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Biomedical subjects

Y Ashino

Publications and source records attributed to Y Ashino.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Prediction of postoperative pulmonary hemodynamics for the second lobectomy after the contralateral lobectomy].

We presented 7 cases who were performed the second lobectomy for the second lung cancer after the first successful lobectomy on the contralateral lung (3 cases for right upper lobectomy + left lower lobectomy and 4 cases for right upper lobectomy + left lower lobectomy). In 6 patients, the predicted postoperative FEV1 estimated by multiplying the preoperative FEV1 by the fraction of perfusion to the contralateral lung was less than 800 ml/m2BSA, which is our first cut-off for identifying lung resection candidates. Unilateral pulmonary arterial occlusion test (UPAO) revealed that total pulmonary vascular resistance (TPVRI) in 3 of those 6 patients was lower than 700 dyne.sec.cm-5/m2BSA, our second cut-off for lung resection. More precise postlobectomy pulmonary hemodynamics in another 3 of those 6 patients were then estimated by adapting selective pulmonary occlusion test (SPAO). Since TPVRI during SPAO was lower than the cut-off value, it was suggested that second lobectomy would be feasible with low incidence of post operative cardiopulmonary complication. There was no serious complications in all 7 cases during their postoperative course. We believe that more precise prediction of postoperative pulmonary hemodynamics by adapting UPAO and SPAO could be one of the tools to minimumize postoperative cardiopulmonary complications in those patients needed second lobectomy for the second lung cancer after the first successful lobectomy on the contralateral lung even though their impaired lung fung function.

Aged↗
PubMed1997

[Ten years experience of home parenteral nutrition or hydration in advanced cancer patients].

From April 1987 to May 1997, ninety-six advanced cancer patients including ninety-one among 159 home care patients and five outpatients were administered parenteral nutrition or hydration. Eventually, 67 patients died at home. We concluded through our experience that advanced cancer patients who were unable to eat or drink might live at home with the support of parenteral nutrition or hydration. But four conditions are needed for satisfactory home care of these patients. First, patients understanding their disease condition therefore together with their family hope for home care. Second, the home care support team is organized in an institution. Third, the home care support team is on call for emergencies. Fourth, the home care support team can not only manage home parenteral nutrition but also provide palliative care, including pain control.

Adult↗
PubMed1996

[Trial of home anti-cancer chemotherapy with infusion of 5-FU and low-dose cisplatin].

We tried home anti-cancer chemotherapy for patients with advanced or recurrent cancer of the digestive system, using two disposable balloon pumps connected to an implantable drug delivery system via central venous line. There were 33 patients under 75 years old, including 20 cases of gastric cancer, 9 cases of colorectal cancer, 2 cases of cholangiocarcinoma and 2 cases of esophageal cancer enrolled in this study. The protocol was combined chemotherapy with continuous intravenous infusion of 5-FU (300 mg/body/day) and low-dose intravenous injection of cisplatin (5 mg/body/day) in 10-day courses for two weeks, and it was repeated 3 times for 6 weeks. Because of side effects such as nausea, vomiting and bone marrow suppression, treatment was discontinued in 12 cases with peritoneal cancer infiltration. In two of 10 with estimable disease, the reduction of the metastatic lymph node was observed, but no effect was shown in the colorectal metastatic liver tumor. Thanks to the portability of the pump with this method, the patient need not undergo hospitalization. Moreover, there is no renal dysfunction or other major side effects, quality of life is not compromised and a return to family and social life is possible. Thus, if the patient cannot take the oral nutrition, it is easy to start home hyper-alimentation.

Aged↗
PubMed1996

[How to palliate the symptoms of terminally ill patients at home].

We reported the kind of symptoms and how they could be palliated in terminally ill patients at home based on our experience of about 9 years. Cancer pain, which was the most frequent symptom, appeared in 67 among 126 patients receiving home care, and it could be effectively controlled with morphine; no patient returned to the hospital because of aggravation of pain. Very few patients stayed in the hospital and never returned home due to uncontrollable pain. Home parenteral infusion was done for 63 patients who were unable to eat or drink because of peritonitis carcinomatosa or cancer cachexia. High fever in the tumor mass was controlled by glucocorticoid hormone, and ascites was drained continuously when the patients suffered from abdominal distension. From analysis of the cases in which home care was interrupted or those in which patients were unable to transfer to home care, symptoms that were difficult to palliate at home were nausea caused by bowel obstruction, acute symptoms (bleeding, disturbance of consciousness, and so on), and dyspnea. But if the patients and family are eager for home care and an adequate medical support system is in place, home care may be possible despite these symptoms.

Hospice Care↗
PubMed1995

[Effects of prostaglandin E1 (PGE1) on pulmonary hypertension and lung vascular remodeling in a rat monocrotaline model of human pulmonary hypertension].

Prostaglandin E1 (PGE1) has been shown to be a potent pulmonary vasodilator in humans and in many animals. The effects of PGE1 on the development of pulmonary hypertension and on pulmonary vascular remodeling were studied in a rat monocrotaline (MCT) model of human pulmonary hypertension. By 3 weeks after injection, MCT (80 mg/kg S.C.) had resulted in high values of mean pulmonary arterial pressure and of the ratio of right ventricular weight to left ventricle+septum weight (RV/LV+S). PGE1 inhibited the development of pulmonary hypertension (300 micrograms/kg) and right ventricular hypertrophy (300 and 100 micrograms/kg) induced by MCT. Three weeks after the injection, the media walls of pulmonary arteries in lungs from rats given MCT were significantly thicker than those from lungs of control rats. PGE1 (300, 100, and 30 micrograms/kg) resulted in significantly less of this morphologic change, in a dose-dependent manner. These results indicate that PGE1 inhibits the development of pulmonary hypertension associated with lung vascular thickening induced by MCT. PGE1 may be useful for the treatment of pulmonary hypertension in humans.

Alprostadil↗
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

[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

[A true aneurysm of the right internal mammary artery, accompanied by diminished grasping power of the right hand].

A 69-year-old man was admitted to our hospital after an abnormal shadow was found on a chest radiograph. The preoperative diagnosis was right subclavian aneurysm. Loss of grip in the right hand developed, and the patient underwent surgery. During surgery, the aneurysm was found to have originated from the right internal mammary artery. The root of the right internal mammary artery was tied and the right subclavian artery, which had been compressed and displaced by the aneurysm, was replaced. A chest radiograph obtained 6 months after surgery showed that the trachea was no longer displaced. However, the gripping force of the right hand had not recovered.

Aged↗
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↗
PubMed1995

[Four important subjects of successful care at home for patients of terminally ill].

From April 1987 to May 1995, we have had care at home for 103 patients of terminally ill, and at this through our experience, we pointed out four important subjects for successful care at home. The first is prompt consultation at anytime when the patient or its family need. It is especially important when the patient's end time is near and previously we must fully instruct to patient's family how to consult and how to care. The second is effective palliative care. In these palliative care pain control with morphine is most important and we must master how to use morphine. The third is truth telling and informed consent. At treatment we have to communicate true information to patient. Home care must be started under patient's will. The fourth is organization of medical care, health care and welfare care. We have to make up network system of these office at first, and finally we have to make up community for supporting patients and these family.

Attitude to Death↗
PubMed1994

[The importance of pain control with morphine for terminally ill patient care for at home].

From April 1987 to June 1994, 81 patients of terminally ill had been care at home. In these home care, 38 patients received pain control with morphine. In 29 patients, pain control had been started before home care but in 9 patients pain control had been started under home care. Routes of morphine administration were oral in 24 cases and rectal in 14 cases. In cases of oral routes, finally 2 cases converted to rectal routes and 2 cases converted to subcutaneous routes. Duration of treatment were from 2 days to 741 days (average 72 days). Dosage of morphine were 7.5 mg to 480 mg (average 116 mg). Two patients lived but 24 patients died at home and 12 patients died at hospital. We concluded that palliative care especially pain control with morphine was very important care for patients of terminally ill who wanted care at home and ultimately die at home. We had to make ourself master of method pain control with morphine.

Administration, Oral↗
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↗