Using either route of epidural injections to deliver steroids for unilateral chronic radiculopathy secondary to herniated intervertebral disc provided significant improvements in patients function and pain relief. However, we could not find a statistically significant difference between two indicated groups either in functional improvement or in reduction in pain, although half-dose of steroids delivered via TF route provided somewhat better long-term pain relief and functional capacity improvements.

The aim of this study was to evaluate the genotoxicity of repeated exposure to isoflurane or halothane and compare it with the genotoxicity of repeated exposure to cisplatin. We also determined the genotoxicity of combined treatment with inhalation anaesthetics and cisplatin on peripheral blood leucocytes (PBL), brain, liver and kidney cells of mice. The mice were divided into six groups as follows: control, cisplatin, isoflurane, cisplatin-isoflurane, halothane and cisplatin-halothane, and were exposed respectively for three consecutive days. The mice were treated with cisplatin or exposed to inhalation anaesthetic; the combined groups were exposed to inhalation anaesthetic after treatment with cisplatin. The alkaline comet assay was performed. All drugs had a strong genotoxicity (P<0.05 vs. control group) in all of the observed cells. Isoflurane caused stronger DNA damage on the PBL and kidney cells, in contrast to halothane, which had stronger genotoxicity on brain and liver cells. The combination of cisplatin and isoflurane induced lower genotoxicity on PBL than isoflurane alone (P<0.05). Halothane had the strongest effect on brain cells, but in the combined treatment with cisplatin, the effect decreased to the level of cisplatin alone. Halothane also induced the strongest DNA damage of the liver cells, while the combination with cisplatin increased its genotoxicity even more. The genotoxicity of cisplatin and isoflurane on kidney cells were nearly at the same level, but halothane caused a significantly lower effect. The combinations of inhalation anaesthetics with cisplatin had stronger effects on kidney cells than inhalation anaesthetics alone. The observed drugs and their combinations induced strong genotoxicity on all of the mentioned cells.

No abstract

In this study, DNA damage in tumour cells, as well as irreversible cell damage leading to apoptosis induced in vivo by the combined application of cisplatin and inhalation anaesthetics, was investigated. The genotoxicity of anaesthetics on Ehrlich ascites tumour (EAT) cells of mice, alone or in combined application with cisplatin, was estimated by using the alkaline comet assay. The percentage of EAT cell apoptosis was quantified by flow cytometry. Groups of EAT-bearing mice were (i) treated intraperitoneally with cisplatin, (ii) exposed to repeated anaesthesia with inhalation anaesthetic, and (iii) subjected to combined treatment of exposure to anaesthetics after cisplatin for 3 days. Sevoflurane, halothane and isoflurane caused strong genotoxic effects on tumour cells in vivo. The tested anaesthetics alone showed no direct effect on programmed cell death although sevoflurane and especially halothane decreased the number of living EAT cells in peritoneal cavity lavage. Repeated anaesthesia with isoflurane had stimulatory effects on EAT cell proliferation and inhibited tumour cell apoptosis (6.11%), compared to the control group (10.26%). Cisplatin caused massive apoptosis of EAT cells (41.14%) and decreased the number of living EAT cells in the peritoneal cavity. Combined cisplatin and isoflurane treatment additionally increased EAT cell apoptosis to 51.32%. Combined treatment of mice with cisplatin and all anaesthetics increased the number of living tumour cells in the peritoneal cavity compared to cisplatin treatment of mice alone. These results suggest that the inhalation of anaesthetics may protect tumour cells from the cisplatin-induced genotoxic and cytotoxic effects.

We studied the relationship of deterioration of cardiorespiratory function with respect to degree and localisation of apex of spinal curvature. The study comprised 33 patients (27 females and 6 males) aged 15 (11-21) years, surgically treated for an average scoliotic angle of 72 ° (55-129 °, after Cobb) which was postoperatively reduced to 32.6 ° (13-74 °). The static and dynamic cardiorespiratory function parameters were tested (pre-operatively and 24 months after surgery) by spirometry and plethysmography, arterial blood gas analysis, and the exercise tolerance test. In terms of the site and apex of the thoracic curve as determined by spine X-ray, patients were divided into two groups: upper thoracic scoliosis with the apex between T5 and T8 and lower thoracic scoliosis with the apex between T9 and Til. Only upper thoracic scoliosis with Cobb angle of more than 70° correlated (r = -1) with restrictive ventilation disorder (vital capacity 68%) and latent hypoxaemia (uptake O₂ ml/kg/min 63%) demonstrated during the exercise tolerance test (p > 0.05). The results of the test have demonstrated that surgically obtained 54% correction of the scoliotic curve improves pulmonary function (p < 0.05). However, the improvement does not match the degree of achieved scoliotic curve correction, what means that even in surgically treated high-angled thoracic scoliosis exists an increased risk of morbidity and mortality.