[An autopsy case of pulmonary metastasis of cholangiocellular carcinoma associated with marked fibrotic change of the lungs].

An autopsy case of pulmonary metastasis of cholangiocellular carcinoma is presented. A 44-year-old woman was admitted to our hospital because of dyspnea, general fatigue and a sense of abdominal fullness on February 5, 1990. In November 1986, at an other hospital, she had been diagnosed as having diffuse metastatic lung tumor and multiple bone metastases, by transbronchial lung biopsy and other examinations. During the clinical course, she was not received chest irradiation and chemotherapy which induced fibrotic change of lungs. Chest X-ray film on December 21, 1986 showed diffuse nodular shadows in both lung fields. Chest X-ray film on February 4, 1990 showed diffuse reticular shadows with marked shrinkage of lung fields. She died two months after admission. The primary site of the carcinoma was not determined clinically, but was revealed by autopsy to be cholangiocellular carcinoma of the liver, with generalized metastasis. Microscopic findings of the autopsied lung showed markedly increased connective tissue around bronchi and blood vessels, in areas where microtubular adenocarcinoma was scattered. This is a very rare case of pulmonary metastasis of cholangiocellular carcinoma, associated with marked fibrotic change of the lungs during about 3.5 years. To our knowledge, this is the first reported case.

Chronic sensory and autonomic neuropathy.

A man with sensory neuropathy had evidence of autonomic failure: abnormal pupils, hypohidrosis, esophageal dilation, diarrhea, hypotension, orthostatic hypotension, sphincter disturbance, and impotence. Functional tests revealed abnormalities of both sympathetic and parasympathetic systems, mainly postganglionic. Autopsy revealed degeneration of posterior columns, posterior nerve roots, posterior root ganglia, and peripheral nerves. Degeneration was also observed in the sympathetic trunk, vagal nerve, and myenteric plexus. Neurons in the intermediolateral columns were preserved. Progressive sensory neuropathy with dysautonomia seems to be a new disease.

Minamata disease (organic mercury poisoning): neuroradiologic and electrophysiologic studies.

We studied 10 patients with Minamata disease (organic mercury poisoning) who have been followed for over 20 years. CT revealed a bilateral, symmetric, low-density area in the visual cortex and diffuse atrophy of the cerebellar hemispheres and vermis, especially the inferior vermis. Computerized quantitative analysis of the tremor of these patients showed a peculiar frequency of 7.075 Hz on postural tremor and 7.501 Hz on action tremor. On studies of short-latency somatosensory evoked potential, all patients showed a lack of the N20 component, the potential of the somatic sensory area.

Electrophysiological characteristics of ischemic cardiac cells in hypoxic and hyperkalemic conditions.

The difference in the electrophysiological properties between the subepicardial cells and the subendocardial cells (Purkinje fibers and ordinary myocardial cells) was examined in dogs using a microelectrode technique. The preparations were obtained one hour after coronary occlusion. Immediately after exposure to a hypoxic solution, spontaneous activities could be recorded in neither the subepicardial nor the subendocardial cells. The electrical activities induced by electrical stimulation disappeared 5-10 min after exposure to the hypoxic solution in the subepicardial cells, while they remained in the subendocardial cells. Vmax, action potential amplitude, action potential duration and resting membrane potential of the subendocardial cells were all reduced significantly in the hypoxic solution containing 7 mK K+ in contrast to those in the hypoxic solution containing 4 mM K+ (p less than 0.001). In the hypoxic solution containing 15 mM K+, all cardiac cells depolarized partially and became electrically quiescent in both normal and ischemic cardiac cells. These findings support the idea that during regional hypoxia and hyperkalemia resulting from acute coronary occlusion, heterogeneous changes in electrical activities occur between the subepicardium and the subendocardium in the ischemic regions.

Effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium of dogs.

The effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium was studied in 45 dogs in vivo. By recording pairs of local electrograms from the endocardium and epicardium and by stimulating the ventricle close to one of a pair of electrodes, we measured conduction times in the subendocardial layer (Endo 1-2), in the subepicardial layer (Epi 1-2), and from the endocardium to the epicardium (Endo-Epi). We then estimated the effect of lidocaine on each of them. In normal myocardium, lidocaine in a therapeutic dose (serum level 2.5 +/- 0.4 micrograms/ml) did not affect any of the three conduction times, but in a larger dose (serum level 6.5 +/- 0.7 micrograms/ml) it prolonged Endo-Epi significantly (P less than 0.05) and Endo 1-2 and Epi 1-2 slightly. In acutely ischemic myocardium caused by single stage ligation of the left anterior descending coronary artery, lidocaine in a therapeutic dose prolonged Endo 1-2 and Endo-Epi significantly (P less than 0.001) in the early stage after administration but did not affect Epi 1-2 simultaneously. Lidocaine in a larger dose, however, prolonged all three conduction times (P less than 0.001). The data indicate that within normal ventricular myocardium, lidocaine does not influence conduction unless its dose is toxic, and that within acutely ischemic ventricular myocardium, at a therapeutic dose, lidocaine prolongs conduction rapidly, but this effect is produced heterogeneously in the ischemic myocardium and is poor in the subepicardial layer.

The effect of cytochalasin B on the superoxide production by alveolar macrophages obtained from normal rabbit lungs.

Resident alveolar macrophages and lung lavage fluids were obtained from normal rabbit lungs. Superoxide production by alveolar macrophages exposed to lung lavage fluids and cytochalasin B was measured by superoxide dismutase-inhibitable nitroblue tetrazolium (NBT) reduction. Glycogen-elicited peritoneal macrophages were used as a control. Cytochalasin B, as well as lung lavage fluids, enhanced superoxide production by resting alveolar macrophages. The cytochalasin B-induced superoxide production was associated with enhanced attachment to glass and with remarkable alterations of the cell surface morphology, probably relating to interference with the microfilament functions of cells. On the other hand, glycogen-elicited peritoneal macrophages showed only a slight production of superoxide when exposed to the same stimulants.

Histochemical studies of lysosomal enzyme and nitroblue tetrazolium reduction of phagocytes in the cerebrospinal fluid of patients with infectious diseases of the central nervous system.

Lysosomal enzyme levels and nitroblue tetrazolium (NBT) reduction of phagocytes in the cerebrospinal fluid (CSF) of patients with infectious diseases of the central nervous system (CNS) were studied histochemically to evaluate the function of phagocytes. Lysosomal enzymes of acid phosphatase and beta-galactosidase were demonstrated in mononuclear phagocytes and leptomeningeal cells, but not in polymorphonuclear leukocytes (PMN) and lymphocytes. In tuberculous meningitis, more than 60% of the cells were positive for the enzymes as compared with less than 30% for other diseases. Besides, the cells which stained highly for the enzymes were often found in the CSF of tuberculous meningitis. The lysosomal enzyme levels in the cells were dependent on the nature of the infection rather than on the intensity of inflammation when judged by total cell count in the CSF. On the other hand, reduced NBT formazan was found in PMN, mononuclear phagocytes, and leptomeningeal cells. The intensity of NBT reduction by these cells correlated well with the total cell count in CSF; i.e., enhanced NBT reduction by phagocytes reflected the intensity of the inflammation in the subarachnoid space. Thus, histochemical study of phagocytes in CSF can provide useful additional aids to the diagnosis of the nature and stage of CNS infection.