Percutaneous Radiofrequency Disc Decompression: A Study of 27 Patients.

BACKGROUND: Percutaneous radiofrequency nucleoplasty is a true minimally invasive technique for treatment for radiculopathy caused by contained disc protrusions. This minimally invasive procedure uses controlled thermoablation for reducing the intervertebral disc and decompressing the lumbar nerve root. Material and Methods: Our study is a prospective analysis of 27 patients aged from 30 to 64 years with lumbar disc protrusion who were treated with percutaneous radiofrequency disc decompression (PRFD) between May 2018 and May 2019. Clinical follow-up was reported at 1 month, 3 months, and 6 months. The outcomes were assessed using a visual analog scale (VAS) and MacNab score. RESULTS: Of the 27 patients, 14 were female and 13 were male. Their mean age was 53 ± 2 years. In all 27 patients, percutaneous radiofrequency nucleotomy was performed. An excellent outcome as reflected by MacNab score was observed in 17 patients (63%), a good outcome in 8 patients (29.7%), and a poor outcome in 2 patients (7.3%). Prior to treatment, the average back and leg VAS scores were 7.95 and 7.82, respectively. At sixth month follow-up, the back and leg VAS scores were reduced to 3.17 and 3.04, respectively. Patients with a poor outcome developed early recurrent disc prolapse and required endoscopic discectomy. CONCLUSION: PRFD is a safe and effective treatment of contained disc protrusion. PRFD is a good alternative to surgery. These procedures significantly increase quality of life in patients with lumbar radiculopathy.

Kinetics of thyroxine (T(4)) and triiodothyronine (T(3)) transport in the isolated rat heart.

The dynamics and kinetics of thyroid hormone transport in the isolated rat heart were examined using the modified unidirectional paired tracer dilution method. The uptake of (125)I-thyroxine ((125)I-T(4)) and (125)I-triiodothyronine ((125)I-T(3)) from the extracellular space into heart cells was measured relative to the extracellular space marker (3)H-mannitol. The thyroid hormone maximal uptake was 54.4 % for (125)I-T(4) and 52.15 % for (125)I-T(3). The thyroid hormone net uptake was 25.69 % for (125)I-T(4) and 25.49 % for (125)I-T(3). Backflux from the intracellular space was 53.17 % for (125)I-T(4) and 61.59 % for (125)I-T(3). In the presence of unlabelled thyroid hormones, (125)I-T(4) and (125)I-T(3) maximal uptakes were reduced from 10.1 to 59.74 % and from 34.6 to 65.3 %, respectively, depending on the concentration of the unlabelled hormone, suggesting a saturable mechanism of the thyroid hormone uptake by the heart cells, with K(m(T4))= 105.46 microM and the maximal rate of (125)I-thyroid hormone flux from the extracellular space to heart cells (V(max(T4))) = 177.84 nM min(-1) for (125)I-T(4) uptake, and K(m(T3)) = 80.0 microM and V(max(T3)) = 118.5 nM min(-1) for (125)I-T(3) uptake. Experimental Physiology (2001) 86.1, 13-18.

Endothelium-dependent relaxation of rat aorta to a histamine H(3) agonist is reduced by inhibitors of nitric oxide synthase, guanylate cyclase and Na,K-ATPase.

The possible involvement of different effector systems (nitric oxide synthase, guanylate cyclase, beta-adrenergic and muscarinic cholinergic receptors, cyclooxygenase and lipoxygenase, and Na(+),K(+)-ATPase) was evaluated in a histamine H(3) receptor agonist-induced ((R)alpha-methylhistamine, (R)alpha-MeHA) endothelium-dependent rat aorta relaxation assay. (R)alpha-MeHA (0.1 nM - 0.01 mM) relaxed endothelium-dependent rat aorta, with a pD(2) value of 8.22 +/- 0.06, compared with a pD(2) value of 7.98 +/- 0.02 caused by histamine (50% and 70% relaxation, respectively). The effect of (R)alpha-MeHA (0.1 nM - 0.01 mM) was competitively antagonized by thioperamide (1, 10 and 30 nM) (pA(2) = 9.21 +/- 0.40; slope = 1.03 +/- 0.35) but it was unaffected by pyrilamine (100 nM), cimetidine (1 muM), atropine (10 muM), propranolol (1 muM), indomethacin (10 muM) or nordthydroguaiaretic acid (0.1 mM). Inhibitors of nitric oxide synthase, L-N(G)-monomethylarginine (L-NMMA, 10 muM) and N(G)-nitro-L-arginine methylester (L-NOARG, 10 muM) inhibited the relaxation effect of (R)alpha-MeHA, by approximately 52% and 70%, respectively). This inhibitory effect of L-NMMA was partially reversed by L-arginine (10 muM). Methylene blue (10 muM) and ouabain (10 muM) inhibited relaxation (R)alpha-MeHA-induced by approximately 50% and 90%, respectively. The products of cyclooxygenase and lipoxygenase are not involved in (R)alpha-MeHA-induced endothelium-dependent rat aorta relaxation nor are the muscarinic cholinergic and beta-adrenergic receptors. The results also suggest the involvement of NO synthase, guanylate cyclase and Na(+),K(+)-ATPase in (R)alpha-MeHA-induced endothelium-dependent rat aorta relaxation.

The evidence for histamine H(3) receptor-mediated endothelium-dependent relaxation in isolated rat aorta.

The presence of histamine H(3) receptors was evaluated on the rat aorta endothelium. In the presence of pyrilamine (1 nM, 7 nM, 10 nM) or thioperamide (1 nM, 10 nM, 30 nM) the concentration-response curve for histamine-induced (0.1 nM - 0.01 mM) endothelium-dependent rat aorta relaxation was shifted to the right without significant change of the E(max) indicating competitive antagonism by pyrilamine (pA(2) = 9.33 +/- 0.34, slope = 1.09 +/- 0.36) or thioperamide (pA(2) =9.31 +/- 0.16, slope=0.94 +/- 0.10). Cimetidine (1 muM) did not influence histamine-induced endothelium-dependent rat aorta relaxation. In the presence of thioperamide (1 nM, 10 nM, 30 nM) the concentration-response curve for (R)alpha-MeHA-induced (0.1 nM - 0.01 mM) endothelium-dependent relaxation was shifted to the right without significant change of E(max) indicated competitive antagonism by thioperamide (pA(2) = 9.21 +/- 0.4, slope = 1.03 +/- 0.35). Pyrilamine (100 nM) or cimetidine (1 muM) did not influence (R)alpha-MeHA-induced endothelium-dependent rat aorta relaxation. These results suggest the presence of a heterogenous population of histamine receptors, H(1) and H(3), on rat aorta endothelium.

Glucagon effect on myocardial transport and utilization of energy-metabolites from the coronary microcirculation in the perfused rabbit heart.

Effect of glucagon on energy-metabolite transport into cardiac muscle was studied during a single transit through the isolated rabbit heart using a rapid paired-tracer dilution method. Kinetic experiments revealed that 1.5 microM glucagon stimulated the influx of palmitate bound to 30 g/litre albumin, by increasing the V 2.3 times and increasing the Km for transport 2.4 times. Tracer uptake of D-glucose, as the only exogenous substrate provided, was increased by 80% by 1.5 microM glucagon. Myocardial utilization of [3H]-or [14C]-labelled short-chain monocarboxylic acids (L-lactate, pyruvate and acetate) was significantly reduced by glucagon, to the same degree as their unidirectional sarcolemmal transport. Inhibition of L-[14C]lactate uptake was dose-dependent and in positive correlation with myocardial lactate production. It is concluded that glucagon may regulate sarcolemmal permeability and myocardial utilization for energy-metabolites from the coronary circulation.

Protective effects of glucagon during the anaphylactic response in guinea-pig isolated heart.

1 Cardiac anaphylaxis and the effects of glucagon pretreatment were studied in guinea-pig isolated hearts actively sensitized to ovalbumin.2 Antigen challenge of the sensitized hearts markedly increased creatine phosphokinase (CPK) activity in the coronary venous effluent. Control values of CPK release from the hearts before challenge were 3.56 +/- 0.15 mu min(-1) mg(-1). In the first 10 min following challenge, CPK release remained stable at increased levels which ranged between 4.88 +/- 0.20 to 5.39 +/- 0.38 mu min(-1) mg(-1). There was no correlation between immunologically released histamine and CPK release.3 Pretreatment of the hearts with glucagon (0.15 mumol l(-1)) exerted a pronounced anti-arrhythmic activity, reducing the conduction arrhythmias and completely preventing automaticity arrhythmias which normally occurred following ovalbumin challenge.4 Anaphylactic histamine release was reduced significantly in the presence of glucagon. The percentage inhibition of histamine release from glucagon pretreated hearts, during the first 10 min after challenge, ranged between 58% and 94% of that from hearts similarly challenged in the absence of glucagon.5 Glucagon significantly elevated sinoatrial nodal automaticity, enhanced atrioventricular conduction, improved coronary flow and reduced contractile force during anaphylaxis. It appears that these effects are caused both by modulating anaphylactic histamine release and by influencing the effects of the released histamine.6 CPK release from the anaphylactic hearts was significantly inhibited in the presence of glucagon. The average percentage inhibition of CPK activity during the first 10 min after challenge ranged between 42% and 98%.7 The findings from this study provide experimental evidence for protective effects of glucagon pretreatment during cardiac anaphylaxis.