[Inhalational nitric oxide therapy for pulmonary hypertension].
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Biomedical subjects
Publications and source records attributed to K Hisano.
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We have treated a case of chronic fatigue syndrome with atopic diathesis was had suffered general malaise, low grade fever, swelling of the lymph nodes, myalgias and arthralgias for a long time. A 29-year-old female, who had been treated for atopic dermatitis for 5 years, complained of general malaise in May 1990. She was admitted to the nearest hospital in December 1990 because of low grade fever, swelling of the lymph nodes and an elevation of antinuclear antibody (2520x). She was transferred to our hospital in May 1991. A diagnosis of collagen disease was not compatible with her condition. In addition to general malaise, fever and lymph node swelling, headache, myalgias, muscle weakness, arthralgias and insomnia were observed, and a diagnosis of chronic fatigue syndrome was made based on the working case definition proposed by Holmes et al. Although eosinophilia, a high serum level of IgE, and elevation of RAST scores, low NK and ADCC activity, and a reduced level of NK cells in the peripheral blood were detected, serum antibodies to a number of viruses were in the normal range. Treatments with non-steroid anti-inflammatory drugs, minor tranquilizers and antidepressant drugs were not effective at all. An administration of magnesium sulphate was intravenously performed once a week in order to improve her condition, especially severe general malaise. After about 6-week's administration of magnesium sulphate, she noticed reduced easy fatigability and an improvement in her impaired daily activities. Finally she was able to leave the hospital in January 1992.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of i.v. administered isosorbide dinitrate (ISDN) on the reduced level of regional myocardial function during coronary occlusion were studied in conscious dogs before and after collateral development and in the absence of persistent coronary stenosis. The animals were instrumented during sterile surgery with a miniature pressure gauge for measuring left ventricular pressure and a cannula for aortic pressure. Two pairs of piezoelectric crystals were placed in normal and ischemic areas to determine regional circumferential length. A hydraulic cuff occluder and a Doppler flow probe were placed around the left circumflex coronary artery. Collaterals were induced to develop by 2 min of coronary occlusion applied repetitively at an interval of 32 min for 2 to 9 days, until the regional dysfunction produced by coronary occlusion had disappeared. Collateral development was estimated according to percentage of systolic shortening and endsystolic length area (ESL area) during the occlusion. Before collateral development, ISDN in a dose of 100 micrograms/kg did not affect the level of regional dysfunction. The ESL area was 250 +/- 54 and 248 +/- 52 mm.sec before and after ISDN, respectively. After collateral development, the ESL area was 51 +/- 13 mm.sec and it decreased by 35% after the i.v. administration of ISDN. The improvement by ISDN of transient myocardial dysfunction was achieved even during electrical tachypacing. Accordingly, the beneficial effects of ISDN on regional wall motion rendered ischemic during transient coronary occlusion were appreciable after coronary collateral development.
Simple method of venoarterial (V-A) bypass was developed for neonatal ECMO. Technical aspects in the management of our device was shown in this report. The most important technique was to keep the flow of ECMO less than 60-80 ml/min/kg. The low flow circulation less than 80 ml/min/kg made puppies alive under apnea experimentally. Clinically we experienced four newborn cases. All cases had severe respiratory failure with AaDO2 above 580 mmHg due to congenital diaphragmatic hernia. Two cases of them were able to survive. Other two cases died from intracranial hemorrhage during ECMO. The oxygenation of all cases was satisfactory under relative low flows. Our simple ECMO circuit was not only easy to operate but also to give less damage to blood.
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The effects of two types of repeated transient coronary artery occlusions on collateral development were examined in chronically instrumented, conscious dogs. A 2-minute coronary occlusion at 32-minute intervals (group 1, n = 11) or a 15-second occlusion at 4-minute intervals (group 2, n = 7) were repeated day and night without interruption. In both groups, the total duration of coronary occlusions each day was the same (90 minutes). Before and after repetitive occlusions of either group, effects of transient 2-minute coronary occlusion on regional segment shortening in the ischemic area were examined to assess the functional state of the collateral vessels. In group 1, systolic segment shortening in the area rendered ischemic was reduced to -97.8 +/- 17.7% of the preocclusive control value during 2 minutes of coronary occlusion. After 125-478 repetitive occlusions (3-11 days), the degree of hypokinesia during the 2-minute occlusion was significantly improved to -0.6 +/- 4.6% of the preocclusive value (p less than 0.001 vs. before the repetition). In group 2, it remained unchanged even after 3,500-5,450 repetitive occlusions (11-16 days): -111.8 +/- 8.2% before and -111.4 +/- 13.8% after the repetition of 15-second occlusions (NS). The ratio of peripheral coronary arterial pressure to aortic pressure during transient-coronary occlusion, measured by selective catheterization, was significantly higher in group 1 than in group 2 (64.4 +/- 5.3% vs. 20.7 +/- 1.3%, p less than 0.001). These findings suggest that myocardial ischemia of 2 minutes but not 15 seconds is vital to provide effective stimuli for angiogenesis.
The effects of i.v. administered isosorbide dinitrate (ISDN) on the reduced level of regional myocardial function during coronary occlusion were studied in conscious dogs before and after collateral development and in the absence of persistent coronary stenosis. The animals were instrumented during sterile surgery with a miniature pressure gauge for measuring left ventricular pressure and a cannula for aortic pressure. Two pairs of piezoelectric crystals were placed in normal and ischemic areas to determine regional circumferential length. A hydraulic cuff occluder and a Doppler flow probe were placed around the left circumflex coronary artery. Collaterals were induced to develop by 2 min of coronary occlusion applied repetitively at an interval of 32 min for 2 to 9 days, until the regional dysfunction produced by coronary occlusion had disappeared. Collateral development was estimated according to percentage of systolic shortening and endsystolic length area (ESL area) during the occlusion. Before collateral development, ISDN in a dose of 100 micrograms/kg did not affect the level of regional dysfunction. The ESL area was 250 +/- 54 and 248 +/- 52 mm.sec before and after ISDN, respectively. After collateral development, the ESL area was 51 +/- 13 mm.sec and it decreased by 35% after the i.v. administration of ISDN. The improvement by ISDN of transient myocardial dysfunction was achieved even during electrical tachypacing. Accordingly, the beneficial effects of ISDN on regional wall motion rendered ischemic during transient coronary occlusion were appreciable after coronary collateral development.
Sixty-seven patients subjected to this study composed of 32 patients treated surgically, 15 patients treated medically and 20 patients examined by autopsy for the past 8 years. Out of 32 surgical cases, 16 were operated on in an acute stage, within 2 weeks after onset and 9 out of these 16 acute cases belonged to DeBakey type I or II and 11 out of 15 autopsy cases belonged to type I or II either. Contrarily most of the medical cases were type III. Both causes of death in the acute autopsy group and operative indications in the acute surgical group were cardiac tamponade, heart failure due to aortic insufficiency, myocardial infarction and aortic rupture. Operative mortality rate was 12.5% in the acute cases and 19% in the chronic cases, late mortality rate was 19% in the acute cases and 0% in the chronic cases. Two cases of operative death had massive bleeding due to aortic rupture and massive myocardial infarction. These were the most dangerous complications of acute aortic dissections. We conclude that all patients with type I or II dissections should be operated on before fatal complications occur.
The mechanisms of epicardial coronary artery dilation after reactive hyperemia were studied in instrumented conscious dogs. A pair of ultrasonic crystals, an electromagnetic flow probe and a cuff occluder were placed on the left circumflex coronary artery in 12 mongrel dogs under sterile conditions. Reactive hyperemia after 20 s of coronary occlusion dilated the epicardial coronary artery by 120 +/- 14 micron (3.8 +/- 0.6%, p less than 0.01) from 3.167 +/- 0.345 mm. This reactive dilation was abolished by flow-limiting coronary stenosis. However, vasodilation after nitroglycerin was 168 +/- 26 micron (5.1 +/- 0.5%) and 162 +/- 27 micron (4.9 +/- 0.6%), respectively, before and after flow limitation. After removal of the endothelium by a balloon catheter, dilation of the epicardial coronary artery after reactive hyperemia was markedly attenuated to 7 +/- 4 micron (p less than 0.01 versus before denudation), despite the presence of a similar degree of reactive hyperemia. The extent of coronary dilation after nitroglycerin was unchanged before and after de-endothelialization. Thus, the endothelium contributed to reactive dilation but not to the nitroglycerin-induced dilation. The negative feedback control of coronary diameter to changes in flow velocity may relate to the regulation of coronary artery tone.
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The effects of glyceryl trinitrate and dipyridamole on induced ischaemia were studied in awake dogs during transient coronary occlusion before and after collateral development. Seventeen dogs were instrumented under sterile conditions with a miniature pressure gauge to measure left ventricular pressure, a cannula for aortic pressure, and pairs of piezoelectric crystals towards the subendocardium of the left ventricle for regional segment length measurements. A hydraulic cuff occluder and Doppler flow probe were placed around the left circumflex coronary artery. Collateral function was increased by repeated 2 min coronary occlusions at 32 min intervals for 2-9 days until regional wall motion returned to preocclusive values, despite the persistence of coronary occlusion. The effects of glyceryl trinitrate and dipyridamole were studied after the initial haemodynamic changes had subsided. Collateral function was quantified by integrating changes in end systolic length of the ischaemic area during coronary occlusion. Before collateral development the end systolic length area was 29.4(2.4) cm X s and was unchanged by glyceryl trinitrate or dipyridamole. After the development of collaterals the end systolic length area decreased from 4.1(1.1) to 2.2(1.0) cm X s (p less than 0.01) after glyceryl trinitrate and increased to 14.9(1.7) cm X s (p less than 0.01) after dipyridamole. Therefore, glyceryl trinitrate acted directly on collaterals and improved the induced ischaemia, whereas dipyridamole exaggerated the regional wall motion abnormality.
The study reviews 18 infants and children with eventration of the diaphragm who were treated over a period of eight years. The affected diaphragm and pulmonary tissue were examined by light and electron microscopy. The 18 patients, ranging in age from 10 days to 6 years, were divided according to Thomas' classification into a group with the congenital (10 patients) and a group with the acquired type (8 patients). Fifteen of these patients underwent surgery with diaphragmatic plication. On microscopic examination, biopsies of the lung showed atelectasis and pneumonia. These pathological changes became increasingly diffuse and severe with age. The diaphragm in patients with the congenital type of eventration was occupied by diffuse fibroelastic tissue. In patients with the acquired type, the cross-striated muscles of the diaphragm showed degenerative changes such as fragmentation, and interstitial fibrosis of the diaphragm became prominent with age. The results of this clinical study suggest that, in order to reduce the pathological changes in the lung, early surgical plication should be performed even in patients with the acquired type, if respiratory and digestive symptoms are noted.
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Coronary blood flow and epicardial coronary artery diameter were simultaneously measured by an electromagnetic or Doppler flow probe and a pair of ultrasonic crystals, respectively, during reactive hyperemia in conscious dogs. Reactive dilation appeared after the full appearance of reactive hyperemia and lasted for a period of 4-20 times the duration of the coronary occlusion. beta-Receptor blockade (propranolol, 1 mg/kg iv) attenuated both the reactive hyperemia in volume by 21-22% (P less than 0.01) and dilative responses of the epicardial coronary diameter by 27-28% (P less than 0.01), despite a nonsignificant attenuation of the resting or peak hyperemic coronary blood flow. When coronary blood flow was held constant during reperfusion, by an occluder distal to the ultrasonic crystals, the reactive dilation disappeared. A peculiar reactive constriction was noted when coronary occlusion was performed proximal to the site of the ultrasonic crystals. Appearance of this constriction was at 149 and 385 s after the release of 5 and 60 s of coronary occlusion, respectively. This late reactive constriction disappeared after pretreatment with alpha- (phentolamine, 1 mg/kg iv) and/or alpha- + beta-blockade, but not with beta-blockade alone, and it was not observed when the coronary diameter was measured proximal to the occluder. Thus reactive dilation of the epicardial coronary artery derives from an increase in coronary flow and is reduced by propranolol via a reduction in the hyperemic flow, suggesting a flow-dependent change in the diameter of the epicardial coronary artery. Reactive constriction is a local phenomenon following marked reduction in the coronary diameter and is abolished by alpha-adrenergic blockade with phentolamine.
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