Biomedical subjects
Publications and source records attributed to T Satake.
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This study was designed to clarify the mechanism of reperfusion arrhythmia. In the mongrel dogs, the left anterior descending coronary artery was occluded for 15 min and then the ligation was released. The dogs were divided into two groups: one was the control group, and the other the indomethacin group in which indomethacin, an inhibitor of prostaglandin (PG) biosynthesis, was premedicated at 30 min before ligation. The ventricular multiple response threshold (VMRT), and plasma levels of K+, PG E and PG F2 alpha were measured in the great cardiac vein before and during occlusion, and after reperfusion. In the control group, during occlusion, VMRT decreased and did not return to normal soon after reperfusion. The levels of PG E and PG F2 alpha in the great cardiac vein did not change significantly during occlusion; however, PG E became significantly elevated after reperfusion. In the indomethacin group, the time course of VMRT was essentially similar to that of the control group during occlusion; however, lowering of VMRT after reperfusion was prevented significantly. The PG F2 alpha level in the great cardiac vein did not elevate after reperfusion or during occlusion. In both groups, the level of K+ in the great cardiac vein was elevated during occlusion, but rapidly decreased to normal after reperfusion. These results suggest that PG E, as a washout metabolite, is a key factor in evoking reperfusion arrhythmia.
Plasma and erythrocyte digoxin concentrations from patients on digoxin maintenance therapy were measured and the results from patients with toxic and those with nontoxic drug levels were compared. Digoxin cumulation and release in plasma and erythrocyte were also studied. Our results indicate that erythrocyte digoxin concentration may be useful in distinguishing toxic and nontoxic drug levels.
Argyrophil cells were seen in 2 of 134 cervical tissue blocks obtained from 18 uteri, but none in the endometrium. In 10 of 30 cases of differentiated endometrial adenocarcinoma cells contained argyrophil granules stained with Grimelius method. These argyrophil reactive glandular cells gave positive d-PAS and Alcian blue (pH 2.5, PH 1.0) reactions, but gave no argyrophil reaction with PAS-Grimelius double staining method. It was also demonstrated that these glandular cells contained sulphomucins, because High iron diamine (HID) method gave positive reaction with HID-Alcian blue pH 2.5 double staining. Dense granules, which were submicroscopically seen in cells of well differentiated endometrial adenocarcinomas, were diagnosed as exocrine secretory granules, because of their localization in the cytoplasm and distinct morphological transformation from condensed vacuoles into mature secretory granules. From these findings, argyrophil granules which were seen in cells of the differentiated endometrial adenocarcinomas were thought not to correspond to endocrine granules but mucosubstances.
To investigate the pathophysiology of ischemic heart disease (IHD), tourniquet ischemia on the upper limb was one and change in platelet aggregation, plasma 6-keto-PGF1 alpha concentrations and plasma thromboxane B2 (TXB2) concentrations were studied. At rest, platelet aggregability and plasma TXB2 concentrations were significantly increased in IHD patients compared with those in normal subjects (p less than 0.001 and p less than 0.001, respectively). In normal subjects, platelet aggregability, plasma 6-keto-PGF1 alpha concentrations and plasma TXB2 concentrations rose significantly during ischemia (p less than 0.05, p less than 0.02 and p less than 0.05, respectively). In addition, plasma 6-keto-PGF1 alpha concentrations were significantly lower in IHD patients than in normal subjects during ischemia (p less than 0.005), though there was no significant change in the level of either group at rest. These results suggest that increase in prostacyclin synthesis in normal subjects during tourniquet ischemia may be a defense mechanism to maintain the balance between prostacyclin and thromboxane A2 (TXA2) and to prevent platelet aggregation induced by the procedure. Increase in platelet aggregation and TXA2 generation in IHD patients at rest indicates a close correlation between IHD and platelet reactivity. Tourniquet ischemia induced a significant increase in prostacyclin generation in normal subjects but not in IHD patients, which suggests the production of prostacyclin was impaired in IHD patients during ischemia. A marked different was obvious in prostacyclin and TXA2 generation between IHD patients and normal subjects, and this difference may play an important role in the pathogenesis of IHD.
We investigated the mechanism of the reperfusion-accelerated mitochondrial dysfunction. To clarify this mechanism, we performed the following experiments using 40 mongrel dogs. Experiment I: Prostaglandin (PG) E and F2 alpha levels in the great cardiac vein (GCV) were examined before, during occlusion and after reperfusion of the left anterior descending coronary artery (LAD). Experiment II: Heart mitochondria were prepared from the normal area and the occluded or the reperfused area after 15 min of the LAD occlusion, or after 5 min of reperfusion following the occlusion with or without premedication of indomethacin. The PGE level in the GCV did not change significantly during occlusion, but increased significantly soon after reperfusion. Mitochondrial dysfunction was caused by occlusion and further accelerated by reperfusion. The PG E level in mitochondria isolated from the reperfused area increased significantly. Indomethacin significantly prevented both the increase in PG E and the acceleration of mitochondrial dysfunction by reperfusion. These results suggest that the increase in PG E level is closely related to the reperfusion-accelerated mitochondrial dysfunction, and that premedication with indomethacin significantly prevented the extension of mitochondrial dysfunction induced by coronary reperfusion.
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Plasma norepinephrine (NE) concentration was measured in blood samples from the pulmonary artery (PA), the superior vena cava (SVC), the inferior vena cava (IVC) and the femoral artery (FA) in 34 patients undergoing diagnostic cardiac catheterization. In patients with pulmonary hypertension, the mean plasma NE concentrations in PA, SVC and FA were significantly higher than that of IVC, but no such difference was found in patients without such hypertension. Except in IVC, the plasma NE concentration in patients with pulmonary hypertension was significantly higher than in others. Furthermore, the plasma NE concentration was positively correlated with the mean pulmonary arterial pressure and inversely related to pulmonary arterial oxygen saturation in patients without a shunt. These results suggest the possibility that vasoconstriction by the sympathetic nervous system may contribute to the development of pulmonary hypertension in patients without the shunt.
Twenty-three patients with chronic respiratory failure and 30 normal subjects were studied to assess the sympathetic nervous activity in chronic hypoxic states, especially in chronic cor pulmonale. Of the 23 patients, 13 had a right ventricular hypertrophy (RVH) pattern on the electrocardiogram. Plasma norepinephrine (NE), dopamine-beta-hydroxylase (DBH), cyclic adenosine 3',5'-monophosphate (cyclic AMP) and cyclic guanosine 3',5'-monophosphate (cyclic GMP) concentrations were measured before and after oxygen inhalation. Plasma NE concentrations were 0.57 +/- 0.07 ng/ml in patients with chronic respiratory failure and 0.22 +/- 0.02 ng/ml in controls (p less than 0.001). Moreover, plasma NE concentrations were higher in patients with RVH than without (p less than 0.05), and these concentrations decreased significantly (p less than 0.05) in the former patients after oxygen inhalation. Plasma cyclic AMP concentrations were 31.2 +/- 2.6 pmol/ml in cases of chronic respiratory failure and 17.4 +/- 0.7 pmol/ml in controls (p less than 0.001) with no difference in plasma cyclic GMP and DBH concentrations. These results suggest that a significant proportion of patients with chronic respiratory failure, especially with cor pulmonale, were in hyper-adrenergic states partially due to hypoxia.
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Peripheral blood lymphocytes from 31 normal subjects and 29 patients with heart diseases were stimulated by isoproterenol, and cyclic AMP level in lymphocytes was assayed. Simultaneously plasma norepinephrine concentration at rest was measured. In normal subjects the generation of cyclic AMP after the stimulation decreased with age. The response of lymphocytes in patients of NYHA classes III and IV was significantly smaller than in the normal, age-matched control. Plasma norepinephrine concentration of patients of classes II, III, and IV rose significantly above normal. In congestive heart failure, a significant correlation between plasma norepinephrine concentration and increase of lymphocyte cyclic AMP was demonstrated. From these results it was suggested that beta-adrenergic receptors in congestive heart failure were desensitized.
The plasma concentrations of norepinephrine (NE), adenosine cyclic 3', 5'-monophosphate (cyclic AMP), and guanosine cyclic 3', 5'-monophosphate (cyclic GMP) were measured serially for 2 weeks after the onset of symptoms in 17 patients with acute myocardial infarction (AMI). The mean concentrations of NE in patients without complications were significantly elevated during the first 2 days following AMI. There was a significant correlation between the maximum concentration of plasma NE and of plasma CK. The mean concentrations of plasma cyclic AMP and cyclic GMP in patients without complications were significantly elevated on the first day and for 8 days respectively following AMI. The concentration of plasma cyclic AMP on admission in patients with complications was significantly higher than that in those without complications. There were significant correlations between the maximum concentration of plasma cyclic AMP and those of plasma CK, GOT, and LDH. Significant but weak correlations between the concentration of plasma NE and those of cyclic AMP and cyclic GMP were found. The results of the present study suggest an enhanced sympathetic nervous system activity at an early stage of AMI, a prolonged enhancement of parasympathetic nervous system activity in the course of AMI, and the potential value of plasma cyclic AMP concentrations as a useful index to estimate the seriousness and size of AMI.