Treatment of symptomatic lumbar spinal degenerative pathologies by means of combined conservative biochemical treatments.

Research in spine surgery has proposed new soft and less invasive techniques. These are the results of our experience with oxygen-ozone therapy, which we could experiment within the Italian National Health System over 3 years. A total of 1,920 patients were admitted on the basis of unselected enrolment because of lumbosciatic pain. Patients were divided into three groups: (A) Patients with degenerative disc disease and arthropathy: 509 (26.5%), (B) Patients with failed back surgery syndrome (FBSS): 1,027 (53.489%), and (C) Patients with pure herniated lumbar disc: 384 (20%). The rationale of the treatment for all these different pathologies we have taken into consideration is the biochemical mechanism by which they can engender pain and dysfunction. Treatment for group A: paravertebral injection and phleboclysis (two cycles of 6 sessions, one each 3 days) +endoscopic neurolysis. Treatment for group B: paravertebral injection and phleboclysis (two cycles of 6 sessions, one each 3 days) + endoscopic neurolysis with intradiscal procedure (named percutaneous peridurodiscolysis). Treatment for group C: paravertebral injection (two cycles of 6 sessions, one each 3 days) + percutaneous discolysis.The perceived quality of result for this minimally invasive procedure makes oxygen-ozone therapy an interesting weapon in the hands of doctors. Furthermore, if the technique loses its clinical effectiveness, it can be repeated without harm for the patient, and costs for the health organization are notably very low, above all if compared to surgical procedures.We underline the need that this treatment should be performed in protected structures, in operative rooms, under anesthesiologic control, and in the hands of specialists.

Adenosine and carnitine derivatives and calcium movements in rat heart sarcoplasmic reticulum.

Many researches indicate that some Ca antagonists modulate Ca fluxes not only at the level of the cytoplasmic membrane but also across the sarcoplasmic reticulum. The present study investigates whether certain compounds like propionylcarnitine or acetylcarnitine which have the capacity to influence cardiac activity might interfere with intracellular Ca movements. The results demonstrate that acetylcarnitine and propionylcarnitine do not affect the calcium intracellular movement in sarcoplasmic reticulum.

Are increased ATP blood levels responsible for PGI2 release from endothelium?

Defibrotide, a polydeoxyribonucleotide with profibrinolytic and antithrombotic properties obtained from mammalian lungs was shown capable of favoring the release of prostacyclin from endothelial cells. We previously evidenced that the use of defibrotide i.p. (32 mg/kg for 30 min) or orally (50 mg/kg for 1 h) induced a significant increase in 2,3-diphosphoglycerate (2,3-DPG) content of blood cells in rats. We tested the in-vivo capacity of defibrotide to modify over 90 min the blood content of ATP, cAMP and 2,3-DPG. Male Wistar rats were anaesthetized with pentobarbital (20 mg/kg) i.p.; the left carotid artery was cannulated with a polyethylene tube, from which 0.4 ml of blood was drawn at 0, 5, 10, 15, 20, 30, 40, 50, 60 and 90 min. At 0 min, defibrotide was administered i.p. or i.v. (through the femoral vein) at the dose of 1 ml containing 80 mg of drug or orally at the dose of 1 ml containing 160 mg of drug. The control rats employed received either the vehicle of the drug or physiologic saline. Our results demonstrated a significant drug-related increase with time (maximal levels were revealed about 20 min after i.v., i.p., or oral defibrotide treatment) of blood ATP content and a significant decrease in cAMP content as compared with the controls. Our data confirm the relation between increased drug-induced prostacyclin production and that of ATP of in blood.

Prostacyclin release from endothelial cells, induced by defibrotide treatment, favours the function of grafted rat hearts and kidneys.

Defibrotide, a single-stranded DNA fraction obtained from mammalian lungs and able to increase prostacyclin production by endothelial cells, has been shown to be efficient in protecting rat organs (heart, kidney and liver) from ischaemic damage. We studied the efficacy of the drug in preserving the function of rat heart and kidney submitted to isotransplantation. Defibrotide was administered to donor Wistar rats at the dose of 32 mg/kg in 1.5 ml of saline. Heart and kidney were isolated and cold-preserved in buffered phosphate medium and continuously infused with defibrotide (32 mg/h) through the innominate or renal artery. Recipient Wistar rats were treated with defibrotide before and after transplantation at the dose of 32 mg/kg/day. Controls were treated with the vehicle of the drug. The function of isografted organs was evaluated at 12 and 24 h and at 2, 4 and 7 days from grafting. Heart function was evaluated by studying creatinine phosphokinase (CPK) and lactic dehydrogenase (LDH) activities of myocardial tissue. Renal function was evaluated by studying serum creatinine and urea levels of kidney-grafted rats. CPK and LDH activities were found to be significantly higher in defibrotide-treated rats than in controls. Creatinine and urea levels remained significantly lower in defibrotide-treated rats than in the controls. The results of the present work indicate that defibrotide treatment is useful to maintain the functionality of grafted hearts and kidneys.

Protective action of propionyl-L-carnitine on toxicity induced by hyperbaric oxygen.

The protective effect of propionyl-L-carnitine against hyperbaric oxygen toxicity was studied by in vivo experiments on mice. The treatment reduced both the percentage of animals with convulsions and the death rate. Tissue signs of toxicity and pulmonary weight increase were less marked in treated animals than in controls. Results may indicate that propionyl-L-carnitine needs to build up to critical levels in cells and mitochondria before its metabolic effects can be fully felt.