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Biomedical subjects

M Oyama

Publications and source records attributed to M Oyama.

At least 91 records · Page 5Linked to original sources
PubMed1983

Characterization of free radical-mediated damage of canine cardiac sarcoplasmic reticulum.

In vitro generation of free radicals by xanthine oxidase acting on xanthine as substrate depressed steady-state calcium uptake by canine cardiac sarcoplasmic reticulum vesicles. The effect of free radicals on the calcium-dependent ATPase activity of the SR vesicles was pH dependent. At pH 7.0, ATPase activity was decreased, but at pH 6.4 it was unchanged. Exposure to free radicals increased the passive permeability of the vesicles to calcium. This increase was inhibited by superoxide dismutase (SOD) at pH 7.0, and SOD plus mannitol at pH 6.4. The increased permeability per se was insufficient to explain the effects of free radicals on ATPase activity, since the calcium ionophore A23187 was unable to mimick these effects. Direct measurement of the number and turnover of the pump units indicated that the number of units was unchanged but turnover was decreased by free radicals at pH 7.0. The overall data suggest at least two mechanisms of free radical damage, one associated with an increase in passive permeability and another associated with an as yet undefined change in some specific steps of the ATPase reaction.

Animals↗
PubMed1983

The effects of thoracic aortic cross-clamping and declamping on visceral organ blood flow.

Blood flow was measured using radioactive microspheres in 11 macaque monkeys 1) before hemorrhage shock, 2) after onset of shock, 3) after aortic cross-clamping and resuscitation, and 4) after release of the cross-clamp and stabilization. Hemodynamic parameters (cardiac output, arterial, right atrial and left atrial pressure) and blood gases were also monitored. Total abdominal organ flow fell with hemorrhage and fell further with aortic clamping. Reinfusion of shed volume did not restore abdominal organ flow (4.7% baselines) but increased LAP and cardiac output to the upper body. Release of the cross-clamp produced profound acidosis that was treated effectively with NcHCO3. After stabilization of blood, flow to kidney remained low (49% baseline) although intestinal flow was increased threefold (320% of baseline). It is clear that thoracic aortic cross-clamping in shock further compromises already reduced visceral blood flow and may contribute to the problem of ischemic multiple organ failure after resuscitation from hemorrhagic shock.

Abdomen↗
PubMed1983

Anaphylaxis-induced increase in plasma cyclic AMP dependent on endogenous catecholamines in rats.

Plasma cyclic AMP levels during anaphylactic shock in rats was studied in 7 groups of animals: (1) control rats; (2) rats with adrenomedullectomy; (3) rats treated with propranolol; (4) rats with reserpinization; (5) rats with 6-hydroxydopamine-induced chemical sympathectomy; (6) rats treated with hexamethonium, and (7) rats treated with cocaine (catecholamine uptake inhibitor). All experiments were carried out in ovalbumin-sensitized rats. Plasma cyclic AMP showed a rapid increase during anaphylactic shock in control rats. Adrenomedullectomy abolished the anaphylaxis-induced increase in plasma cyclic AMP, while hexamethonium had no effect. Propranolol caused a dose-dependent abolition of the increase. The treatment of rats with reserpine, 6-hydroxydopamine or cocaine partially inhibited the increase in plasma cyclic AMP. The results show that the adrenal medulla is the major source of catecholamines during anaphylactic shock, and that catecholamines in the adrenergic neuronal terminals may be partly responsible for the anaphylaxis-induced increase in plasma cyclic AMP.

Adrenal Medulla↗
PubMed1983

Proportion regulation without pattern formation in Dictyostelium discoideum.

When shaken in a glucose-albumin-cAMP medium, dissociated aggregative cells formed small clumps, in which both prespore and prestalk cells differentiated in essentially the same proportions as in a slug. Immunocytochemical staining of sections of such clumps revealed that the two types of cells showed no particular pattern of distribution, unlike the two-zoned prestalk-prespore pattern as observed in the slug. Cells dissociated at stages later than the onset of aggregation always produced a constant proportion of prespore cells, irrespective of the initial proportion when transferred to the culture. Furthermore, prestalk cells fractionated from slugs and transferred to the culture restored almost the normal prespore protortion through conversion of the cell types, whereas proportion of unfractionated slug cells remained unchanged. We conclude from these findings that the normal prestalk-prespore pattern is not required for proportion to be regulated.

Cell Aggregation↗
PubMed1982

Comparison of three different assays for the assessment of ciguatoxin in fish tissues: radioimmunoassay, mouse bioassay and in vitro guinea pig atrium assay.

Moderate correlation was shown between the following tests: RIA: mouse bioassay (r = 0.58); RIA: guinea pig atrium assay (r = 0.62); guinea pig atrium assay: mouse bioassay (r = 0.62). All three assay procedures showed good correlation when ciguatoxin was present in tissues in high concentrations. The results also suggest that more than one structurally related toxin may be present in the fish tissues.

Animals↗
PubMed1982

Free radical damage to sarcoplasmic reticulum of masseter muscle by arachidonic acid and prostaglandin G2.

In vitro generation of free radicals by xanthine oxidase acting on hypoxanthine as a substrate induced a decreased calcium uptake velocity and reduced calcium-dependent ATPase activity of isolated sarcoplasmic reticulum (SR) vesicles from canine masseter muscle at pH 7.0. At pH 5.5 calcium uptake velocity was also reduced but ATPase activity was unaffected. Application of arachidonic acid or prostaglandin G2 induced the depression of both calcium uptake velocity and ATPase activity. The effect of arachidonic acid and prostaglandin G2 on ATPase activity depended on the pH. At pH 7.0, ATPase activity was decreased, but at pH 5.5 it was unchanged. These effects were reversed by superoxide dismutase (SOD) at pH 7.0, and by SOD plus mannitol at pH 5.5. Prostaglandin H2, prostaglandin E2 and 11,14,17-eicosatrienoic acid had no effect on calcium uptake velocity and ATPase activity at both pH 7.0 and pH 5.5. These results suggest that damage to the masseter muscle is caused by a free radical superoxide anion generated as a result of increased prostaglandins synthesis, and by the production of more lethal hydroxyl radical switched from the production of superoxide anion at low pH.

Adenosine Triphosphatases↗
PubMed1982

Effects of cyclic AMP on contact formation and differentiation in Dictyostelium discoideum.

It has been shown previously that Dictyostelium discoideum NC4 cells dissociated at the early aggregation stage form cell clumps and differentiate into prespore cells in a shaking culture containing glucose, albumin, EDTA and cyclic AMP. In this culture system, we found that the cells neither differentiate nor form cell clumps in the absence of cyclic AMP. Wheat-germ agglutinin (WGA) completely inhibited the cyclic AMP-induced formation of cell contact and the inhibition was nullified by the addition of N-acetyl-D-glucosamine. When the cells were prevented from forming contact by either rapid shaking or the addition of WGA, they were unable to differentiate even in the presence of cyclic AMP, indicating that contact formation is a prerequisite for prespore differentiation. Cells dissociated from migrating slugs formed cell clumps in shaking culture, with or without cyclic AMP, and the cell contact was sensitive to WGA. In the absence of cyclic AMP, prespore cells lost their differentiated state, even though the cells were in contact. This indicates that cyclic AMP has a second effect, that of pomoting differentiation, in addition to the effect of inducing contact formation. Both effects were required for prespore differentiation of strain NC4 cells.

Cell Adhesion↗
PubMed1980

Quantitative effect of a single large dose of methylprednisolone on infarct size in baboons.

Despite numerous studies directed at determining the ability of glucocorticoids to minimise myocardial ischaemic damage following acute coronary occlusion, there remains no clear consensus concerning their usefulness. Within an ischaemic region, glucocorticoids produce membrane stabilising effects which decrease the autolytic effects of marked cellular swelling and lysosomal membrane rupture. Their use has also been associated with a decreased cellular lysis due to infiltrating inflammatory cells and with an increase in collateral blood flow. The use of glucocorticoids has remained clinically attractive due to experimental observations regarding these local actions; however, the potential of these actions to enhance long-term viability of ischaemic myocardium has remained uncertain. A major problem in the comparison of the extent of infarction between treated and untreated animals has been the variability in infarct size that results from coronary artery ligation at any given anatomical site. In the experimental baboon model which we have employed, we have previously shown that the ultimate epicardial area of infarction, as well as the volume of infarction as assessed histologically at 7 days post occlusion, shows a good linear relationship to the area of ischaemic injury at 1-hour post occlusion, as assessed by high resolution epicardial ST segment mapping. In this way animals may serve as their own controls and as long as an intervention is initiated at 1 h or later post occlusion, then the epicardial area or transmural volume of histologically assessed infarction at 7 days can be compared with the predicted epicardial area or transmural volume of infarction and hence determine the effect of that intervention in altering infarct size. This experimental model does not rely on a comparison of the absolute magnitude of infarcts between treated and untreated animals and, therefore, avoids the error introduced by the inherent variability in infarct size between animals after coronary occlusion.

Animals↗
PubMed1980

Prostaglandin E2 and cyclic nucleotides during anaphylactic shock in rats.

Anaphylactic shock was induced with ovalbumin in sensitized rats and the relationship between PGE2 and cyclic nucleotides in lung tissue and plasma histamine during anaphylactic shock was studied. PGE2 level and cyclic AMP/cyclic GMP ratio decreased with this ovalbumin-challenge, and the former reached a minimum value 40 sec after the challenge while the latter reached a minimum value 20 sec later. The plasma histamine level was elevated and reached a maximum value concomitant with the minimum value in the cyclic AMP/cyclic GMP ratio. Dibutyryl cyclic AMP elevated the PGE2 level significantly and inhibited the ovalbumin-induced elevation of plasma histamine, however, this effect was abolished by the administration of indomethacin. PGE2 infusion elevated the cyclic AMP level as well as the cyclic AMP/cyclic GMP ratio, in a time-dependent manner, and inhibited the ovalbumin-induced elevation of plasma histamine during 10 min infusion. There was a significant correlation between the cyclic AMP level and the cyclic AMP/cyclic GMP ratio, both elevated by PGE2 infusion. Thus, anaphylactic elevation of the plasma histamine level results from a decrease in the levels of PGE2 in lung tissue rather than a decrease in the cyclic AMP/cyclic GMP ratio, albeit these decreases being coincident during anaphylactic shock.

Anaphylaxis↗