Biomedical subjects
Publications and source records attributed to M Umemoto.
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The role of histamine H1- and H2-receptors in mediating the response produced by histamine was investigated on rat ocular surface. Histamine caused a dose-dependent increase in microvascular permeability on this surface. Response to histamine was significantly inhibited by pretreatment with chlorpheniramine (an H1-antagonist) but was unchanged by cimetidine (an H2-antagonist). No additive effect was shown when chlorpheniramine and cimetidine were used in combination. Moreover, dimaprit, a selective histamine H2-receptor agonist, failed to elicit a dose-dependent vasopermeability response. Chlorpheniramine significantly reduced increase in microvascular permeability associated with immediate hypersensitivity, although cimetidine did not. The addition of cimetidine to chlorpheniramine did not lead to greater reduction than that achieved with chlorpheniramine alone. We conclude that the microvascular permeability response to histamine is predominantly mediated by H1-receptors on rat ocular surface.
The effect of disodium cromoglycate (DSCG) on the anaphylactic reaction was re-evaluated by measuring the amount of leaked dye into tissues of rat conjunctiva 48 h after passive sensitization with IgE antibodies against ovalbumin. In the rat sensitized with mouse monoclonal IgE (titer 4), DSCG produced a dose-dependent inhibitory effect when used in a dose range between 1 and 5%; at more than 2%, the effect was statistically significant. On more severe anaphylactic reactions induced with the same antibody at titer 10, DSCG had no significant effect when applied in doses of less than 5%. On the other hand, DSCG (2%) had no significant effect on the sensitization with either rat polyclonal IgE or mouse polyclonal IgE (titer 4). These findings indicate that DSCG has a potential benefit when used in moderate anaphylactic reactions and has a strictly specific effect depending on the origin of the antibody.
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A long-term follow-up study on pulmonary function in twelve lobectomized children under ten years of age at the time of surgery was performed to determine the patterns of compensation. In the patients over ten years old at the time of the test performed over two years postoperatively, there was neither compensatory regeneration nor compensatory overdistension of the remaining lung tissue. However, there appeared to be an increase in the vital capacity, probably due to the growth of surrounding tissue such as thorax, respiratory muscles, and diaphragm. In contrast, the children tested under the age of eight years showed evidence of mild overdistension during the early postoperative period, but not at two years. There was no sign of overdistension in the patients over ten years of age at the time of testing.
While oxygen-derived free radicals have been implicated in the pathogenesis of myocardial injury, the exact nature of this injury is still unclear. To test the hypothesis that oxygen-induced injury may influence the recovery of cardiac function from ischemic damage, we used an oxygen free radical scavenger, superoxide dismutase (SOD), together with catalase, during the reperfusion of isolated canine heart which had been subjected to 15 min of normothermic ischemic arrest followed by 2 hr of hypothermic cardioplegic preservation using a modified Collins solution. Determinations of thiobarbituric acid reactive substances and coenzyme Q10 within the myocardium showed that the treatment with SOD and catalase was capable of inhibiting lipid peroxidation induced by reperfusion. This inhibition was apparently associated with the improvement of myocardial energy metabolism and cardiac performance. Coronary flow was significantly higher in the heart treated with SOD and catalase during the working stage with a corresponding increase in oxygen consumption. Myocardial adenosine triphosphate (ATP) was partially, but significantly restored during reperfusion in these hearts whereas no restoration was observed in the heart without the enzymes. The treatment with SOD and catalase also improved left ventricular stroke work index and left ventricular maximum dp/dt at an early stage of the working mode. These results suggest that the use of SOD and catalase during reperfusion can protect the ischemic heart against reperfusion injury by scavenging oxygen-derived free radicals.
Three series of experiments were undertaken to determine whether the residual catecholamine (CA) terminals or intrinsic neurons of ventral tegmentum (VT) in rats given 6-hydroxydopamine (6-OHDA) after desmethylimipramine (DMI) in the lateral ventricles at birth, mediated VT self-stimulation (SS). In Experiment I, male pups were injected bilaterally on days 3 and 5 with 6-OHDA (total dose 200 micrograms) or with the vehicle after pretreatment with DMI (50 mg/kg, IP) 30 min earlier. Each subject, 150 days old, was implanted bilaterally in the VT with electrode-cannula units. Both the dopamine (DA)-depleted and control groups yielded similar percentages of self-stimulators. The rate of responding was, however, slightly but significantly lower in the DA-depleted group than in the controls. In Experiment II, 8 DA-depleted and 7 control rats were pretreated with pargyline (50 mg/kg, IP) and then given unilateral injections of 6-OHDA in the VT, in the tissue below the SS electrode. These intracerebral injections of 6-OHDA had no effect on VT SS in both groups. Seventeen controls and 12 DA-depleted rats, in Experiment III, were given injections of kainic acid (KA; 5 nM) either ipsilaterally or contralaterally. The ipsilateral injection abolished SS (14 days of testing), whereas the contralateral injection had no effects on ipsilateral SS in both groups. Histochemical fluorescence study in Experiment I and II showed that the neonatal treatment with DMI + 6-OHDA had reduced the number of DA-containing perikarya in the VT and that reinjection of 6-OHDA into the VT caused the disappearance of the residual CA terminals in tissue surrounding the electrode tip.
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This study was designed to investigate the relationship between myocardial oxygen consumption and oxygen-induced myocardial injury. Dog hearts were exposed to 40 min normothermic ischemia and then reperfused for 10 min with three oxygenated perfusates containing different hemoglobin concentrations and with moderate hemodilution. The experimental groups consist of a moderate hemodilution group (Group M) receiving 8 g/dl of hemoglobin, an extreme hemodilution group (Group E) given 4 g/dl of hemoglobin, and a hemoglobin-free autologous plasma group (Group F). Hearts in the non-ischemic control group (Group C) were also perfused with moderate hemodilution throughout. In Group C, Group M and Group E, the O2 tension of perfusates was maintained at about 100 mmHg and in Group F, at over 300 mmHg. Oxygen extraction at 5 min after reperfusion in Group C was 14%, in Group M and Group E less than 10%, but in Group F 70%. Oxygen consumption in Group F was more than twice that in Group E and surpassed that in Group C. Group M also showed a significant increase in oxygen consumption compared with Group E at 5 min after reperfusion. Among the ischemic groups, Group E showed improvement of left ventricular function almost comparable to Group C accompanied by a rapid decrease in myocardial lactate, improved preservation of myocardial adenine nucleotides and prevention of myocardial lipid peroxidation. In contrast, Group F showed persistently higher values of lipid peroxides and lactate, the poorest recovery of adenine nucleotides, and impairment of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
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Recent advances in echocardiography have revealed that hypertension causes several types of cardiac hypertrophy. We classified hypertensive patients by type of cardiac hypertrophy, and evaluated left ventricular function and the severity of hypertension. The subjects consisted of 257 hypertensive patients, 13 patients with cardiac hypertrophy, and 95 normotensive controls. The hypertensives were classified in four groups: no hypertrophy, concentric hypertrophy, asymmetrical septal hypertrophy (ASH), and asymmetrical apical hypertrophy (AAH). The normotensive patients with cardiac hypertrophy included nine with ASH and four with AAH. Cardiac functions in these patients were determined by echocardiography, RI-angiocardiography and cardiac catheterization. The results were as follows: Among 257 hypertensive patients, the incidence of concentric hypertrophy, ASH, and AAH was 53%, 10%, and 4%, respectively. In patients with AAH and hypertension, the hypertensive blood pressure levels and hypertensive organ involvements were mild. The blood pressures of most of these patients fell to the normal range after admission. The cardiac index and left ventricular systolic function (FS, mVCF, and ejection fraction) were significantly higher in AAH with hypertension than in the other hypertensive groups or in the normotensive controls. The hypertensive patients showed lower E-F slopes and higher A/E ratios than the normotensive controls, as well as the normotensive patients with ASH or AAH. Cardiac function did not differ appreciably between normotensive AAH and hypertensive AAH. Left ventricular dimension and left ventricular end-diastolic volume index were larger in AAH with hypertension. The total peripheral resistance of the hypertensive AAH was significantly lower than that of the hypertensives with concentric hypertrophy (p less than 0.01), though it was higher than that of the normotensive AAH (p less than 0.01). It was, therefore, concluded that mild hypertension observed in patients with AAH may be the result of regulatory mechanisms in the hyperkinetic states.
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The role of the dopaminergic input to the medial prefrontal cortex (MFC) on self-stimulation (SS) was investigated in adult rats injected neonatally with 6-hydroxydopamine (6-OHDA). Each subject on day 3 or 5 received bilateral intraventricular injection of 6-OHDA (total dose 200 micrograms, 50 micrograms/injection/2.5 microliters vehicle which contained 1 mg/ml ascorbic acid) or of the vehicle alone after pretreatment with desmethylimipramine (50 mg/kg i.p.) 30 min earlier. At 150 days of age, the animals were implanted with monopolar (100 microns) stainless steel electrodes in the MFC. One long (10 h) and 5 short (2 h) SS sessions resulted in similar percentages of responders for the brain reward in test and control subjects, and similar response rates in both groups. Biochemical assays of the levels of norepinephrine (NE) and dopamine (DA) in the frontal cortex showed depletion of DA 90% in the test animals, but no depletion of NE. Histochemical fluorescence visualization of the catecholamine input verified the biochemical results in the MFC. These results are viewed as negative evidence for the hypothesis that DA innervations in the MFC are critical neural substrates for SS, and suggest that activation of intrinsic neurons in the MFC are responsible for SS in the region.
Two patients with monoclonal IgM-secreting neoplasms are presented. Though both patients could be diagnosed as Waldenström's macroglobulinemia, the clinicopathologic features were quite contrastive. Most neoplastic cells in Case 1 showed lymphocytic morphology with rather leukemic process, while those in Case 2 were highly polymorphic with solid proliferation. The clinical and morphologic heterogeneity in these cases and cases in the literature is discussed, and the possible requirement to establish a system for the subclassification of IgM-secreting neoplasms is insisted.