[Low dose CT protocol--capability for early detection of lung carcinoma].

Lung carcinoma is the most common cause of death among men who died from cancer; also, among women, the incidence of this disease is on the increase. Use of multislice computed tomography (MSCT) has enhanced detection capability for pulmonary nodules. Nowadays, low radiation dose CT technique (LDCT) increases interest in lung cancer screening. This study is a part of the project whose aim is early diagnosis and well-timed treatment of lung carcinoma. Participants in this screening were above the age of 40, both smokers and non-smokers, who have undergone MSCT examination of lungs following low-dose protocol (LDCT). In the first ten months of the study, 375 volunteers have been examined. Overall number of detected nodules was 361; and 303 of these nodules have been characterized as non-calcificated. 95 participants (24.27%) had at least one non-calcificated nodule. 17 patients were referred to pulmologist and for further clinical evaluation. LDCT significantly increases detection of small, non-calcificated pulmonary nodules, and, therefore, gives higher opportunity to detect early lung carcinoma.

The mechanism of alpha2-adrenergic inhibition of sympathetic ganglionic transmission.

UNLABELLED: Alpha2-adrenergic agonists produce analgesia and reduce hemodynamic stress through central and peripheral mechanisms, but the effect of adrenergic agonists on pre- and postganglionic sites has not yet been clarified. In this study, we examined the effects of dexmedetomidine (DMT), an alpha2-agonist, on neural conduction and neurotransmitter release in sympathetic ganglia. The stellate ganglia from 48 mongrel dogs were isolated, desheathed, and superfused with Krebs' solution. Compound action potentials were evoked, and chromatography was used to detect acetylcholine released by preganglionic stimulation in the presence or absence of DMT. To further elucidate the mechanism of alpha2 effects, DMT was applied in combination with the alpha2-antagonist atipamezole (AT) or the imidazoline antagonist idazoxan (ID). In other experiments, DMT was applied in the presence of exogenous nicotinic stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide or muscarinic stimulation with (+)cis-dioxolane. DMT dose-dependently inhibited synaptic transmission with a 50% effective dose of 71.6 (26.0-174.3) microM. Neurotransmitter release was reduced 25% by 70 microM DMT during low-frequency (0.4 Hz) stimulation, but this effect was abolished at higher frequency (5 Hz) stimulation. AT but not ID blocked the inhibitory action of DMT. DMT inhibited the excitatory postsynaptic response to exogenous muscarinic stimulation but not nicotinic stimulation. These results indicate that alpha2-receptor activation depresses ganglionic transmission through postsynaptic inhibition of muscarinic stimulation, although reduction of neurotransmitter release through a presynaptic autofeedback mechanism is also involved. IMPLICATIONS: This article provides novel insights into the mechanism of drug action of alpha2-receptor agonists in the sympathetic ganglia of dogs by directly measuring the relative contribution of pre- and postganglionic receptors. Our study indicates that the central sympatholytic effects of alpha2-adrenoceptor stimulation are augmented by peripheral inhibition of ganglionic transmission.

Direct comparative effects of isoflurane and desflurane on sympathetic ganglionic transmission.

Although the sympathetic ganglion is an important site of peripheral regulation, few studies have examined the effect of anesthetics on synaptic transmission. In the present study we compared the actions of desflurane with those of isoflurane on synaptic transmission and neurotransmitter release in the stellate ganglion. In the electrophysiologic group, 14 stellate ganglia were isolated from adult mongrel dogs after halothane anesthesia, desheathed, and superfused with Krebs' solution. Compound action potentials (CAP) were induced by supramaximal stimulation of the preganglionic T3-ramus at a low frequency of 0.4 Hz and were recorded from the postganglionic ventral ansa subclaviae. Each ganglion was exposed to two levels of anesthetics (equivalent to 1 and 2 minimum alveolar anesthetic concentration [MAC]), followed by an anesthetic-free washout period. While equianesthetic concentrations of isoflurane and desflurane caused essentially equipotent suppression of ganglionic transmission, desflurane was more efficacious than isoflurane, both with respect to the onset of and recovery from the inhibition of synaptic activity. In the electrochemical group, 25 ganglia were exposed to both anesthetics at a high concentration (equivalent to between 1.82 and 1.95 MAC) during maximal and submaximal current stimulations, and the release of actylcholine (ACh) in the superfusate was measured with liquid chromatography. Although desflurane and isoflurane caused a significant depression of CAP, neither anesthetic inhibited the release of ACh in the superfusate at either maximal or submaximal current stimulations. These results indicate that the suppression of ganglionic activity is equipotent for both anesthetics based on equivalent MAC values, but that desflurane is more efficacious than isoflurane with respect to onset and recovery at the higher concentrations of anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)