Developmental cellular electrophysiologic effects of propafenone on the rabbit atrioventricular node.

Transmembrane recordings and surface electrograms were used to evaluate the influence of propafenone on the cellular electrophysiology of isolated neonatal and adult rabbit atrioventricular node (AVN) preparations. An automatic interval of 863 +/- 82 ms (mean +/- SEM, n = 14) in neonates was found to be significantly shorter than the 1510- +/- 205-ms (n = 12) automatic interval observed in adults. Propafenone in a concentration of 5 x 10(-6) M significantly increased the automatic interval of neonatal pacemakers but not that of the adult preparations. These changes in automaticity produced by propafenone were not dependent on the adrenergic receptor-blocking action of the drug. The pacemaker escape time after overdrive pacing was also shorter in the neonate than in the adult. Propafenone prolonged the escape time of the neonatal tissues but not those of the adult. AVN refractory period, A-H interval, and antegrade Wenckebach rate were comparably increased in a concentration-dependent manner in both age groups. The maximum diastolic potential was decreased by propafenone in the neonatal atrionodal tissue but not in other regions of the AVN and not in any region of the adult AVN. Action-potential duration was increased in all regions of the AVN in both age groups. Action-potential amplitude and maximum upstroke velocity were decreased by propafenone in both age groups. Unlike other excitable tissues of the heart, the action-potential duration of AVN nodal cells increased with decreasing pacing intervals as the pacing interval approached the Wenckebach interval.(ABSTRACT TRUNCATED AT 250 WORDS)     

Substance P- and calcitonin gene-related peptide-immunofluorescent nerves in the repair of experimental bone defects

Summary Healing of an experimental bony defect in the rat's tibia was studied with an immunofluorescent technique to clarify when and where substance P (SP) and calcitonin gene-related peptide (CGRP) would develop. The normal tibia showed a few SP- and CGRP-immunofluorescent nerve fibres. In the experimental tibia, the number of these fibres increased on the 6th day after operation, reached a peak of proliferation on the 15th day and reverted to normal after the 24th day. The changes were associated with the development and decay of callus tissue suggesting that harmful stimuli from the injured site in a bone could be mediated by sensory nerves throughout the repair period. Most of the SP- and CGRP-immunofluorescence was seen near the vessels, frequently in the same nerve fibres. The SP- and CGRP-immunofluorescent nerves seemed to take part jointly in callus formation through the enhancement of local blood flow.

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Résumé Le procesus de guérison d'une perte de substance osseuse expérimentale a été étudié sur le tibia du rat par immunofluorescence afin de déterminer quand et où la substance P (SP) et la calcitonine peptide d'origine génique (CGRP) se développeraient. Le tibia normal ne montre qu'un petit nombre de fibres nerveuses immunofluorescentes SP et CGRP. Dans le tibia d'expérimentation, les fibres nerveuses immunofluorescentes SP et CGRP augmentent en nombre à partir du 6ème jour, atteignent leur maximum de prolifération le 15ème jour et reviennent à l'état normal après le 24ème jour post-opératoire. Ces modifications sont étroitement associées au développement et à la disparition du cal, suggérant ainsi que les stimuli nocifs provenant de la lésion osseuse pourraient être inactivés par les nerfs sensitifs durant la période de réparation. En outre, la plus grande partie de l'immunofluorescence SP et CGRP a été observée à proximité des vaisseaux, souvent dans les mêmes fibres nerveuses. Il semble que les nerfs immunofluorescents SP et CGRP participent conjointement à la formation du cal en augmentant la vascularisation locale.

     

Alteration of second-messenger ligand binding following 2-hr hemispheric ischemia in the gerbil brain.

The alterations of second-messenger ligand binding and cerebral blood flow (CBF) were evaluated in the gerbil brain after 2-h unilateral common carotid artery occlusion. [3H]Forskolin (FK) and [3H]phorbol-12,13-dibutyrate (PDBu) were used as specific ligands for adenylate cyclase (AC) and protein kinase C (PKC) activity estimation, respectively. CBF was determined at the end of the experiment by the [14C]iodoantipyrine method. A quantitative autoradiographic method permitted simultaneous measurement of the three parameters in the same brain. The levels in the caudate-putamen, globus pallidus, and hippocampus were analyzed. The animals were divided into three groups: Group 1 with severe ischemia (CBF in the lateral nuclei of the thalamus (CBFt) less than 50 ml/100 g/min), Group 2 with mild ischemia (CBFt greater than or equal to 50 ml/100 g/min), and the Sham Group. The PDBu binding revealed a statistically significant increase in the caudate-putamen, lateral nuclei of the thalamus and hippocampus (CA1 and CA3 regions and dentate gyrus) on the ischemic side in Group 1 as compared to that in Group 2 and the Sham Group. In contrast, the FK binding did not show any significant changes in any of the regions. These data and our previous findings for 6-h ischemia suggest that (1) PKC translocation to the cell membrane may occur at the early ischemic phase in particular regions including the caudate-putamen, lateral nuclei of the thalamus and hippocampus, with the translocated PKC gradually diminishing during the subsequent ischemic period; and (2) the suppression of the AC system observed in 6-h ischemia may not appear in the early ischemic phase.     

Necrosis observed on CT enhancement is of prognostic value in soft tissue sarcoma.

Fifty-one patients with deep-seated soft tissue sarcoma of the extremities and trunk wall were examined with contrast-enhanced CT for presence of nonenhanced tumor areas (CT necrosis). After a median follow-up time of 3 years, 19 of the 41 patients with CT necrosis had developed metastases, compared to none of the 10 patients who had tumors without CT necrosis. Tumors with CT necrosis were larger than tumors without, but in tumors of similar size, absence of CT necrosis was a favorable prognostic sign.     

Determination of ion recombination loss by two-voltage method for pulsed radiation beams.

The ion recombination loss is one of the most important correction factors for dosimetry using ionization chamber especially for the measurement of high-intensity pulsed radiation beam. The two-voltage method has been used frequently for the correction of ion recombination loss. Several ways to approximate the method are presented. Comparisons were carried out to check the validity of the approximation. Using four ionization chambers of different types and shapes, measurements were made to obtain the optimal value of the ratio for the two voltages.     

Age-related alterations of NMDA-receptor properties in the mouse forebrain: partial restoration by chronic phosphatidylserine treatment.

The effect of aging on the properties of N-methyl-D-aspartate (NMDA) receptors in the forebrain of female NMRI mice was investigated using the antagonist [3H]MK-801 as radioligand. Compared to young (3 months) mice, aged (20 months) mice showed changes of the properties of the NMDA receptor at three different levels: (1) the density was reduced by about 35%; (2) the efficacy of L-glutamate and glycine for stimulating specific [3H]MK-801 binding was enhanced, probably because more NMDA receptor-associated ion channels are closed under baseline conditions in the aged brain; (3) the affinity of L-glutamate and glycine to its binding sites at the NMDA receptor complex was also enhanced. Chronic treatment of aged mice with phosphatidylserine (20 mg/kg, i.p., once daily) for three weeks completely normalized enhanced efficacy and affinity of L-glutamate and glycine and elevated NMDA receptor density by approximately 25%. These findings are consistent with the assumptions that deficits of the NMDA receptor are one of the mechanisms of age-related cognitive impairment and that the beneficial effects of phosphatidylserine treatment on cognitive deficits of aged individuals might be partially due to the effects of this drug on age-related NMDA receptor deficits.     

Value of MR imaging in the evaluation of chronic infiltrative lung diseases: comparison with CT.

The value of MR imaging was compared with that of high-resolution CT in assessing chronic infiltrative lung disease in 25 patients. The cases included nine patients with usual interstitial pneumonia, six with sarcoidosis, four with hypersensitivity pneumonitis, and six with miscellaneous conditions. The diagnosis was proved by biopsy (n = 17) or by means of clinical, laboratory, and radiologic criteria (n = 8). All patients had 1.5-T MR imaging and CT of the chest. Cardiac-gated T1-, proton density-, and T2-weighted spin-echo sequences were obtained. Initially, the MR images were assessed independently; later they were compared directly with the corresponding CT scans. In six patients, MR images and CT scans were obtained before open lung biopsy, and the images and scans were assessed prospectively. CT was superior to MR imaging in the anatomic assessment of the lung parenchyma and in showing fibrosis. However, areas of air-space opacification (ground-glass opacities) were seen as well on MR as on high-resolution CT. In the six patients who had open lung biopsy, areas of air-space opacification seen on MR and on CT corresponded to areas of active alveolitis or air-space infiltrates pathologically. Follow-up in six patients showed equal degrees of change in the air-space opacification over time on MR and CT. We conclude that, although MR imaging is inferior to high-resolution CT in the assessment of chronic infiltrative lung diseases, it may play a role in the assessment and follow-up of patients with air-space opacification.