Biomedical subjects

Y Hoshikawa

Publications and source records attributed to Y Hoshikawa.

At least 55 records · Page 3Linked to original sources

PubMed1995

[Effect of adhesiveness of white blood cells on pulmonary vascular permeability and resistance].

We studied pulmonary vascular injury evoked by mechanically activated white blood cells (WBCs). In isolated perfused rat lungs, changes in pulmonary vascular resistance were measured, and a gravimetric method was used to measure the pulmonary vascular filtration coefficient, which was taken as an index of pulmonary vascular injury. WBCs were activated by gentle agitation in a glass container for 10 sec. The filtration coefficient was measured under baseline conditions, and then inactive or activated WBCs were added to the perfusate. The perfusion was stopped for 90 minutes and then the lungs were reperfused. The expression of CD18 on the surface of WBCs was measured by flow cytometry. The filtration coefficient and the pulmonary vascular resistance in lungs exposed to activated WBCs were about 2.5 times and 3.3 times higher, respectively, than those in the lungs exposed to inactive WBCs. These results indicate increases in resistance and in pulmonary vascular permeability. The results of flow cytometry indicated that the mechanical agitation increased the expression of CD18 on the surface of WBCs. In conclusion, WBCs in which adhesiveness has been increased can induce pulmonary vascular injury and can increase pulmonary vascular resistance.

Animals↗

PubMed1995

[Neutrophil elastase in postoperative pleural effusion of patients who had undergone pulmonary resections].

We determined whether activity of neutrophil elastase increases in pleural effusion after lobectomy for the neoplasm in the lung. Samples of pleural effusion were obtained 3 and 24 h postoperatively and samples of the peripheral blood were obtained preoperatively, 3 h, 24 h, and 1 w postoperatively, then the neutrophil counts, the levels of neutrophil elastase and alpha 1-antitrypsin by enzyme-linked immunosorbent assay, the activity of neutrophil elastase using succinyl-(L-alanine) 3-p-nitroanilide were measured. We found that the levels of neutrophil elastase increased 170 times greater in pleural effusion than in peripheral blood 3 h after lobectomy. However, the levels of alpha 1-antitrypsin did not increase in pleural effusion. The activity of neutrophil elastase increased to 0.54 +/- 0.1 mumol/min/l in pleural effusion 3 h after lobectomy, however the activity of neutrophil elastase was under the sensitivity level of detection in the peripheral blood after lobectomy. In conclusion, there is an imbalance between the levels of neutrophil elastase and alpha 1-antitrypsin in pleural effusion after lobectomy, the imbalance resulting in the increased activity of neutrophil elastase which probably is relating to tissue injury in the pleural spaces.

Aged↗

PubMed1995

[Hydraulic conductivity of the visceral pleura with hemodynamic lung edema in dogs].

Hydraulic conductivity of the visceral pleura was measured in situ in anesthetized dogs. There were two groups: control (n = 7), and edema (n = 5). The 7th intercostal space of the left thorax was opened. In each group, a hemispherical capsule, filled with physiological salt solution, was attached to the visceral pleura of left lobe by negative pressure made with a vacuum pump. In the edema group, pulmonary venous pressure was increased by ligation of the pulmonary vein. The transpleural fluid flow (V) was measured at different intracapsular pressures (delta P). The hydraulic conductivity was calculated from the relation between the fluid flow rate (v) and the intracapsular pressure, i.e., the slope of the linear regression line. The hydraulic conductivities in the control and edema groups were 1.49 +/- 0.68 and 3.19 +/- 1.13 nL.min-1.cmH2O-1.cm-2, respectively. We conclude that the pleural tissue may play an important role in hydraulic conductivity of the visceral pleura when pulmonary venous pressure is high.

Animals↗

PubMed1995

[Vasoactive intestinal peptide (VIP)-induced pulmonary vasodilation mediated by EDRF/NO in isolated perfused rat lungs].

We studied the effects of Vasoactive Intestinal Peptide (VIP) on the pulmonary circulation in isolated perfused rat lungs. VIP caused pulmonary vasodilation in a dose-dependent manner. This effect was inhibited by pretreatment with L-N omega-nitro-arginine (L-NNA), a competitive inhibitor of endothelium-derived relaxing factor (EDRF/NO), but not by meclofenamate, a cyclooxygenase inhibitor. Addition of L-arginine, a substrate of EDRF/NO, after treatment with L-NNA reversed VIP-induced pulmonary vasodilation. These results indicate that VIP causes pulmonary vasodilation, and they suggest a role for EDRF/NO in VIP-induced pulmonary vasodilation in isolated rat lungs.

Animals↗

PubMed1995

[Surgical treatment of lung cancer over 80 years of age: investigation from post operative complications].

Seventeen patients with lung cancer over 80 years were treated surgically from 1983 through 1993 in our department. Thirteen patients were male and four were female. The histology of the tumor was adenocarcinomas, squamous, large and small cell carcinomas, in 9, 6, 1 and 1 cases, respectively. More than single lobectomy was performed in each patient. Unilateral pulmonary occlusion test was applied in patients whose expected contralateral FEV1.0/BSA was less than 800 ml.m2, or expected residual FEV1.0/BSA was less than 850 ml.m-2. Postoperative cardiovascular complications, such as PAT, PAC, PVC or Af, were seen in 9 patients, respiratory problems, namely, sputa retention, retained secretions or atelectasis, in 7 patients. Blood chemistry and hematology were performed for about three weeks after operations, and found increases in serum transaminases, and leukocytosis. However, there were no operative death. We conclude that some patients over 80 years of age are candidates for surgery after careful cardiopulmonary preoperative evaluation.

Adenocarcinoma↗

PubMed1995

[Role of cyclooxygenase metabolites in the increase in pulmonary vascular permeability caused by mechanically activated white blood cells].

To study the role of cyclooxygenase metabolites in changes in the pulmonary vasculature induced by mechanically activated white blood cells (WBCs), the effects of activated and inactive WBCs, and of a cyclooxygenase inhibitor, were studied in isolated perfused lungs from Sprague-Dawley rats. WBCs were activated by gentle agitation in a glass container for 10s. Baseline measurements were made, and then activated or inactive WBCs were added to the perfusate. Perfusion was stopped for 90 minutes, and then started again. The effects of the cyclooxygenase inhibitor meclofenamate on the pulmonary vascular filtration coefficient and on pulmonary vascular resistance were also measured. In the group that received activated WBCs, the pulmonary vascular filtration coefficient and the pulmonary vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the group that received inactive WBCs. However, this apparent increase in the filtration coefficient caused by activated WBCs was partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of WBCs to the pulmonary vascular endothelium. These date indicate that WBCs that have been made to adhere to vessel walls can induce pulmonary vascular injury via cyclooxygenase products.

Animals↗

PubMed1995

[Contribution of oxidative stress to pulmonary hypertension induced by chronic hypoxia].

Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with media wall thickening of pulmonary arteries in rats. Platelet-activating factor plays an important role in the pulmonary vascular remodeling induced by chronic hypoxia, and reactive oxygen species are involved in tissue injury induced by platelet activating factor. We therefore hypothesized that reactive oxygen species contribute to the pulmonary hypertension induced by chronic hypoxia, and examined the effect of N-acetyl-L-cysteine (NAC), a free radical scavenger and the precursor of glutathione sulfhydryl (GSH), on hypoxia-induced pulmonary hypertension. We used a chemiluminescence-HPLC assay to measure the levels of phosphatidylcholine hydroperoxide (PCOOH) in the rat lungs exposed to hypoxia. Three weeks of normobaric hypoxia (FiO2 = 0.1) with NAC significantly reduced pulmonary hypertension, right ventricular hypertrophy, and media wall thickening of the pulmonary arteries. NAC had no effect on the hematocrit of normoxic or chronically normobaric hypoxic rats. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. Lung PCOOH levels were significantly higher in the hypoxic rats than in the control rats, and those in the NAC-treated rats were significantly lower than those in the hypoxic rats that were not given NAC. These results indicate that hypoxia induces oxidative stress in the lung tissue, and that oxidative stress may have a role in the development of pulmonary hypertension induced by chronic hypoxia in rats.

Acetylcysteine↗

PubMed1995

[Role of peptide leukotrienes in monocrotaline-induced lung disease].

Monocrotaline (MCT) causes lung inflammation and right ventricular hypertrophy associated with lung vascular thickening in rats. We hypothesized that peptide leukotrienes play a role in MCT-induced lung disease, and examined the effect of ONO 1078, a specific antagonist of LTC4, D4 and E4 receptors on MCT-induced right ventricular hypertrophy and on lung vascular thickening. Next, we measured leukotriene C4 (LTC4) levels in the lung tissue of MCT-treated rats. Within 3 weeks after the injection MCT had caused an increase in the ratio of right ventricular weight to left ventricle+septum weight (RV/(LV+S)) and an increase in media wall thickness of the muscular arteries of the lung. In rats given both ONO 1078 and MCT, these changes were significantly less severe than in rats given MCT only. The LTC4 levels in MCT-treated rats were significantly higher than in saline-treated control rats. These results indicate that this antagonist of peptide leukotriene receptors inhibits right ventricular hypertrophy induced by MCT, and suggest a role for peptide leukotrienes in the inflammatory process that contributes to lung vascular remodeling in MCT-treated rats.

Animals↗

PubMed1994

Trichostatin A induces morphological changes and gelsolin expression by inhibiting histone deacetylase in human carcinoma cell lines.

Trichostatin A (TSA) is a Streptomyces metabolite which specifically inhibits mammalian histone deacetylase at a nanomolar concentration and causes accumulation of highly acetylated histone molecules in mammalian cells. The effects of TSA on the morphology and the cell cycle of the human carcinoma cell lines, T24 and HeLa, were investigated. The morphology of T24 and HeLa cells dramatically changed and actin stress fibers reappeared during the treatment with TSA. The morphological change was not observed with chemically synthesized (S)-TSA and trichostatic acids, which are inactive to inhibit histone deacetylase. Cell cycle progression of these cells was blocked by TSA at G1 phase (HeLa) or G1 and G2 phases (T24). An RNA synthesis inhibitor, actinomycin D, and a protein synthesis inhibitor, cycloheximide, inhibited the morphological changes by TSA, suggesting that TSA induces expression of a new gene(s) followed by de novo protein synthesis, which is required for the actin microfilament reorganization. An approximately 7-fold (T24) or 12-fold (HeLa) increase in the intracellular level of gelsolin, an actin regulatory protein, was found in the cells treated with TSA for 24 h. These results suggest that gelsolin is one of the putative proteins necessary for the morphological changes of human carcinoma cells induced by TSA.

Actins↗

PubMed1994

The granulocyte colony-stimulating factor produced in the human lung and its effect on liquid movement in the rabbit lung.

Levels of the granulocyte colony-stimulating factor (G-CSF) were determined in the plasma and resected lung tissue from patients who underwent pulmonary resection. Moreover, the effect of recombinant human (rh) G-CSF on the permeability of pulmonary endothelium and on liquid clearance from the alveolar spaces was investigated in rabbits. The plasma levels of G-CSF increased from 30 pg/ml preoperatively to 409 +/- 236 pg/ml 3 h postoperatively (P < 0.05), while the levels of G-CSF in the resected lung tissue were increased in the alveolar fluid, to 1,834 +/- 1,054 pg/ml, and in the pulmonary blood, to 5,466 +/- 2,019 pg/ml. It was found that rh G-CSF 25 micrograms administered into the subcutaneous tissue of rabbits increased extravascular lung water to 3.45 +/- 0.26 vs 2.98 +/- 0.20 in control experiments (P < 0.05); however, rhG-CSF 0.75 microgram/kg administered into the alveolar spaces did not affect liquid clearance from the alveolar spaces. The findings of this study led us to conclude that G-CSF is synthesized in the human lung and increases the permeability of pulmonary endothelium, but not liquid clearance across the alveolar epithelium.

Animals↗

PubMed1994

[Effect of amurinone on human pulmonary artery in vitro].

We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 microM), a cyclooxygenase inhibitor, or L-NG-nitroarginine (100 microM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

Adult↗

PubMed1994

[Lung 3H-thymidine incorporation in monocrotaline (MCT)-treated rats--role of platelet-activating factor (PAF)].

Monocrotaline (MCT) causes chronic pulmonary hypertension associated with pulmonary vascular thickening in rats. Since components of the pulmonary vascular thickening are reflected in increased DNA synthesis in medial smooth muscle cells, and since platelet-activating factor (PAF) has been reported to contribute to the pulmonary hypertension induced by MCT, we examined the effect of WEB 2170, a specific PAF receptor blocker, on MCT-induced pulmonary vascular thickening and in vitro 3H-thymidine incorporation into lung tissue, as an index of stimulation of cell proliferation. In MCT-treated rats, pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular thickening developed at 3 weeks after injection. Also, in MCT-treated rat lung tissue, there was a significant increase in the in vitro 3H-thymidine incorporation rate. In WEB 2170-treated MCT rats, these changes were significantly less severe than those observed in rats receiving MCT alone. We conclude that PAF plays a role in the inflammatory process that contributes to the development of pulmonary hypertension and vascular remodeling associated with increased lung cell proliferation in MCT-treated rats.

Animals↗

PubMed1994

[A case of lung cancer combined with ocular myopathy and idiopathic thrombocytopenic purpura which was presumed to be caused by heart catheterization].

A 61-year-old patient was admitted to our hospital because of a chest abnormal shadow. He was suffered from ocular myopathy for more than 4 years. A lab data on the admission showed only a slight thrombocytopenia. After the unilateral pulmonary arterial occlusion test for the preoperative evaluation of thoracotomy, the hemorrhagic tendency was appeared. A detailed examination proved idiopathic thrombocytopenic purpura which was presumed to be caused by the heart catheterization. We employed high-dose intravenous gamma-globulin infusion and concentrated platelet transfusion for 5 days for preventing hemorrhagic complications during the thoracotomy. The partial resection was undergone for the left upper lobe tumor, which was proved as large cell carcinoma. The postoperative hemorrhage was well controlled. We conclude that the high-dose intravenous gamma-globulin infusion and/or concentrated platelets transfusion should be positively employed for the patients with even slight thrombocytopenic purpura.

Carcinoma, Non-Small-Cell Lung↗

PubMed1993

[Biliary lithotripsy using super fine cholangioscopy with the deviced bended sheath].

Percutaneous transhepatic cholangioscopy (PTCS) is an useful technique to evaluate or treat biliary diseases, although PTCS is an invasive method for the patients. We used 5 F or 7 F of super fine cholangioscopy to treat two cases of choledocholithiasis after surgery without dilatation of drainage tract. We developed different types of bended sheath for supplement of lack of angle system in this cholangioscope. Furthermore, by using bended sheath, cholangioscopic view improved, because saline was injected at the same time via the sheath. We emphasize that super fine cholangioscope with bended sheath is a safe and useful modality for evaluation of biliary disease.

Adult↗

PubMed1993

[Changes in right ventricular hemodynamic function by unilateral pulmonary arterial occlusion test].

We performed unilateral pulmonary arterial occlusion test (UPAO) for the preoperative evaluation of lung function in patients undergoing lung resection. In this test, the main pulmonary artery of either side is occluded to simulate postoperative functional status. In order to evaluate the right ventricular hemodynamic function, we measured right ventricular ejection fraction (RVEF) and right ventricular end-diastolic volume index (RVEDVI) throughout UPAO by thermodilution method. We investigated the relationships between changes in right ventricular hemodynamic function and postoperative complications related to cardiac functions, namely arrhythmias or heart failure. Thirty-four patients without heart disease prior to lung resection were examined by UPAO, and RVEF and RVEDVI were measured. Analyses demonstrated that changes in RVEF were inversely correlated with changes in RVEDVI. In 6 cases, RVEDVI increased from control by over 20% during UPAO. All of these patients had postoperative cardiac complications. The hypothetical ventricular function curves showed a large increase in RVEDVI relative to right ventricular stroke work index (RVSWI), suggesting a decrease in right ventricular function. In conclusion, these results suggest that changes in RVEDVI during UPAO may predict postoperative cardiac complications in patients undergoing pulmonary resection.

Adult↗

PubMed1992

[CT of intestinal injuries following blunt trauma].

We retrospectively reviewed 53 CT scans in 42 patients with surgically proven intestinal injury following blunt abdominal trauma. Free air and localized low density fluid were specific signs of intestinal injury. Free peritoneal fluid without a known source, thickened bowel wall, and thickened mesentery were non-specific ones. Specific and non-specific findings were demonstrated in six (22%) and 23 (85%) of 27 CT scans performed within four hours following trauma, and 19 (73%) and 26 (100%) of 26 CT scans performed after four hours, respectively. CT is useful for the diagnosis of blunt intestinal injuries, but early diagnosis is difficult because of the lack of specific signs.

Abdominal Injuries↗

PubMed1992

[MR imaging of corpus callosal injuries].

The MR imaging and CT findings of corpus callosal injury were analyzed in 32 of 224 patients with acute head injuries. MR imaging was more sensitive than CT in the detection of callosal injuries. All 9 hemorrhagic lesions were visualized on both MR imaging and CT. Fifteen of 23 nonhemorrhagic lesions were not visualized on CT, although all nonhemorrhagic lesions were visualized on MR imaging. Twenty-four lesions of the corpus callosum were located in the splenium, but no lesion was located in the rostrum. Diffuse axonal shear injuries were visualized in 25 patients with callosal injury as associated traumatic lesions. Twenty-three patients with callosal injury had low initial Glasgow Coma Scale scores (less than 9), but 9 patients had high scores. Associated diffuse axonal shear injuries, especially in the brain stem could be a possible explanation for this difference. MR imaging is useful to detect traumatic lesions of the corpus callosum.

Accidents, Traffic↗

PubMed1992

Idiopathic acro-osteolysis in an elderly woman. A 10-year follow-up.

We report a case of idiopathic acro-osteolysis in an 80-year-old, otherwise normal woman. The patient first presented at the age of 70 years with a 3-year history of progressive shortening of the left toes. There was no history of trauma or bone disorders. She had osteolysis of the left second to fourth distal phalanges. Angiography was normal. During follow-up over 10 years the osteolysis gradually progressed and spread to affect the right toes.

Age Factors↗