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Biomedical subjects

H Miyoshi

Publications and source records attributed to H Miyoshi.

At least 253 records · Page 14Linked to original sources
PubMed1989

Long-term prognosis of esophageal variceal cases treated with injection sclerotherapy.

One hundred fifty-two patients with esophageal varices underwent a total of 485 injection sclerotherapy procedures (mean, 3.2 times per each case). During 5 years of observation, 20 cases (13.2%) died following injection sclerotherapy. The 3-year survival rates, based on the Kaplan-Meier method, were 42% for emergency cases, 75% for elective cases and 90% for prophylactic cases. Significant differences (P less than 0.05) by the generalized Wilcoxon test were observed in the survival rates between emergency cases and prophylactic cases, and also between elective cases and prophylactic cases. Two cases (8.6%) of failure to control acute hemostasis were experienced. Twenty cases of bleeding after sclerotherapy were experienced, and 8 died of bleeding. The three-year bleeding rate according to the Kaplan-Meier method was 59% for emergency cases, 25% for elective cases and 7% for prophylactic cases. A significant difference (P less than 0.05) by the generalized Wilcoxon test was observed in the bleeding rate between elective cases and prophylactic cases. Non-bleeding rate (100%-bleeding rate) after sclerotherapy showed almost the same values as the survival rate. These results indicate that upper digestive tract hemorrhage influences the prognosis of patients after sclerotherapy.

Adult↗
PubMed1989

Hypothalamic growth hormone-releasing factor (GRF) participates in the negative feedback regulation of growth hormone secretion.

Effects of growth hormone (GH) excess on immunoreactive hypothalamic GH-releasing factor (GRF) and somatostatin (SRIF) were studied in rats. Hypothalamic GRF content significantly reduced after 7-day daily treatment with 160 micrograms of rat GH or after inoculation of GH-secreting rat pituitary tumors, MtT-F4 for 9 or 13 days and GH3 for 3 months. Basal and 59 mM K+-evoked release of GRF from incubated hypothalami diminished, more than the content, by 43-51% in MtT-F4 tumor- or by 67-83% in GH3 tumor-bearing rats. In contrast, there was a small but significant increase in content or release of SRIF in rats harboring the GH3 or MtT-F4 tumor, respectively. These results indicate the existence of a negative feedback loop via hypothalamic GRF as well as SRIF in control of GH secretion.

Animals↗
PubMed1989

Differentiation between septic and postburn insulin resistance.

Sepsis and extensive burn injury produce clinical syndromes characterized in part by "insulin resistance," but it is unclear if these insulin resistant states are identical. To test if the maximal biological effectiveness of insulin is altered in septic or burned patients, eight septic patients and eight nonseptic patients recovering from severe burn injury were studied using the hyperinsulinemic eukalemic euglycemic clamp technique. Compared with bed-rested controls, the septic patients showed an insulin-induced plasma clearance of potassium, which was 183% higher (P less than .001), and a concomitant glucose clearance, which was 52% lower (P less than .001). Nonseptic burn patients also had a 91% increase in potassium clearance (P less than .05), but their maximal insulin-stimulated glucose uptake was not different from that of bedrested controls. When septic patients were compared with their nonseptic burned counterparts, there was no difference in potassium clearance in response to insulin, but glucose uptake by the septic patients was 47% lower (P less than .001). Insulin infusion completely suppressed hepatic glucose production in both septic patients and in nonseptic burn patients. The percent of whole body glucose uptake that was oxidized was not different between the septic patients and the nonseptic postburn patients in both the basal and insulin-stimulated states (38% and 51% v 38% and 42%, respectively). It is concluded that septic and postburn insulin resistance differ in that peripheral glucose uptake in sepsis, but not nonseptic burn injury, is refractory to pharmacologic insulin stimulation, whereas in both states insulin effectively stimulates potassium uptake.

Adult↗
PubMed1989

Glucagon and hepatic glucose production: modulation by low-dose bradykinin infusion.

The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers. Studies were performed during constant insulin concentration as achieved by simultaneous somatostatin infusion and insulin replacement. In the basal period glucagon was infused at a rate of 0.5 ng/kg min. Then, glucagon infusion rate was increased to 3 ng/kg min to test the response to hyperglucagonemia. In a second set of experiments BK was infused concomitantly with the high dose glucagon. Each subject served as his own control. BK infusion did not prevent the glucagon-induced rise in hepatic glucose production and glucose cycling. However, at a later stage BK accelerated the negative feedback mechanisms activated by glucagon (decrease in hepatic glucose production) significantly. These findings suggest that intravenous BK may interact with mechanisms involved in the down-regulation of hepatic glucagon effects.

Adult↗
PubMed1989

Effect of rice fiber on human fecal microflora.

The effects of brown rice, containing fourfold as much dietary fiber as polished rice, on the human fecal microflora were determined. Significantly increased numbers of Bifidobacterium adolescentis and Enterococcus faecalis were observed during the brown rice intake, whereas the total counts and the numbers of bacteroides, Eubacterium aerofaciens, and Escherichia coli during the intake were lower than those before and after the intake. Lower numbers of clostridia and low incidences of Clostridium paraputrificum and C. perfringens were observed during the brown rice intake.

Adult↗
PubMed1989

Role of insulin and glucose oxidation in mediating the protein catabolism of burns and sepsis.

We have investigated the responsiveness of protein kinetics to insulin and the role of glucose oxidation rate as a mediator of the protein catabolic response to burn injury and sepsis by assessing the response of leucine and urea kinetics to a 5-h hyperinsulinemic euglycemic clamp with and without the simultaneous administration of dichloroacetate (DCA) (to further increase glucose oxidation via stimulation of pyruvate dehydrogenase activity) in eight severely burned and eight septic patients. Leucine and urea kinetics were measured by the primed-constant infusions of [1(-13)C]leucine and [15N2]urea. Compared with controls, basal leucine kinetics (flux and oxidation) were significantly elevated (P less than 0.01) in both groups of patients. Hyperinsulinemia elicited significant (P less than 0.05) decreases in leucine kinetics in both groups of patients. Consistent with this observation, hyperinsulinemia caused urea production to decrease significantly (P less than 0.05) in both patient groups. The administration of DCA to patients during hyperinsulinemia elicited a significant increase in glucose oxidation rate compared with the clamp rate (P less than 0.05), and the percent of glucose uptake oxidized increased from 45.5 +/- 5.5 to 53.5 +/- 4.8%; yet the response of leucine and urea kinetics to the clamp plus DCA was not different from the response to the clamp alone. These results suggest that the maximal effectiveness of insulin to suppress protein breakdown is not impaired and that a deficit in glucose oxidation or energy supply is probably not playing a major role in mediating the protein catabolic response to severe burn injury and sepsis.

Adolescent↗
PubMed1989

An investigation on the inactivation process of sodium currents in single frog ventricular cells.

The characteristics of sodium currents (INa) in single frog ventricular cells were studied with the oil gap method. This method improves time- and space-control of the membrane potential under the voltage clamp, thereby making possible accurate analysis of fast events of INa. In this preparation the threshold of INa was about -60 mV and the reversal potential was 58 mV, which is close to the value calculated by the Nernst equation for sodium ions. Because the instantaneous current-voltage (I-V) relationship is linear, the ease of permeation of sodium ions through Na+ channels is well expressed by the chord conductance. The falling phase of INa and the time course of recovery from inactivation follow a time course of single exponential function. The time constants for on- and off-processes of inactivation at the same membrane potential are very close to each other, indicating only a single state of inactivation. Though almost all properties of INa were well described by Hodgkin-Huxley's model, a clear delay of onset of inactivation was demonstrated by two-pulse experiment. In this report the modified kinetics scheme was proposed which can account for both a delay of onset of inactivation development and a falling phase of INa that follows a single exponential time course.

Animals↗
PubMed1988

Quantitative analyses of the uncoupling activity of substituted phenols with mitochondria from flight muscles of house flies.

Uncoupling activity with flight-muscle mitochondria from house flies was measured for a series of weakly acidic uncouplers (substituted phenols) and compared with the protonophoric potency across lecithin liposomal membranes. The activity was linearly related to the protonophoric potency when such factors as the stability of anionic species in the membrane phase and the difference in the pH conditions of the extramembranous aqueous phase were taken into account. Relationships of the flight-muscle activity with activities measured previously with rat-liver mitochondria and spinach chloroplasts were linear. Our findings were further evidence for the shuttle-type mechanism of the uncoupling action of weakly acidic uncouplers.

Adenosine Triphosphate↗
PubMed1988

Evaluation of the isotopic equilibration between lactate and pyruvate.

When an isotopic tracer is infused for the purpose of determining the rate of turnover or oxidation of a substrate, it is assumed that the resulting isotopic enrichment by the tracer will reflect the kinetics of only the pool of interest. However, this may not be the case when carbon-labeled lactate is infused, since rapid isotopic exchange with the intracellular pyruvate and alanine pools could potentially occur. Therefore we have determined the extent of isotopic exchange occurring during the infusion of [3-13C]lactate into six anesthetized dogs. In the steady state, pyruvate enrichment was 91 +/- 2.2% (means +/- SE) of the lactate enrichment, and alanine enrichment was 81 +/- 3.3% of the pyruvate enrichment and 72 +/- 2.6% of the lactate enrichment. In contrast, when [3-13C]alanine was infused (n = 2), pyruvate (and lactate) enrichment was 9.9% of the alanine enrichment. We therefore conclude that there is rapid isotopic equilibration between lactate and pyruvate but that interaction with alanine reflects the true metabolic flux rates, rather than isotopic exchange. Consequently, lactate kinetics, as traditionally determined, more accurately reflect whole body pyruvate kinetics.

Animals↗
PubMed1988

Effect of isotope infusion and sampling sites on glucose kinetics during a euglycemic clamp.

The importance of the location of isotope infusion and blood sampling on calculating glucose kinetics was studied in five mongrel dogs in the basal state and when glucose turnover was increased during a hyperinsulinemic euglycemic clamp. [U-14C]glucose was infused into the pulmonary artery, unlabeled glucose was infused into a femoral vein to maintain euglycemia, and blood was sampled from the right atrium (AV mode) and the femoral artery (VA mode). In the basal state there was no difference between the AV or VA mode in plateau specific activity; hence, the calculated rate of appearance of glucose was the same with either mode. During the euglycemic clamp procedure, plateau specific activity of the AV mode was significantly lower than that of the VA mode (P less than 0.05). The rate of appearance of glucose calculated from the VA mode was almost identical to the rate of infusion of unlabeled glucose (13.0 +/- 1.4 vs. 12.6 +/- 1.4 mg.kg-1.min-1, respectively), but the rate of appearance of glucose calculated from the AV mode was 12% greater. This study demonstrates that the calculation of glucose kinetics is sensitive to differences in sampling site when the turnover rate is high relative to the mass flow rate (cardiac output times substrate concentration).

Animals↗
PubMed1988

Hormonal control of substrate cycling in humans.

Recent studies have established the existence of substrate cycles in humans, but factors regulating the rate of cycling have not been identified. We have therefore investigated the acute response of glucose/glucose-6P-glucose (glucose) and triglyceride/fatty acid (TG/FA) substrate cycling to the infusion of epinephrine (0.03 microgram/kg.min) and glucagon. The response to a high dose glucagon infusion (2 micrograms/kg.min) was tested, as well as the response to a low dose infusion (5 ng/kg.min), with and without the simultaneous infusion of somatostatin (0.1 microgram/kg.min) and insulin (0.1 mU/kg.min). Additionally, the response to chronic prednisone (50 mg/d) was evaluated, both alone and during glucagon (low dose) and epinephrine infusion. Finally, the response to hyperglycemia, with insulin and glucagon held constant by somatostatin infusion and constant replacement of glucagon and insulin at basal rates, was investigated. Glucose cycling was calculated as the difference between the rate of appearance (Ra) of glucose as determined using 2-d1- and 6,6-d2-glucose as tracers. TG/FA cycling was calculated by first determining the Ra glycerol with d5-glycerol and the Ra FFA with [1-13C]palmitate, then subtracting Ra FFA from three times Ra glycerol. The results indicate that glucagon stimulates glucose cycling, and this stimulatory effect is augmented when the insulin response to glucagon infusion is blocked. Glucagon had minimal effect on TG/FA cycling. In contrast, epinephrine stimulated TG/FA cycling, but affected glucose cycling minimally. Prednisone had no direct effect on either glucose or TG/FA cycling, but blunted the stimulatory effect of glucagon on glucose cycling. Hyperglycemia, per se, had no direct effect on glucose or TG/FA cycling. Calculations revealed that stimulation of TG/FA cycling theoretically amplified the sensitivity of control of fatty acid flux, but no such amplification was evident as a result of the stimulation of glucose cycling by glucagon.

Adult↗