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Biomedical subjects

H Otani

Publications and source records attributed to H Otani.

At least 199 records · Page 11Linked to original sources
PubMed1989

[The experimental study on long-term cardiac preservation: the efficacy of low-flow continuous perfusion with fluorocarbon].

We compared the effect of simple immersion and continuous perfusion on long-term cardiac preservation, and evaluated the effectiveness of perfusion with oxygenated fluorocarbon solution. The isolated rabbit hearts were preserved for 24 hours at 4 degrees C using the following five preservation techniques: (1) simple immersion with Collins M solution (Group I), (2) perfusion with oxygenated Collins M solution at a flow rate of 10 ml/hr (Group II), (3) perfusion with the same solution as in Group II at a flow rate of 20 ml/hr (Group III), (4) perfusion with oxygenated Collins M solution containing 10% fluorocarbon at a flow rate of 10 ml/hr (Group IV), (5) perfusion with the same solution as in Group IV at a flow rate of 20 ml/hr (Group V). The hearts of Group I showed a significant decrease of myocardial ATP and an increase of myocardial lactate during preservation compared to the hearts of perfusion groups. Assessment of isovolumic left ventricular function following 24-hour preservation using a support animal showed a significant decrease of Max dp/dt and increase of end-diastolic pressure in the hearts of Group I. Perfusion with fluorocarbon (Group IV and V) significantly increased oxygen consumption compared to Group II and III in association with minimum accumulation of myocardial lactate, indicating that aerobic metabolism during preservation is better maintained in the fluorocarbon-perfused hearts. Moreover, CPK release and myocardial water gain during preservation were significantly less, and left ventricular function following preservation was significantly better in these hearts. Increasing the flow rate from 10 ml/hr to 20 ml/hr resulted in sustained increase in perfusion pressure (1.80 +/- 0.53 to 3.70 +/- 0.34 mmHg) and myocardial water content (79.2 +/- 0.4 to 87.2 +/- 0.3%) during preservation in the hearts of Group III, but it did not further improve left ventricular function despite significant enhancement of myocardial oxygen uptake in both Group III and V. These results suggest that hypothermic low-flow continuous perfusion with oxygenated Collins M solution is superior to simple immersion with the same solution for long-term cardiac preservation, and that the addition of fluorocarbon to the perfusate enhances the efficacy of such a perfusion.

Animals↗
PubMed1989

[Successful treatment with a small dose of N4-behenoyl-1-beta-D-arabinofuranosylcytosine in a case of chronic myelomonocytic leukemia in blastic crisis].

A 56-year-old female was admitted for the examination of leukocytosis in May, 1982. The hematological examination showed hemoglobin 12.0g/dl, platelets 14.5 X 10(4)/microliters and leukocytes 18,000/microliters with 28% of monocytes. A bone marrow aspiration revealed granulocytic hyperplasia. Granulocytes showed nuclear abnormalities, such as folding or lobulation. From these data, a diagnosis of chronic myelomonocytic leukemia (CMMoL) was made and followed with no treatment for 2 years. However, fever, bone pain, anemia, thrombocytopenia and the increase of monoblasts in the peripheral blood and bone marrow were observed in May, 1984. These findings indicated that she was in the blastic phase. She was treated by intensive combination chemotherapy (BHAC-AMP), but did not attain any remission. Therefore, a small dose of N4-behenoyl-1-beta-D-arabinofuranosylcytosine (BH-AC; 1 mg/kg/day) was administered for 70 days. As a result, complete remission was obtained and continued for 37 months with the same therapy. The experience of this case suggests that small dose of BH-AC could be applied to a case of CMMoL in blastic crisis.

Antineoplastic Agents↗
PubMed1989

Improvement of myocardial function by trifluoperazine, a calmodulin antagonist, after acute coronary artery occlusion and coronary revascularization.

Activation of an intracellular calcium-calmodulin complex may play an important role in myocardial injury induced by ischemia and reperfusion. Trifluoperazine, a calmodulin antagonist, was used before ischemia to enhance myocardial preservation by preventing intracellular calcium accumulation. The experimental model used an isolated in situ pig heart (19 control animals and 15 trifluoperazine-treated animals) subjected to occlusion of the left anterior descending coronary artery for 60 minutes followed by 60 minutes of hypothermic potassium crystalloid cardioplegic arrest and 60 minutes of reperfusion. Myocardial segmental function measured by ultrasonic crystals showed that active systolic segment shortening was abolished in the distribution of the left anterior descending artery after 60 minutes of occlusion irrespective of the treatment, whereas that not in the distribution of the left anterior descending artery increased by about 15% in both groups of animals. Restoration of systolic segment shortening in the distribution of the left anterior descending artery 60 minutes after reperfusion was 12% and 42% of baseline levels in untreated and trifluoperazine-treated animals, respectively (p less than 0.01). This improvement in segmental function by trifluoperazine was reflected in significantly (p less than 0.05) better global myocardial contractility and compliance and in significantly (p less than 0.01) greater total coronary blood flow and myocardial oxygen consumption. Trifluoperazine also increased myocardial creatine phosphate content in the distribution of the left anterior descending artery (p less than 0.01) during reperfusion, and creatine kinase release was reduced (p less than 0.05). Our results suggest that trifluoperazine improved regional myocardial function after acute occlusion of the left anterior descending artery and reperfusion and that global cardiac performance was thereby improved. The beneficial effects of trifluoperazine may be exerted by prevention of myocardial injury associated with the calcium-calmodulin complex in ischemic and reperfused myocardium.

Adenosine Triphosphate↗
PubMed1989

Characterization of very low density lipoprotein from Watanabe heritable hyperlipidemic rabbits.

We investigated the properties of very low density lipoprotein (VLDL) from two types of Watanabe heritable hyperlipidemic (WHHL) rabbits: one with a high incidence of coronary atherosclerosis (type 1), and the other with a low incidence (type 2). When incubated with mouse peritoneal macrophages, VLDL from type 1 WHHL rabbit (type 1-VLDL) stimulated cholesteryl ester synthesis 10.5-fold more than VLDL from the type 2 WHHL rabbit (type 2-VLDL) did. Moreover, a similar difference was seen in the stimulation of cholesteryl ester synthesis in peritoneal macrophages isolated from the WHHL rabbits. The mass ratios of cholesterol to protein in type 1- and type 2-VLDL were 5.69 and 2.05, respectively. Agarose gel electrophoresis of type 1-VLDL showed beta mobility, and that of type 2-VLDL showed pre-beta mobility. No difference was seen between the sizes of VLDL particles of the two types. The amount of apolipoprotein E in type 1-VLDL was greater than that in type 2-VLDL. In conclusion, the difference between type 1 and type 2 WHHL rabbits is at least partly due to the presence in type 1 animals of VLDL particles rich in cholesteryl esters and apolipoprotein E, particles which are very similar to beta-VLDL in conformation.

Animals↗
PubMed1988

Development of the choroid plexus anlage and supraependymal structures in the fourth ventricular roof plate of human embryos: scanning electron microscopic observations.

The developing anlage of the choroid plexus and supraependymal structures in the fourth ventricular roof plates of nine normal human embryos ranging from Carnegie stages 14 to 19 were investigated with scanning electron microscopy. In the human embryos at stage 18, the first semimacroscopic choroidal anlage developed in the form of bilateral evaginations that ran dorsomedially and caudally from the bilateral corners of the rhombencephalon. The anlage became evident with even smaller and parallel ridges in the embryo at stage 19. Embryos at earlier stages exhibited surface membrane modifications such as convexity, microvilli, cilia, and spherical protrusions at the middle one-third of the rhombencephalon, which corresponded to the future choroidal anlage region. Two morphologically different groups of supraependymal cells (SE cells) were elucidated throughout the stages examined. Type 1 SE cells has spindle or tear-drop-like bodies, frequently with one or more long cytoplasmic processes. Type 2 SE cells were globular, with numerous fine pseudopodial processes. Type 1 SE cells were distributed mainly at the future choroidal anlage regions or on the anlage itself and were less frequently located at the rostral end of the roof. We found no general pattern in the distribution of type 2 SE cells. Supraependymal fibers (SE fibers) were seen as fine processes that were distributed similarly to type 1 SE cells and extended transversely for a long distance.

Cell Differentiation↗
PubMed1988

Development of mitochondrial helical sheath in the middle piece of the mouse spermatid tail: regular dispositions and synchronized changes.

Morphologic changes in the development of the mitochondrial helical sheath in the mouse spermatid tail were examined with the scanning electron microscope (SEM) using the osmium-DMSO-osmium method and classified into several stages. During late spermiogenesis, spherical mitochondria gathered around the forming spermatid tail. The shape of these mitochondria gradually changed from spheroid to long and rod-like. Mitochondria first were arranged in four longitudinal rows (stage 1) that twisted dextrally, and the mitochondria began to stagger (stage 2). They became elongated and arranged into a staggered pattern; they then attached to each other in an end-to-end fashion to form a sinistral double helix around the core of the axoneme (stage 3). These end-to-end contacts were observed in every second gyre on the four lines surrounding the core of the axoneme at stage 3. Mitochondria further elongated and end-on touching appeared with every third gyre on the five longitudinal lines that surround the core of the axoneme (stage 4). The direction of the helix, always sinistral, was clearly discernible only in the later stages. Disposition of the mitochondria in the spermatid tail was regular throughout development, which indicates that these mitochondria elongate simultaneously and also at the same rate. On any given cracked surface of the seminiferous tubule, spermatid tails with the same stage of mitochondria predominantly were observed. This ultrastructural finding appears compatible with the histologic synchronism, (termed the "wave") in differentiating germ cells.

Animals↗
PubMed1988

Improved myocardial performance induced by clofibrate during reperfusion after acute myocardial infarction.

The increase of cellular fatty acids appears to be one of the causes of the myocardial injury during ischemia and reperfusion. This study was designed to examine whether a hypolipidemic drug such as clofibrate can reduce the myocardial injury during ischemia and reperfusion. Clofibrate was fed to experimental pigs for 9 days. Isolated in situ hearts from both experimental and control pigs were subjected to 60 min of regional ischemia induced by occluding the left anterior descending coronary artery, followed by 60 min of global ischemia by hypothermic cardioplegic arrest and 60 min of reperfusion. The clofibrate feeding resulted in the better cardiac performance as judged by increased coronary blood flow, improved left ventricular function, and reduced myocardial injury as judged by creatine kinase release. Although the clofibrate-fed animals contained higher levels of thiobarbituric reactive materials, the free fatty acid levels of plasma and myocardium were much lower compared with control animals. The clofibrate feeding was also associated with increased peroxisomal catalase and beta-oxidation of fatty acids. These results suggest that decreased levels of free fatty acids in the plasma and the myocardium and increased catalase activity induced by antilipolytic therapy appear to provide beneficial effects to the myocardium during ischemia and reperfusion.

Animals↗
PubMed1988

Alpha 1-adrenoceptor-mediated phosphoinositide breakdown and inotropic response in rat left ventricular papillary muscles.

alpha 1-Adrenoceptor stimulation of rat left ventricular papillary muscles by phenylephrine in the presence of propranolol resulted in rapid breakdown of phosphatidylinositol 4,5-bisphosphate (PI-4,5-P2) and a triphasic inotropic response in a concentration-dependent manner. The release of inositol trisphosphate (IP3) was maximum within 30 seconds and remained high for at least 30 minutes. The IP3 formation was associated with a rapid, but small, increase in contractile force followed by a transient decline in the contractility prior to the development of a sustained and more pronounced positive inotropic response. Inhibition of PI-4,5-P2 hydrolysis by the alpha 1-adrenergic antagonist prazosin or the PI-4,5-P2 phosphodiesterase inhibitor neomycin blocked all components of the inotropic responses. Combined addition of 2,3-diphosphoglyceric acid, a competitive inhibitor of IP3 phosphatase, with phenylephrine doubled the IP3 formation and potentiated the initial phases of inotropic responses but had no effect on the sustained positive inotropic response. Nifedipine and Mn2+ did not block the transient inotropic responses but inhibited the sustained positive inotropic response. alpha 1-Adrenoceptor stimulation resulted in restoration of slow responses in the high K+-depolarized muscles in the time course similar to that of the development in the sustained positive inotropic response. Addition of phorbol-12,13-dibutyrate alone or in combination with caffeine or A23187 failed to produce a sustained positive inotropic effect, but pretreatment with this phorbol ester (1-100 nM) for 30 minutes resulted in dose-dependent potentiation of alpha 1-adrenoceptor-mediated sustained positive inotropic effect associated with enhanced slow responses. These results suggest that the inotropic effects mediated by cardiac alpha 1-adrenoceptor stimulation occur through the phosphodiesteratic cleavage of PI-4,5-P2, such that IP3 may produce transient inotropic effects by mobilizing intracellular Ca2+, while diacylglycerol, along with cofactors that are also generated on alpha 1-adrenoceptor stimulation, may provoke a sustained positive inotropic effect by potentiating slow Ca2+ channels through activation of protein kinase C.

2,3-Diphosphoglycerate↗
PubMed1988

Enhanced phosphodiesteratic breakdown and turnover of phosphoinositides during reperfusion of ischemic rat heart.

In this study, we examined phosphoinositide metabolism during ischemia and reperfusion using an isolated and perfused rat heart. When myocardial phosphoinositides were prelabeled with [3H]inositol, reperfusion after 30 minutes of normothermic global ischemia resulted in significant accumulations of radiolabeled inositol phosphate, inositol bisphosphate, and inositol trisphosphate. Isotopic incorporation of [3H]inositol into phosphatidylinositol, phosphatidylinositol-4-phosphate, and phosphatidylinositol-4,5-bisphosphate was increased significantly in the heart reperfused with [3H]inositol after 30 minutes of ischemia compared with that perfused with [3H]inositol after 30 minutes of nonischemic perfusion. However, isotopic incorporation of [3H]glycerol into diacylglycerol, phosphatidic acid, and all of the three phosphoinositides was diminished in the reperfused hearts. Reperfusion of the ischemic heart prelabeled with [14C]arachidonic acid resulted in significant increases in [14C]diacylglycerol and [14C]phosphatidic acid. The enhanced accumulations of [3H]inositol phosphates during reperfusion were not affected by treatment with prazosin plus atropine or indomethacin, but were inhibited by hypoxic reperfusion, reperfusion with Ca2+-free buffer, or by mepacrine. These results suggest that myocardial reperfusion stimulates phosphodiesteratic breakdown and turnover of phosphoinositides, and increased Ca2+ influx caused by reperfusion may be involved in the mechanism of stimulation of phosphatidylinositol-specific phospholipase C activity in the rat heart.

Animals↗
PubMed1988

Judgments of horizontality of still water: effects of perceptual and cognitive factors.

Three experiments examined failure to solve the Piagetian water-level horizontality task in terms of artifacts of experimental procedure, perceptual characteristics of the task, and the physical principles involved in the task. The possibility that rotational set accounts for task failure was examined in Exp. 1 (N = 154 college students) with no evidence of an effect, although the spatial tasks used correlated with performance on the horizontality task for women but not for men. In Exp. 2 (N = 159) a procedure of focussing attention on the movement of water and air using a carpenter's level also did not affect horizontality performance. However, Exp. 3 confirmed that performance (N = 57) on the horizontality task was related to understanding the basic principle of the level. These results were discussed in terms of possible experiences of the subjects as well as the relative contributions of perceptual and cognitive factors.

Adult↗
PubMed1988

Positive inotropic effect and phosphoinositide breakdown mediated by arachidonic acid and prostaglandin F2 alpha.

We investigated the mechanism of arachidonate- and prostaglandin-induced alteration of cardiac contractile activity in isolated rat left ventricular papillary muscles. Superfusion with 10(-6) to 10(-4) M arachidonic acid resulted in a slow developing positive inotropic effect (PIE) in a concentration-dependent manner. The PIE was abolished by pretreatment with 10(-5) M indomethacin. Prostaglandin (PG) F2 alpha also produced a significant PIE in a concentration-dependent manner, but the EC50 value was approximately 2 orders of magnitude lower and the maximum contractile response was 2-fold higher than those of arachidonate. PGE2 and PGI2 were without an effect on contractile force at concentrations ranging from 10(-9) to 10(-6) M. Both arachidonate and PGF2 alpha provoked slow responses in the partially depolarized muscles in a time course similar to that of development in the PIE. Neither arachidonate nor PGF2 alpha affected tissue levels of cyclic AMP and cyclic GMP, but these molecules increased accumulations of [3H]inositol phosphates (IPs) in a concentration-dependent manner similar to that observed for their PIE. The enhanced accumulation of [3H]IPs induced by arachidonate was abolished by pretreatment with 10(-5) M indomethacin. Although an increase in [3H]IP level was relatively rapid in PGF2 alpha-treated tissues, maximum accumulations of [3H]IPs were identical between arachidonate- and PGF2 alpha-treated tissues. Thus, for comparable increases in [3H]IPs, there was a greater PIE with PGF2 alpha than with arachidonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Alkaline phosphatase activity of the IVth ventricular choroidal epithelium of rats during embryonic and neonatal development.

The cytochemical localization of alkaline phosphatase (AlPase) activity in the developing IVth ventricular choroidal epithelium was investigated in embryonic and neonatal rats. During the initial development of the choroidal primodium the flattened and/or cuboidal epithelial cells of the ventricular roof were changed to columnar cells with well-developed microvilli and apical tight junctions. When compared to AlPase activity on the lateral plasma membranes of the surrounding ependymal cells, these columnar cells of the choroidal primodium revealed activity on the lateral and luminal plasma membranes, but no activity was found on the basal surface of these cells. On the other hand, the epithelial cells in the neonatal choroid plexus showed a continuous morphological alteration from columnar cells with short microvilli to mature cuboidal cells with numerous long microvilli. AlPase activity in immature columnar cells was observed on all plasma membranes, except for the apical junctional area of the lateral surface. With maturing of the choroidal epithelial cells, the activity appeared to be eliminated from the lateral and luminal plasma membranes of the cuboidal cells, and mature choroidal epithelial cells showed activity on the basal surface only. These findings suggest that AlPase may play an important role in the membrane activity of epithelial cells differentiating between the primitive epithelial cells of the ventricular roof and the mature choroidal epithelial cells.

Alkaline Phosphatase↗
PubMed1988

Effect of ischemia and reperfusion of the myocardium on in vitro beta-oxidation of fatty acids.

The in vivo oxidation of perfused [14C]-labeled fatty acids has been shown to decrease dramatically in hypoxic hearts. This study addresses the influence of ischemia and reperfusion on the enzymic activities of beta-oxidation of fatty acids in mitochondria and of peroxisomal origin. The rate of beta-oxidation of fatty acids in the isolated mitochondria from myocardium of swine fed control diet declined about 20% by the ischemic insult induced by hypothermic cardioplegic arrest. Upon reperfusion, the rate of mitochondrial beta-oxidation returned to a normal level. In clofibrate-fed animals, the rate of mitochondrial beta-oxidation did not vary significantly between control, ischemic, and perfused tissues. Furthermore, neither in control nor in clofibrate-fed animals did the rates of peroxisomal beta-oxidation of fatty acids vary significantly in the ischemic or reperfused tissues as compared to that of preischemic controls. These results suggest that ischemia does not contribute to any loss of enzymic activity in beta-oxidation of fatty acid cycles either in mitochondria or peroxisomes. Furthermore, the feeding of 0.5% (w/w) clofibrate to pigs increased the rate of mitochondrial beta-oxidation of fatty acids only by 50% while that of peroxisomes increased threefold. A similar threefold increase in catalase activity was also produced by clofibrate feeding. These results suggest that the heart plays a role in the hypolipidemic action of clofibrate.

Animals↗
PubMed1988

The effect of temperature and hematocrit level of oxygenated cardioplegic solutions on myocardial preservation.

The ideal temperature and hematocrit level of blood cardioplegia has not been clearly established. This study was undertaken (a) to determine the optimal temperature of blood cardioplegia and (b) to study the effect of hematocrit levels in blood cardioplegia. A comparison of myocardial preservation was done among seven groups of animals on the basis of variations in hematocrit levels and temperature of oxygenated cardioplegic solution. The experimental protocol consisted of a 2-hour hypothermic cardioplegic arrest followed by 1 hour of normothermic reperfusion. Group 1 received oxygenated crystalloid cardioplegic solution at 10 degrees C. Groups 2 through 7 received oxygenated blood cardioplegic solution with the following hematocrit values and temperatures: (2) 10%, 10 degrees C; (3) 10%, 20 degrees C; (4) 10%, 30 degrees C; (5) 20%, 10 degrees C; (6) 20%, 20 degrees C; and (7) 20%, 30 degrees C. Parameters studied include coronary blood flow, myocardial oxygen extraction, myocardial oxygen consumption, and myocardial high-energy phosphate levels of adenosine triphosphate and creatine phosphate during control (prearrest), arrest, and reperfusion. Myocardial oxygen consumption at 30 degrees C during arrest was significantly higher than at 10 degrees C and 20 degrees C, which indicates continued aerobic metabolic activity at higher temperature. Myocardial oxygen consumption and the levels of adenosine triphosphate and creatine phosphate during reperfusion were similar in all seven groups. Myocardial oxygen extraction (a measure of metabolic function after ischemia) during initial reperfusion was significantly lower in the 30 degrees C blood group than in the 10 degrees C blood group at either hematocrit level and in the oxygenated crystalloid group, which suggests inferior preservation. The hematocrit level of blood cardioplegia did not affect adenosine triphosphate or myocardial oxygen consumption or extraction. It appears from this study that blood cardioplegia at 10 degrees C and oxygenated crystalloid cardioplegia at 10 degrees C are equally effective. Elevating blood cardioplegia temperature to 30 degrees C, however, reduces the ability of the solution to preserve metabolic function regardless of hematocrit level. Therefore, the level of hypothermia is important in blood cardioplegia, whereas hematocrit level has no detectable impact, and cold oxygenated crystalloid cardioplegia is as effective as hypothermic blood cardioplegia.

Adenosine Triphosphate↗
PubMed1988

Enhanced myocardial preservation by nicotinic acid, an antilipolytic compound. Improved cardiac performance after hypothermic cardioplegic arrest.

The effect of nicotinic acid, an antilipolytic drug, on myocardial preservation was studied on the basis of cardiac performance after 2 hours of cardioplegic arrest. Isolated in situ pig hearts were subjected to 120 minutes of hypothermic potassium (35 mEq) crystalloid cardioplegic arrest followed by 60 minutes of reperfusion. The experimental group received nicotinic acid 0.08 mmol/L 15 minutes before cardioplegic arrest, whereas the control group received 15 minutes of unmodified perfusion. There was a marked decline in myocardial creatine phosphate levels during cardioplegic arrest in both groups that returned to the baseline level during reperfusion without a significant intergroup difference, and adenosine triphosphate levels remained stable throughout the experiment in both groups. Myocardial oxygen consumption during reperfusion was significantly higher in hearts treated with nicotinic acid, which was consistent with a significantly greater cardiac contractile force as evaluated by isovolumetric left ventricular pressure measurements. There appeared to be less cardiac membrane damage as measured by creatine kinase release during reperfusion, which was significantly inhibited by treatment with nicotinic acid. The present study supports the conclusion that nicotinic acid improves cardiac performance after hypothermic cardioplegic arrest.

Adenosine Triphosphate↗
PubMed1987

Role of xanthine oxidase inhibitor as free radical scavenger: a novel mechanism of action of allopurinol and oxypurinol in myocardial salvage.

Xanthine oxidase (XO) has been hypothesized to be a potential source of oxygen-derived free radicals during reperfusion of ischemic myocardium based on the fact that allopurinol, a XO-inhibitor, can reduce reperfusion injury. In this communication we report that both allopurinol and oxypurinol, the principle metabolite of allopurinol, prevent the reperfusion injury in isolated pig heart. However, we found that neither pig heart nor pig blood contain any XO activity. Our study showed a direct free radical scavenging action of these XO-inhibitors during ischemia and reperfusion, as judged by the reduction of free radical signals when compared using an Electron Paramagnetic Resonance Spectrometer. Using a Luminometer, we also confirmed that both allopurinol and oxypurinol can scavenge ClO2, HOCl, and significantly inhibit free radical signals generated by activated neutrophils. These XO-inhibitors, however, failed to scavenge O2. and OH. radicals. Our results suggest that these XO-inhibitors salvaged the ischemic-reperfused myocardium by scavenging free radicals, and not by inhibiting XO in the pig heart.

Adenosine Triphosphate↗
PubMed1987

Fourth ventricular floor in human embryos: scanning electron microscopic observations.

The ultrastructural surface features of the normal fourth ventricular floor of seven human embryos ranging from Carnegie stage 14 to stage 19 (crown-rump length: 7.6-16.2 mm) were examined by using scanning electron microscopy (SEM). Low-power SEM views showed the median sulcus, sulcus limitans, and neuromeres, transient structures characteristic of the earlier embryonic period. High-power SEM observation revealed supraependymal cells (SE cells) and supraependymal fibers (SE fibers) which exhibited a characteristic localization, as well as generalized surface-membrane modifications such as microvilli and cilia. SE cells could be classified into two major groups. The type 1 SE cells seem to possess neuronal functions, as deduced from morphological similarities to their counterparts in adults and the specialized distribution closely related to neuromeres. The type 2 SE cell morphologically resembled the phagocytic SE cell described in related literature. SE fibers ran a course either rostrocaudally in the median sulcus or mediolaterally on the neuromeres, most frequently near the interneuromeric cleft; they made contact with type 1 SE cells and ependymal surface modifications and then penetrated the ependymal layer.

Cerebral Ventricles↗