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Biomedical subjects

H Kitagawa

Publications and source records attributed to H Kitagawa.

At least 325 records · Page 18Linked to original sources

Cardiopulmonary values in dogs with artificial model of caval syndrome in heartworm disease.

Cardiopulmonary values were determined in dogs with an artificial model of heartworm caval syndrome, which was produced by insertion of heartworm-like silicone tubes into the tricuspid valve orifice and right atrium. Fifteen to 25 tubes with some knots were inserted in 6 dogs (knot group), and 7 to 11 tubes (small-number group) or 29 to 37 tubes (large-number group) without a knot in 3 dogs, respectively. After tube insertion, angiographic contrast medium infused into the right ventricle regurgitated to the right atrium in all cases, and the regurgitation was the most severe in the large-number group. On electrocardiographic findings, the atrial and/or ventricular premature beat developed. The height of a- and v-wave of right atrial pressure curves elevated in all groups. The elevation in v-wave was obvious in the large-number group. The pulmonary arterial pressure tended to fall or to elevate slightly, and total pulmonary resistance increased in all groups. The right cardiac output decreased significantly in all cases. The right heart hemodynamics of the model might resemble those in spontaneous cases without disturbed pulmonary circulation.

Angiocardiography↗

Intracellular production of adrenal renin in the fetal mouse. An immuno-electron microscopical study.

Renin-containing cells in fetal adrenal glands of the mouse were investigated with the protein A-gold immunocytochemical technique. On Day 14 of gestation, a small number of specific granules were weakly immunoreactive and were distributed in the Golgi region. Sometimes, apparent exocytosis of gold-labelled particles could be seen opening into the extracellular space. On Day 16 of gestation, numerous gold particles were demonstrated in the Golgi region as well as in the specific secretory granules. Immunoreactivity of the specific granules was increased as compared with Day 14, though some granules were observed to have no reaction with the antibody. On Day 18 of gestation reactivity for renin decreased, while a few clustered immunoreactive granules were demonstrated just beneath the cell membrane. No gold particles were observed in the Golgi apparatus during this period and more granules negative for renin were noted than on Day 16 of gestation. These results suggest that renin is produced and released temporarily by adrenal cortical cells in the late fetal life of the mouse.

Adrenal Glands↗

Cardiopulmonary function values before and after heartworm removal in dogs with caval syndrome.

Cardiopulmonary function values were determined before and after surgical removal of adult heartworms in 25 dogs with spontaneous and 4 dogs with drug-induced caval syndrome (CS). Fifteen dogs with spontaneous CS (recovery group) and 4 dogs with drug-induced CS (drug-induced CS group) recovered after removal, and 10 dogs with spontaneous CS were euthanatized or died (nonsurviving group). Before heartworm removal, injected radiographic contrast medium was regurgitated from the right ventricle to the right atrium. Mean pulmonary arterial pressure and total pulmonary resistance were not statistically different between the recovery and nonsurviving groups of dogs, but the end-diastolic right ventricular pressure (mean +/- SD, 6.9 +/- 9.1 mm of Hg) and the a (8.7 +/- 9.2 mm of Hg)- and v (6.3 +/- 8.5 mm of Hg)-waves of the right atrial pressure curve in the recovery group were less, respectively, than the end-diastolic right ventricular pressure (17.3 +/- 6.0 mm of Hg) and the a (15.8 +/- 6.1 mm of Hg)- and v (21.4 +/- 6.9 mm of Hg)-waves in dogs of the nonsurviving group. After heartworm removal, contrast medium regurgitation disappeared, and cardiac output of the right ventricle increased in dogs of the recovery (from 2.08 +/- 0.72 to 2.38 +/- 0.68 L/min; P less than 0.05) and drug-induced CS (from 1.42 +/- 0.19 to 1.88 +/- 0.26 L/min, P less than 0.05) groups. However, regurgitation remained, and cardiac output did not increase in some dogs of the nonsurviving group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of heptaminol AMP amidate on T cell populations of peripheral blood lymphocytes and splenocytes in mice.

Heptaminol AMP amidate (HAA), a nucleotide derivative increased the percentage of T cell surface phenotypes on peripheral blood lymphocytes (PBL) of mice primed with sheep red blood cells. The T cell surface phenotypes Thy1.2, Lyt1, L3T4 and Lyt2 increased on the PBL of HAA administered mice to 136, 145, 144 and 153%, respectively over those on the PBL of control mice.

Adenosine Monophosphate↗

A monoclonal antibody directed to Tn antigen.

A murine monoclonal antibody, MLS 128, that was assigned to an anti-Tn antibody has been established by immunizing mice with human colonic cancer cells (LS 180). MLS 128 bound to mucin glycopeptides from LS 180 cells and their asialo forms to the same extent as well as to ovine submaxillary mucin (OSM) and asialo OSM. Special non-sialylated GalNAc residue(s) attached to a certain peptide region in the antigens seems to be involved in the binding since N-acetylgalactosaminidase treatment of the antigen abolished the binding and pronase digestion diminished the binding markedly.

Acetylgalactosamine↗

Occurrence of tetra- and pentasaccharides with the sialyl-Le(a) structure in human milk.

The occurrence of two novel oligosaccharides in human milk was investigated. These oligosaccharides were purified by affinity chromatography on a column of an immobilized monoclonal antibody, MSW 113. Structural studies, involving 500-MHz 1H NMR spectroscopy and fast atom bombardment-mass spectrometry, indicated the structures of these compounds to be NeuAc alpha 2----3Gal beta 1----3(Fuc alpha 1----4) GlcNAc and NeuAc alpha 2----3Gal beta 1----3(Fuc alpha 1----4) GlcNac beta 1----3Gal. This constitutes the first evidence for the occurrence of N-acetylglucosamine or galactose as the reducing-end residue of human milk oligosaccharides. These two oligosaccharides bound MSW 113 to nearly the same extent as sialyl-Lea hexasaccharide but to another sialyl-Le(a) structure-directed monoclonal antibody, NS-19-9, only weakly.

Antigens, Tumor-Associated, Carbohydrate↗

Renin immunohistochemistry in the adrenal gland of the mouse fetus and neonate.

The development of renin-containing cells in fetal and neonatal adrenal glands of the mouse was studied using immunohistochemistry. On days 13-14 of gestation, immunoreactivity for renin was first observed in a few cortical cells of the gland, appearing as small patchy or granular reaction products in the perikaryon. The mitotic configurations of the cells demonstrating immunoreactivity were noted. On day 16 of gestation, a number of intensively immunoreactive cells were distributed in the aortal side of the cortical zone. On day 18 of gestation, and day 1 postparturition, a small number of potent immunoreactive cells were still found in the cortical area. Immunoreactivity of the cytoplasm was observed in the cells, some showing an intensive reaction and others possessing numerous tiny granules just below the cell membrane. On days 3, 5, and 7 after birth, no renin-containing cells were found in the adrenal gland. The ratio of the numbers of renin-positive cells in certain areas to the numbers in the entire cortical area was significantly increased on day 16 of gestation, but there was no sexual difference in the ratios. The ratios were decreased subsequently until day 1 after birth. The possible significance of renin synthesis in specific adrenal cells in fetal life is discussed with respect to an important involvement of angiotensin II in the morphogenesis of the adrenal gland of the mouse.

Adrenal Glands↗

Vascular access in the neonate following extracorporeal membrane oxygenation.

An infant maintained on extracorporeal membrane oxygenation (ECMO) has unlimited vascular access. When the infant is returned to conventional ventilator therapy, the need for vascular access persists for days to weeks. Providing alternative central venous access may be problematic, particularly while the infant is still heparinized during the first 12 hours after decannulation. In this study, secondary central venous catheters (CVC) were placed, at the time of decannulation, into the internal jugular vein from which the venous bypass cannula is removed. Fifty-four of 90 infants supported with ECMO had secondary CVCs placed (60%) and vascular access maintained for 2 to 122 days (mean, 17.5 days). Four catheters were removed for culture-proved line sepsis (7.4%). Neck wounds were reexplored for bleeding, while on bypass, in 2 of 4 patients in the sepsis group. There were no deaths related to catheter sepsis. Catheter-related septic infants had been on bypass for 50 to 88 hours (mean, 72.7 hours) as compared with 11 to 312 hours (mean, 104 hours) for the entire ECMO group, P = NS. This experience (942 catheter-days) suggests that secondary CVC placement into the vein used for bypass is safe with infectious complications comparable to catheters placed through primary wounds. Infants requiring neck explorations for bleeding while on bypass are not candidates for secondary CVC placement.

Catheterization, Central Venous↗

Complications of lateral C1-2 puncture myelography.

This study reviewed the technical complication of 112 cases of lateral C1-2 puncture myelography for cervical spinal cord disorders. Spinal cord puncture and contrast injection, puncture between the occiput and C1, and blood vessel puncture were the main complications. These principally depended on the positioning of the patient's neck (hyperextension) and misdirection of the x-ray beam. For preventing major arterial puncture, the authors also reviewed 164 vertebral angiograms and determined the pathway of the vertebral arteries and the incidence of anomaly.

Female↗

Effects of heptaminol AMP amidate (HAA) on cyclic AMP level and mitogen-induced proliferation of murine spleen cells.

Heptaminol AMP amidate (HAA), a nucleotide derivative, was found to elevate the intracellular cyclic AMP (cAMP) level of cultured mice spleen cells in a time- and dose-dependent manner. Theophylline and imidazole, when added to the spleen cell culture simultaneously with HAA, respectively caused a further rise and a fall of the cAMP level increased by HAA alone. When comparatively higher doses of the T cell mitogen concanavalin A (Con A) were used in the culture, Con A-induced cell proliferation was mildly inhibited in the culture of spleen cells pooled from HAA administered mice in comparison to the culture of spleen cells pooled from saline treated mice. On the other hand, when another T cell mitogen phytohemagglutinin P (PHA) was used in different concentrations in the culture, there was a trend of enhanced cell proliferation in the culture of spleen cells pooled from HAA administered mice in comparison to the responses in the culture of spleen cells pooled from saline treated mice. The present results supported the previous findings that HAA-mediated immunopotentiation was closely related with a cAMP level elevating property of HAA, and the compound also enhanced the function of helper T cells.

Adenosine Monophosphate↗

Development of artificial model of caval syndrome in canine heartworm disease.

In order to develop an artificial model of caval syndrome (dirofilarial hemoglobinuria), heartworm-like silicone tubes were inserted into the tricuspid valve orifice and right atrium of dogs. Fifteen to 25 tubes with some knots were inserted through the posterior vena cava in 6 dogs (knot-tube group), 7 to 12 tubes without knot (small-number group) through the jugular vein in another 5 dogs, or 25 to 35 tubes (large-number group) in yet another 5 dogs. The tubes remained in the right atrium, and a part of them protruded into the tricuspid valve orifice. The number of tubes at the tricuspid valve orifice was the greatest in the large-number group. After tube insertion, the signs of so-called "caval syndrome", such as systolic cardiac murmur, jugular pulse, anemia, and so on, were observed in almost all cases of the 3 groups, the signs were severest in the large-number group. Urine hemoglobin was detected in almost all cases of the knot-tube and large-number groups, and in 1 case in the small-number group. Ascites was observed in 1 case of the knot-tube group at 6 weeks, in 1 case of the small-number group at 7 days and in 3 cases of the large-number group at 7 days after insertion.

Animals↗

Contribution of live heartworms harboring in pulmonary arteries to pulmonary hypertension in dogs with dirofilariasis.

To investigate whether adult heartworms harboring in the pulmonary arteries contribute to pulmonary hypertension, we determined the cardio-pulmonary values immediately before and after removal of heartworms from the pulmonary arteries and before and after insertion of live worms in their place. In 10 heartworm-infected dogs, 8 to 46 worms were removed. The mean pulmonary arterial pressure fell significantly from 24.5 +/- 7.9 mmHg to 16.3 +/- 4.9 mmHg (p less than 0.01) immediately after removal. The right cardiac output decreased in 7 of the 10 cases. The total pulmonary resistance and right ventricular stroke work index also decreased. At 24 hours after removal, live heartworms were put back into the pulmonary arteries of their host dog. The mean pulmonary arterial pressure elevated significantly (p less than 0.01) immediately after insertion. The right cardiac output further decreased in 7 of the 10 dogs, and the total pulmonary resistance and right ventricular stroke work index increased. Separate from this, 12 to 42 heartworms were transplanted into the pulmonary arteries of 5 heartworm-free dogs. Immediately after transplantation, the pulmonary arterial pressure did not show any significant change. However, the stroke volume decreased, and the total pulmonary resistance increased. These facts suggest a contribution of live heartworms to the pulmonary hypertension, although there is a complicated interaction among the presence of heartworms, the pulmonary lesions and the pulmonary hypertension.

Animals↗

Localization of immunoglobulins in the chicken oviduct.

Studies were made on the distribution of lymphoid tissues and immunoglobulin (Ig: IgA, IgG and IgM)-containing cells (cIg: cIgA, cIgG and cIgM) and the localization of immunoglobulins (Igs) in the oviducal walls of laying hens. Lymphocyte accumulations were occasionally observed, located mainly in the middle infundibulum and in the regions from the isthmus to the vagina. The number of cIgG significantly predominated over that of cIgA or cIgM in the mucosal connective tissue of the magnum and the isthmus. In contrast, in the regions other than the magnum and the isthmus, these three types of cIg were fewer in number. Igs were localized in some superficial epithelial cells (SECs) and glandular cells (GlCs) of the oviduct. Many IgG-containing SECs were found in the infundibulum, the isthmus, and the cranial and major uterus. IgA- or IgM-containing SECs were rare throughout the oviduct. Three types of Ig-containing GlCs were numerously found in the magnum, though lymphocyte accumulations were scarce there. In the isthmus, many IgG-containing GlCs were found, while IgA- or IgM-containing GlCs were rarely observed. Ig-containing GlCs in the magnum were considerably decreased in number after the egg passage. The results suggest that the maternal Igs are transferred to the egg mainly through GlCs in the magnum of the chicken oviduct, and that the oviducal lymphoid tissues have little relationship to the passive immunity.

Animals↗

The development of the pecten oculi in the chick.

The development of the pecten oculi, a structure peculiar to the avian eye, was studied by scanning electron microscopy (SEM) correlated with light microscopy (LM) in embryonic and adult chickens. The development of the chick pecten was divided into 4 phases: (1) formation of the primordial pecten (Hamburger-Hamilton's stages 27 to 29), (2) formation of the plate-like pecten (stages 30 to 34), (3) pleat formation and pigmentation (stages 35 to 37), and (4) bridge formation and high-vascularization (stage 38 to adult). The primordial pecten is formed entirely from the ectoderm by fusion of the inwardly-projecting edges of the optic fissure. The primordial pecten grows into a tall, thin plate rising from a broad base. The pecten begins to fold slightly at stage 35. The number of pleats increases rapidly, from 7 at stage 35, to 16 at stage 36, 18 at stage 37, and 19 to 20 at stage 40. The bridge begins to form at stage 38 by a swelling of the apical edge of the pecten and completes its development by the twentieth post-hatch day. Blood vessels appear first in the broad base of the plate-like pecten, then become more numerous and gradually extend into the pleats. The pecten becomes more vascular than cellular at stage 43, and it is highly vascularized in the adult. The pleat surface becomes conspicuously irregular with increased vascularization. The peripectinate cells, located on the pecten, are already present at stage 27.

Animals↗