[Spinal-continuous epidural anesthesia].
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Biomedical subjects
Publications and source records attributed to M Tagami.
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The purpose of this study is to investigate the effect of hyperventilation on the spinal pain modulating system by using naloxone. Under enflurane anaesthesia, cats were prepared with midcollicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was adjusted to produce hypocapnia of PCO2 20-25 mmHg. After activities of WDR cells were well suppressed, naloxone 0.1 mg.kg-1 was given intravenously. Changes of firings of WDR cells were investigated. Returning to normocapnia, recovery of firings was followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Naloxone significantly antagonized the suppressive effects of hyperventilation upon the activity of WDR cell. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to pain modulating system by endogenous opiates.
Foal diarrhea due to serotype 3 rotavirus broke out on a foal-raising farm in the years 1987 and 1989. In 1989, all of the foals, regardless of whether or not they suffered from diarrhea, received bovine colostral immunoglobulin (Ig) powder orally for 3 to 5 days during the epidemic. The morbidity of the diarrhea was lower than that observed in 1987, when the Ig powder was not administered to foals. These data suggested that the administration of Ig powder might partially prevent foal diarrhea with rotavirus infection.
Nodular hepatic lesions caused by larval Echinococcus multilocularis were found in a four-year-old female thoroughbred race horse born and raised in Hokkaido. Before detection of the infection, the infected animal was transported around Honshu for racing. The present disclosure of hydatidosis in a race horse raises concern over the potential danger of spreading the infection throughout Japan by horses possibly infected in Hokkaido.
The purpose of this study is to investigate the effects of hyperventilation on the wide dynamic range (WDR) cell of the dorsal horn of the feline lumbar spinal cord. Cats received midcollicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells were sampled with microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period with PaCO2 of 35-45 mmHg, respiratory rate and tidal volume were adjusted to make a level of hypocapnia as low as 20-25 mmHg. The recovery of cell activity was followed when normocapnia was restored. Hypocapnia with PaCO2 of 25-30 mmHg and 20-25 mmHg suppressed the activity of WDR cell significantly. At PaCO2 of 25-30 mmHg, the spontaneous activity was suppressed for about 20% and evoked activity for 27%. At PaCO2 of 20-25 mmHg, the spontaneous activity was suppressed for about 50% and evoked activity for 33%. The results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell.
In this study bovine aortic endothelial cells were co-cultured with astrocytes from fetal Wistar Kyoto rats. Endothelial cells growing on type-I collagen, co-cultured with astrocytes, showed various stages of development. Although some cells appeared to be mature, horseradish peroxidase penetrated within 1 min of incubation through the intercellular junctions of these endothelial elements maintained on type-I collagen. In contrast, endothelial cells on type-IV collagen, co-cultured with astrocytes, were well developed; their intercellular junctions were well established, and plasmalemmal vesicles reduced in number. As a result, horseradish peroxidase was unable to penetrate through the endothelial cells grown on type-IV collagen and co-cultured with astrocytes because of the reduced extent of the junctional and vesicular transport. These findings reveal that (1) type-IV collagen is essential for the differentiation of endothelial cells, (2) endothelial cell-astrocyte interactions occur during co-culture, and (3) endothelial permeability depends on astrocyte-produced factors, in addition to type-IV collagen.
A 50-year-old female patient was admitted because of an enormously enlarged spleen and thrombocytopenia. Ultrasonography and magnetic resonance imaging revealed multiple space-occupying lesions in the spleen. She was diagnosed as having Gaucher's disease based on the low level of beta-glucosidase activity in leukocytes and Gaucher's cells present in bone marrow aspirate. Severe hypersplenism necessitated splenectomy. Pathological studies of the excised spleen, including ultrastructural examinations, demonstrated that multiple space-occupying lesions in the spleen were composed of typical Gaucher cells.
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We examined ultrastructurally cerebral pericytes and astrocytes in 20 normotensive Wistar Kyoto rats and 60 asymptomatic stroke-prone spontaneously hypertensive rats, which were sequentially killed at 4-52 weeks of age. Another 30 SHRSP were killed soon after they showed symptoms of stroke. We found two kinds of pericytes around the capillaries; granular pericytes and filamentous pericytes. Granular pericytes possibly serve as scavenger cells in the central nervous system and became active and grew in size with time. In contrast, filamentous pericytes degenerated during the development of hypertension. Degeneration of the filamentous pericytes was involved in an increase of endothelial permeability. Increased permeability caused focal and then circumferential swelling of the astrocytes around the capillaries. Swelling of the astrocytes seemed to accelerate the production of attachment plaques. Following this increase in the number of attachment plaques, numerous astrocytic filaments were produced within the cytoplasm. As a result, fibrous astrocytes were fully developed. Adjacent to the fibrous astrocytes we detected opening of the interendothelial junctions as well as dead neurons. From these observations we propose that astrocytes perform the main function in trophic interactions among cerebral endothelial cells, astrocytes, and neurons and that dysfunction of astrocytes disturbs the neural environment, resulting in neuronal death.
We examined the ultrastructure of cerebral pericytes and astrocytes in 20 normotensive Wistar-Kyoto rats and 60 asymptomatic stroke-prone spontaneously hypertensive rats killed at 4-52 weeks of age. Another 30 stroke-prone spontaneously hypertensive rats were killed soon after they showed symptoms of stroke. We found two kinds of pericytes around the capillaries: granular pericytes and filamentous pericytes. Granular pericytes possibly serve as scavenger cells in the central nervous system and became active and grew in size with time. In contrast, filamentous pericytes degenerated during the development of hypertension. Degeneration of the filamentous pericytes was involved in an increase of endothelial permeability. Increased permeability caused focal and then circumferential swelling of the astrocytes around the capillaries. Swelling of the astrocytes seemed to accelerate the production of attachment plaques. Following this increase in the number of attachment plaques, numerous astrocytic filaments were produced within the cytoplasm. As a result, fibrous astrocytes were fully developed. Adjacent to the fibrous astrocytes we detected opening of the interendothelial junctions as well as dead neurons. From these observations we propose that astrocytes perform the main function in trophic interactions among cerebral endothelial cells, astrocytes, and neurons and that dysfunction of astrocytes disturbs the neural environment, resulting in neuronal death.
Epizootiological and virological studies were conducted on foal diarrhea occurring in 3 foal-raising locations in a light horse farm from March to July, 1987. At the first location, although 27 (75%) of 36 foals had developed diarrhea, the isolation rate of rotavirus (RV) was low (5/14 feces, 36%). Many of the foals had the disease as early as 23 days after birth. At the second and third locations, 21 (27%) of 78 foals and 41 (76%) of 54 foals were affected with diarrhea. Isolation rates of RV were 90% (20/22 feces) and 100% (26/26 feces), respectively. The diseased cases were observed throughout the short period from June to early July and on foals aged from 63 to 65 days. These findings suggested the importance of RV as a causal agent of foal diarrhea at the latter location, RV and/or other agents at the former location. All the 3 strains of RV represented from each location were identified as serotype 3 by plaque reduction neutralization test against the antiserums of serotypes 1 to 6 of RV. However, the 3 strains showed low cross-reactivity with antiserum of the serotype 3 of the equine RV.
A study concerning subjective symptoms of spasms which occur during 24 hours was carried out in 13 quadriplegic patients. All had spasms. Tonic and clonic spasms occurred involving their limbs and trunk. Extensor spasms occurred more often in the lower limbs than in the upper limbs. The duration of spasms was 8 seconds on average and the frequency was 15 times on average per day. The spasms which were severe tended to last longer in duration and were more frequent in occurrence. No spasms occurred without a trigger. The activities in daily living were interfered with by spasms in most patients. Most of these activities also triggered spasms.
Smooth muscle cells were isolated and cultured from the aortic media of age-matched, stroke-prone and stroke-resistant spontaneously hypertensive rats (SHRSP, SHRSR:SHRs) and Wistar-Kyoto rats (WKY), and the growth rate of cells from the three strains was compared. Under electron microscopical observation the cells were identified as modified (or synthetic-type) smooth muscle cells. Cells occurring at low densities showed the same morphology for both SHRs and WKY, but cells occurring at higher densities were observed to be smaller in SHRs than in WKY. An analysis of the growth curves of cells showed a significantly enhanced replication rate in cells from SHRs compared with those from WKY, especially in the early passages. In later passages (repeated until the 9th passage), however, this distinction was not clear. These growth characteristics were also confirmed in cells from both 12- and 24-week-old, age-matched SHRs and WKY. We could not find any difference between the growth characteristics of cells from SHRSP and SHRSR. It is possible to hypothesize from these findings that the abnormality relating to hypertension (hypertension being a common characteristic of SHRSR and SHRSP) is found in the smooth muscle cells, and is reflected as an enhanced growth rate when they are exposed to mitogenic stimuli, such as in atherosclerosis.
Cholera toxin subunit B suppressed the proliferation of cultured vascular smooth muscle cells from the thoracic aorta of Wistar-Kyoto rats (WKY), stroke-resistant spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP). Since cholera toxin subunit B did not stimulate cyclic AMP accumulation in vascular smooth muscle cells, the effect of cholera toxin subunit B might be due to another mechanism. Cholera toxin subunit B bound to the surface of vascular smooth muscle cells and was rapidly incorporated into them. The morphological structure of vascular smooth muscle cells was transformed from the synthetic type to the non-synthetic type, in which microfilaments and intermediate filaments were abundantly formed, while rough endoplasmic reticulum was decreased after CTB treatment.
We performed ultrastructural studies of intracerebral vessels in stroke-prone spontaneously hypertensive rats (SHRSP). The initial vascular lesions observed in the asymptomatic SHRSP were focal cytoplasmic necrosis in the outer layers of the media. Focal cytoplasmic necrosis progressed into wide-spread medial necrosis with time. In the SHRSP with cerebral infarctions we discovered that numerous monocytes adhered to the endothelium of the arteries having advanced medial damage. Following the adherence of the monocytes to the endothelium enormous amounts of plasma components entered and accumulated in the arterial wall. The accumulation of the plasma components, especially fibrin, thickened the wall, narrowed the lumen and resulted in occlusion with resultant cerebral infarctions. A lot of activated platelets are seen adhering to the endothelium of the capillaries and the venules around the cerebral infarctions. These results suggest that the monocytes and the platelets may be closely related to the occurrence of cerebrovascular occlusions. The occlusions may result in further cerebral blood flow reduction and continuous deterioration.
In numerous investigations using cultured smooth-muscle cells, investigators have consistently added 10-20% fetal calf serum (FCS) to the medium to maintain viable cells. In the present study we utilized an optical technique to investigate whether smooth-muscle cells, cultured with or without FCS, maintain their contractile activity in vitro. With such optical measurement, we were able to detect signals due to spontaneous contractions, in muscle cells cultured in FCS-free medium for up to 8 days, and, for the first time, were also able to observe the conduction of these cell contractions. The ultrastructural characteristics of cultured smooth-muscle cells during contractile activity, were also examined by electron microscopy. The cells were mature and well-differentiated, and were packed with numerous myofilaments. They had developed long cell processes, and were linked to one another by gap junctions. These observations indicated that the smooth-muscle cells, cultured without FCS for 7 to 8 days, were morphologically mature and maintained their contractile activity, whereas the cells cultured in FCS-containing medium showed no detectable signs of contractile activity.
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The distribution of 3H-diltiazem in myocardial cell organelles was studied using an electronmicroscopic autoradiographic technique. At 3, 5 and 10 min after 3H-diltiazem injection, silver grains, which indicate the existence of diltiazem, were detected in plasma membranes and intracellular organelles. Silver grains in T systems were observed more frequently at 3 min than at 5 and 10 min. In contrast, silver grains in sarcoplasmic reticula and mitochondria apparently increased with the passage of time. These findings suggest that diltiazem is transported through the T system and may accumulate within the sarcoplasmic reticula and mitochondria. Furthermore, our study revealed morphologically for the first time that the intracellular sites of action where diltiazem was directed were possibly the mitochondria.