral disc herniation treated by spinal endoscopic technique from April 2019 to March 2021 were collected, including 19 males and 11 females;aged from 19 to 76 years with an average of (44.03±16.92) years old. All patients had a single segmental lesion with prolapse of the nucleus pulposus. Among them, there were 3 cases on L2,3, 3 cases on L3,4, 15 cases on L4,5, and 9 cases on L5S1. During operation, posterior bone of vertebral body and pedicle notch were removed by a drill under the endoscope to enlarge the ventral space. And the free nucleus pulposus was exposed and completely removed. The intraoperative blood loss, operation time, hospital stay and postoperative neurological complications were recorded, and Japanese Orthopaedic Association (JOA) score, Oswestry Disability Index (ODI) and visual analogue scale (VAS) were compared before operation, 2 days, 3 months and 1 year after operation, and Macnab standard was used to evaluate clinical efficacy.@*RESULTS@#All operations were successful and the free nucleus pulposus was completely removed. Pain in the lower back and legs was significantly relieved on the day after operation. Two patients experienced transient pain and numbness in lower limbs after operation, and no serious nerve injury complications occurred. ODI and VAS at each time point after surgery were significantly lower than those before surgery (P<0.01), and JOA score was significantly higher than before surgery (P<0.01). The excellent and good rates of Macnab were 66.67% (20/30), 83.33% (25/30) and 90.00% (27/30) on 2 days, 3 months and 1 year after operation, respectively.@*CONCLUSION@#For severe free lumbar intervertebral disc herniation, using of a drill under endoscope to expand the ventral space can smoothly remove the free nucleus pulposus and avoid nerve damage.

Involvement of veratridine-induced increase of reverse Na(+)/Ca(2+) exchange current in intracellular Ca(2+) overload and extension of action potential duration in rabbit ventricular myocytes / 生理学报

The objectives of this study were to investigate the effects of veratridine (VER) on persistent sodium current (I(Na.P)), Na(+)/Ca(2+) exchange current (I(NCX)), calcium transients and the action potential (AP) in rabbit ventricular myocytes, and to explore the mechanism in intracellular calcium overload and myocardial contraction enhancement by using whole-cell patch clamp recording technique, visual motion edge detection system, intracellular calcium measurement system and multi-channel physiological signal acquisition and processing system. The results showed that I(Na.P) and reverse I(NCX) in ventricular myocytes were obviously increased after giving 10, 20 μmol/L VER, with the current density of I(Na.P) increasing from (-0.22 ± 0.12) to (-0.61 ± 0.13) and (-2.15 ± 0.14) pA/pF (P < 0.01, n = 10) at -20 mV, and that of reverse I(NCX) increasing from (1.62 ± 0.12) to (2.19 ± 0.09) and (2.58 ± 0.11) pA/pF (P < 0.05, n = 10) at +50 mV. After adding 4 μmol/L tetrodotoxin (TTX), current density of I(Na.P) and reverse I(NCX) returned to (-0.07 ± 0.14) and (1.69 ± 0.15) pA/pF (P < 0.05, n = 10). Another specific blocker of I(Na.P), ranolazine (RAN), could obviously inhibit VER-increased I(Na.P) and reverse I(NCX). After giving 2.5 μmol/L VER, the maximal contraction rate of ventricular myocytes increased from (-0.91 ± 0.29) to (-1.53 ± 0.29) μm/s (P < 0.01, n = 7), the amplitude of contraction increased from (0.10 ± 0.04) to (0.16 ± 0.04) μm (P < 0.05, n = 7), and the baseline of calcium transients (diastolic calcium concentration) increased from (1.21 ± 0.08) to (1.37 ± 0.12) (P < 0.05, n = 7). After adding 2 μmol/L TTX, the maximal contraction rate and amplitude of ventricular myocytes decreased to (-0.86 ± 0.24) μm/s and (0.09 ± 0.03) μm (P < 0.01, n = 7) respectively. And the baseline of calcium transients reduced to (1.17 ± 0.09) (P < 0.05, n = 7). VER (20 μmol/L) could extend action potential duration at 50% repolarization (APD(50)) and at 90% repolarization (APD(90)) in ventricular myocytes from (123.18 ± 23.70) to (271.90 ± 32.81) and from (146.94 ± 24.15) to (429.79 ± 32.04) ms (P < 0.01, n = 6) respectively. Early afterdepolarizations (EADs) appeared in 3 out of the 6 cases. After adding 4 μmol/L TTX, APD(50) and APD(90) were reduced to (99.07 ± 22.81) and (163.84 ± 26.06) ms (P < 0.01, n = 6) respectively, and EADs disappeared accordingly in 3 cases. It could be suggested that: (1) As a specific agonist of the I(Na.P), VER could result in I(Na.P) increase and intracellular Na(+) overload, and subsequently intracellular Ca(2+) overload with the increase of reverse I(NCX). (2) The VER-increased I(Na.P) could further extend the action potential duration (APD) and induce EADs. (3) TTX could restrain the abnormal VER-induced changes of the above-mentioned indexes, indicating that these abnormal changes were caused by the increase of I(Na.P). Based on this study, it is concluded that as the I(Na.P) agonist, VER can enhance reverse I(NCX) by increasing I(Na.P), leading to intracellular Ca(2+) overload and APD abnormal extension.