Laitinen's stereo-adapter: application to the fractionated cerebral irradiation under stereotaxic conditions

Radiosurgery is a technique which provides a single high dose of radiation very precisely to an intracranial lesion. The volume of tissue treated is small enough to avoid undue biological damage. This treatment requires very sophisticated apparatus and often considerable modifications in the treatment apparatus. The authors have closen to elaborate a system which makes it possible to deliver conventional fractionated irradiation, using a non-invasive stereotactic head frame called "Laitinen stereo-adapter". By fractionating the dose, most benign or low-grade malignant brain tumours can be treated, whatever their volume. The stereo-adapter and the target localization process are described. It can be used with C.T. scanning, angiography or M.R.I. The treatment apparatus is a linear accelerator delivering a 10 M.V. photon beam and treatment is made in the precise positioning of the target localization. The geometrical accuracy of the repeated mountings was studied in a preliminary study, showing a mean discrepancy of less than 1 mm in the three space planes. The geometrical accuracy of the radiation treatment was also studied on a phantom and the precision evaluated at less than 1 mm. The addition of extra collimators with a precollimation system decreased the lateral penumbra to 2-3 mm. Careful dosimetry was performed for each collimator. The use of non-coplanar arcs makes it possible to obtain a steep dose fall off outside the target volume. The dose planning calculations were compared to photodensitometry and thermoluminescent measurements, showing a good correlation. Each technical point will be discussed.(ABSTRACT TRUNCATED AT 250 WORDS)     

MRI dosimetry: a fast quantitative MRI method to determine 3D absorbed dose distributions

RATIONALE AND OBJECTIVES: Magnetic resonance imaging (MRI) techniques seem to be very promising for 3D dosimetry studies, but long imaging acquisition time limits their use. A new fast T1 mapping protocol, easy to implement on a conventional MR imager, has been used to determine dose distributions on Fricke gels. METHODS: The method has been tested on manganese chloride (MnCl2) doped ferrous gelatin gels. The T1 measuring times range from 1 minute 40 seconds to 3 minutes 30 seconds for a 256x256 matrix image. RESULTS: The two- and three-dimensional profiles agree with those obtained with conventional dosimetry techniques (ion chambers). The precision and the spatial resolution principally depend on the signal-to-noise ratio of the used imaging RF coil. For example, for a surface coil, the accuracy is about 2.5% with a 1.56 mm spatial resolution. CONCLUSION: These preliminary results support the feasibility of the proposed technique for accurate MRI dosimetry studies and also have potential for various clinical quantitative MRI applications.     

Pulmonary injury from proton and conventional radiotherapy as revealed by CT

OBJECTIVE: Although radiation therapy is used in early-stage inoperable lung cancer, it often results in injury to functional lung tissue. A study was undertaken to determine the frequency and severity of pulmonary injury revealed by CT in patients who had undergone conformal proton (to a limited volume) radiation therapy. We compared these findings with those from a group of patients who had undergone a combination of photon and conformal proton (to a larger volume) radiation therapy. CONCLUSION: Proton radiation therapy was associated with a lower frequency of pulmonary injury than the combined regimen. Injury correlated well with the volume of normal lung that was irradiated. Conformal proton radiation therapy appears to be able to reduce the incidence and severity of pulmonary injury revealed by CT.     

Acute interactions between -DOPA and the neurotoxic effects of 1-methyl-4-phenylpyridinium or 6-hydroxydopamine in mice

We have compared the effects of an i.p. pretreatment with L-DOPA (200 mg/kg) associated with benserazide (25 mg/kg) on neurotoxic effects of either 6-hydroxydopamine (6-OHDA) (50 microg, 10 microl per mouse) or 1-methyl-4-phenylpyridinium (MPP+) (17.5 microg, 10 microl per mouse). The striatal dopamine (DA) content, the vesicular monoamine transporter (VMAT2) density, as well as the hypothalamic norepinephrine (NE) content were measured 8 days after treatments. The L-DOPA-benserazide pretreatment worsened by 65% the 6-OHDA-induced depletion in striatal DA. On the contrary, it reduced by 42% the MPP+-induced depletion in striatal DA and by 54% the MPP+-induced decrease in VMAT2 density. It was noticed that the L-DOPA-benserazide pretreatment did not modify the marked decrease in hypothalamic NE content induced by 6-OHDA.     

Effect of low concentrations of K+ and Cl− on the Na+-dependent neuronal uptake of [3H] dopamine

The specific uptake of [³H] dopamine (DA) was studied using a crude synaptosomal fraction obtained from rat striatum. In a medium containing a 10 mM NaHC03/NaH2PO4 buffer and no added K⁺ ions, addition of NaCl elicited an increase in DA uptake for Na⁺ concentrations from 10 to 60 mM, and then a decrease of uptake for Na⁺ concentrations up to 130 mM. These data confirm that rather low NaCl concentrations produce a maximal DA uptake. This biphasic curve of uptake resulted from significant changes in the V _max of the DA uptake. Except for 10 mM Na⁺, this curve was not significantly modified when 9 mM NaHCO₃/NaH₂PO₄ were replaced by 9 mM NaCl. This result indicates that the Cl^– dependence of the DA uptake is mainly secondary to the Na⁺ dependence. Addition of KCl up to 3 mM did not modify the ascending part of the NaCl-dependent uptake curve. In contrast, the reduction in uptake produced by high Na⁺ concentrations was prevented in a concentration-dependent manner by KCl; this effect resulted from a decrease in the K_m and an increase in the V _max for the uptake.Measurements of membrane potential, with the help of the fluorescent probe 3,3-diethylthiadicarbocyanine iodide [DiSC₂(5)] and purified synaptosomes prepared from rat striatum and cerebral cortex, revealed that addition of 3 mM KCl to a medium containing a high Na⁺ concentration and no K⁺ ions produced a marked and stable decrease in the fluorescence level. This decrease which corresponds to an increase in membrane polarization was blocked by 0.1 mM ouabain. These data suggest that low K⁺ concentrations are likely to prevent the decrease in uptake elicited by high Na⁺ concentrations by restoration, via a Na⁺/K⁺ ATPase-mediated mechanism, of the membrane potential and/or a transmembrane electrochemical Na⁺ gradient more favourable to DA uptake.     

Pulmonary gas exchange capacity is reduced during normovolaemic haemodilution in healthy human subjects

Purpose

To test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic haemodilution.

Methods

Pulmonary gas exchange capacity was evaluated in seven healthy subjects by measuring the lung diffusion of carbon monoxide (DLCO). During the measurement, various breath-holding times, inspiratory volumes, and sitting or supine positions, were randomly selected in an attempt to alter pulmonary capillary perfusion. KCO was calculated as the percentage of theoretical values of the ratio of DLCO by alveolar volume and normalized by sex, age, and height. Normovolaemic haemodilution (NH) was performed by bleeding an average blood volume of 1 L with simultaneous Dextran 60 replacement to obtain an haematocrit below 35%.

Results

After NH, haemoblogin concentration [Hb] decreased from 14.94 ± 0.96 to 12.5 ± 0.98 g · dl^?1 (P < 0.001). KCO decreased (P < 0.02) but remained closely correlated to [Hb] at every lung volume (< 0.02). Breathholding time and body position had no effect.

Conclusion

Moderate NH impairs pulmonary gas exchange capacity in awake, resting healthy subjects. There is no evidence of any compensatory mechanism since the KCO vs [Hb] relationship is unchanged.     

Succinylcholine does not worsen bupivacaine-induced cardiotoxicity in pentobarbital-anaesthetized dogs

The intravascular injection of a large dose of bupivacaine induces electrophysiological cardiac impairment, mainly by slowing ventricular conduction velocity, and haemodynamic depression, by a decrease in myocardial contractility. When cardiotoxicity occurs, succinylcholine rapidly stops convulsions. However, the possible interactions between bupivacaine and succinylcholine on cardiac electrophysiology and haemodynamic status have never been investigated. Thus, we used an experimental electrophysiological model involving closed-chest dogs. Three groups (n = 6) of pentobarbital-anaesthetized dogs were given 0.2 mg.kg-1 atropine iv. Dogs in Group 1 were given saline. The others received 4 mg.kg-1 bupivacaine iv over ten seconds. Dogs in Group 2 were then given saline and those in Group 3 were then given 2 mg.kg-1 succinylcholine iv from one to two minutes after the administration of bupivacaine. The following electrophysiological variables were measured: heart rate represented by RR interval (RR), PR, atria-His (AH), and His-ventricle (HV) intervals, QRS duration, and QT interval corrected for heart rate (QTc). The following haemodynamic variables were measured: mean aortic pressure (MAoP), the peak of the first derivative of left ventricular pressure (LV dP/dt max), and LV end diastolic pressure (LVEDP). Comparison between Groups 1 and 2 showed that bupivacaine induced more than 100% HV interval lengthening and QRS widening (P less than 0.01), prolonged QTc interval by more than 25% (P less than 0.01), and decreased LV dP/dt max by more than 50% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Developmental toxicities of ethylbenzene, ortho-, meta-, para-xylene and technical xylene in rats following inhalation exposure.

The developmental toxicities of ethylbenzene, o-, m-, p-xylene and technical xylene were studied in Sprague-Dawley rats after inhalation exposure. Animals were exposed to either of these agents at 100, 500, 1000 or 2000 ppm, for 6 h/day, during days 6-20 of gestation. All the agents tested caused maternal toxicity expressed as a reduction in maternal body weight gain at 1000 and 2000 ppm. Decreased corrected weight gain and food consumption were observed at 1000 and 2000 ppm ethylbenzene, o-, m- or p-xylene, and at 2000 ppm technical xylene. No evidence of teratogenic effects was found after exposure to any of these agents up to 2000 ppm. Fetal toxicity evidenced by significant decreases in fetal body weights occurred at concentrations of 500 ppm or greater of o-xylene or technical xylene, and 1000 ppm or greater of ethylbenzene, m- or p-xylene. A significant increase in the mean percentage of fetuses per litter with skeletal variations was also noted at 2000 ppm ethylbenzene, o- and p-xylene. In summary, all tested agents produced developmental toxicity at 1000 and 2000 ppm, concentrations that also produced significant maternal toxicity. With o-xylene and technical xylene, developmental toxicity also occurred at 500 ppm, in the absence of maternal toxic effects. However, the only indication of a treatment-related effect was a slight decrease in fetal weight.