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Biomedical subjects

K Ogino

Publications and source records attributed to K Ogino.

At least 91 records · Page 5Linked to original sources
PubMed1997

Interrelating of ventricular pressure and intracellular calcium in intact hearts.

Although the mechanistic link between variations in intracellular calcium and its effects on myofilament regulatory proteins and subsequent impact on cardiac muscle force production have been known for some time, characterization of cardiac contractile properties are predominantly confined to phenomenological descriptions of the relationship between either muscle length and force or ventricular pressure and volume. However, as recognition of the limitations of these theories grow, investigators have begun to look toward more fundamental theories of cardiac contraction to explain whole heart function. The goal of the present study was first to explore, on a theoretical level, the degree of complexity required in a biochemical model necessary to adequately explain both equilibrium and twitch contraction behavior of cardiac muscle. Central to this analysis was a critical examination of the evidence for and against the importance of a calcium-free, force-generating state. Next, we determined whether such theories can actually account for the interrelationships between the experimentally measured time courses of pressure generation and the calcium transient measured from intact ventricles during both normal twitches as well as during complex contraction sequences. The results of this analysis provide strong support for a four-state model, including the calcium-free, force-generating state. These results will help guide the continuing quest for a mechanistic theory of ventricular function.

Aequorin↗
PubMed1997

Evaluation of pharmacological profile of meloxicam as an anti-inflammatory agent, with particular reference to its relative selectivity for cyclooxygenase-2 over cyclooxygenase-1.

We studied the anti-inflammatory activity of meloxicam on rat carrageenin-induced pleurisy and its toxicity for rat gastric mucosa, relative to its in vitro inhibitory potency against partially purified cyclooxygenase (COX)-1 and COX-2 preparations in order to clarify the pharmacological profile of the compound as an anti-inflammatory agent. In rat carrageenin-induced pleurisy, the plasma exudation rate peaked at 5 h, at which time COX-2 was detectable in cells from the pleural exudate. Meloxicam and piroxicam (1 and 3 mg/kg) and NS-398 (3 mg/kg) showed almost equal anti-inflammatory potency against 5-hour pleurisy. A single oral administration of the compounds caused a dose-dependent increase in the number of rats with gastric mucosal erosion. The ED50 value for meloxicam (5.92 mg/kg) was significantly higher than that for piroxicam (1.76 mg/kg), indicating that meloxicam is safer. Indometacin showed intermediate safety (2.59 mg/kg). In in vitro experiments, indometacin inhibited COX-1 about 1.7 times more potently than COX-2. NS-398 inhibited COX-2 with an IC50 of 0.32 microM, but never affected COX-1 activity, even at 100 microM. In the same assay system, meloxicam inhibited COX-2 about 12 times more selectively than COX-1. Piroxicam, however, inhibited both isoforms almost equally. These results indicate that meloxicam is a potent anti-inflammatory agent with low gastric toxicity. One reason for its in vivo pharmacological profile may be related to its relative selectivity for COX-2 over COX-1. Thus, meloxicam may belong to a group of COX-2 selective anti-inflammatory agents with a better safety profile than conventional COX-1 and COX-2 nonselective anti-inflammatory agents.

Administration, Oral↗
PubMed1997

Impaired cytosolic Ca2+ response to glucose and gastric inhibitory polypeptide in pancreatic beta-cells from triphenyltin-induced diabetic hamster.

Oral administration of a single dose of triphenyltin compounds induces diabetes with decreased insulin secretion in rabbits and hamsters after 2-3 days without any morphological changes in pancreatic islets. In the present study, to test the possibility that the impaired insulin secretion induced by triphenyltin compounds could result from an impaired Ca2+ response in pancreatic beta-cells, we investigated the effect of triphenyltin-chloride (TPTCl) administration on the changes in the cytoplasmic Ca2+ concentration ([Ca2+]i) induced by secretagogues, such as glucose, high K+, gastric inhibitory polypeptide (GIP), and acetylcholine (ACh) in hamster pancreatic beta-cells. TPTCl administration caused partial suppression in 10 mM K+-induced rise in [Ca2+]i without suppressing the increase in [Ca2+]i evoked by 20-50 mM K+. Administration of TPTCl strongly inhibited the rises in [Ca2+]i induced by 27.8 mM glucose, 100 microM ACh in the presence of 5.5 mM glucose, and by 100 nM GIP in the presence of 5.5 mM glucose. In the ACh-induced response, TPTCl administration strongly suppressed the late sustained phase, while weakly suppressing the initial rise in [Ca2+]i. TPTCl administration significantly suppressed the rise of cAMP content in islet cells induced by 100 nM GIP with 1 mM 3-isobutyl-1-methylxanthine in the presence of 5.5 mM glucose (P < 0.01, N = 5-11). TPTCl administration also impaired the insulin secretion in islet cells induced by 27.8 mM glucose, 100 nM GIP in the presence of 5.5 mM glucose, and 100 microM ACh in the presence of 5.5 mM glucose (P < 0.05, N = 9-16). We conclude that the pathology of triphenyltin-induced diabetes in hamsters involves a defect in cellular Ca2+ response due to a reduced Ca2+-influx through voltage-gated Ca2+ channels.

Acetylcholine↗
PubMed1996

Role of prostaglandin H synthase-2 in prostaglandin E2 formation in rat carrageenin-induced pleurisy.

Rat carrageenin-induced pleurisy was used to clarify the role of prostaglandin H synthase (PGHS)-2 in acute inflammation. Intrapleural injection of 0.2 ml of 2% lambda-carrageenin induced accumulation of exudate and infiltration of leukocytes into the pleural cavity. When PGHS-1 and -2 proteins in the pleural exudate cells were analyzed by Western blot analysis, PGHS-2 was detectable from 1 hr after carrageenin injection. Its level rose sharply, remained high from 3 to 7 hr after injection, and then fell to near the detection limit. PGHS-1 was also detected, but kept almost the same level throughout the course of the pleurisy. Levels of prostaglandin (PG) E2 and thromboxane (TX) B2 in the exudate increased from hour 3 to hour 7, and then declined. Thus, the changes of the level of PGE2 were closely paralleled those of PGHS-2. The selective PGHS-2 inhibitors NS-398, nimesulide and SC-58125 suppressed the inflammatory reaction and caused a marked decrease in the level of PGE2 but not in those of TXB2 and 6-keto-PGF 1 alpha. These results suggest that the PGHS-2 expressed in the pleural exudate cells may be involved in PGE2 formation at the site of inflammation.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Responses of plasma norepinephrine and renin-angiotensin-aldosterone system to dynamic exercise in patients with congestive heart failure.

BACKGROUND: Neurohormonal activation is present and neurohormonal responses to dynamic exercise are altered in congestive heart failure (CHF). Responses of plasma norepinephrine in various degrees of heart failure have been investigated, but the responses of the renin-angiotensin-aldosterone system have not been studied in relation to the severity of CHF. The aim of this study was to determine if the responses of the renin-angiotensin-aldosterone system to exercise are augmented according to the severity of CHF. METHODS AND RESULTS: Ventilatory and neurohormonal responses were assessed in 38 patients with CHF (New York Heart Association class: I, 13 patients; II, 14 patients; III, 11 patients) and 11 normal subjects during symptom-limited cardiopulmonary exercise testing. Plasma norepinephrine, renin activity, angiotensin II, and aldosterone were measured at rest and at peak exercise. The increments in neurohormones were divided by peak oxygen consumption, and these ratios (norepinephrine exercise ratio, plasma renin activity-exercise ratio, angiotensin II-exercise ratio, aldosterone-exercise ratio) were compared among groups. Peak oxygen consumption and anaerobic threshold decreased progressively with the severity of CHF. Neurohormonal profiles at rest showed that plasma norepinephrine levels were significantly higher, and the renin-angiotensin-aldosterone system was augmented only in patients with class III CHF. Neurohormones increased during exercise both in patients with CHF and in normal subjects, but patients with class III CHF had significantly higher plasma renin activity (10.11 +/- 2.32 ng/mL/h), angiotensin II (73.9 +/- 14.2 pg/mL), and aldosterone (265.2 +/- 61.1 pg/mL) than did normal subjects. Plasma renin activity-exercise ratio, angiotensin II-exercise ratio, and aldosterone-exercise ratio in patients with class III CHF were significantly higher compared to normal subjects. This augmentation of the renin-angiotensin-aldosterone system was not observed in class I or II patients. Peak plasma norepinephrine levels were not different among normal subjects and subgroups of CHF patients, but the norepinephrine-exercise ratio was significantly higher in classes II and III CHF compared to normal subjects. CONCLUSIONS: These data suggest that neurohormonal excitation during exercise increases along with the severity of CHF when normalized for peak exercise level.

Aldosterone↗
PubMed1996

Triphenyltin chloride induces glucose intolerance by the suppression of insulin release from hamster pancreatic beta-cells.

UNLABELLED: We performed an intravenous glucose tolerance test (IVGTT) after the administration of triphenyltin chloride (TPTCl-Ad) in hamsters in order to confirm the presence of glucose intolerance and to clarify the pathogenesis of TPTCl-induced glucose intolerance. On the 1st, 2nd, 3rd, 4th and 7th days after TPTCl-Ad or the administration of sesame oil alone as a control, glucose was injected at a dose of 0.05 g glucose/100 g B.W., and then PG, IRI and TG were measured on 0, 1, 2, 3, 5 and 10 min after IVGTT. The TPT concentration in the pancreas was measured by gaschromatography and the morphological findings with a transmission electron microscope were compared between the TPTCl-Ad and the control hamsters. FPG on the 1st and the 2nd days after TPTCl-Ad were significantly higher than those in control, but those on the 4th and the 7th day recovered up to the control level. In contrast, basal IRI levels showed reciprocal results compared to the FPG levels. delta IRI/ delta PG on the 1st day after TPTCl-Ad was significantly reduced compared to the control. Fasting TG on the 1st day after TPTCl-Ad was much higher than the control. TPT-concentration on the 1st day after TPTCl-Ad showed peak values and its concentration gradually decreased. Electron microscopic findings in the pancreas after TPTCl-Ad indicated neither destruction nor lymphocyte infiltration of the pancreas. CONCLUSIONS: The present data suggest that the administration of TPTCl in hamsters induces a functional transient damage on islet cells but not a morphological disorder, which shows an essentially different nature from the change in the pancreas induced by viral infection or by a large amount of streptozotocin.

Animals↗
PubMed1996

Changes in activity of superoxide dismutase in the human endometrium throughout the menstrual cycle and in early pregnancy.

To investigate the possible role of the superoxide radical and its scavenging system in the human endometrium, the immunohistochemical distribution of superoxide dismutase (SOD), activities of SOD and lipid peroxide concentrations were studied in the human endometrium throughout the menstrual cycle and in early pregnancy. The endometrial epithelium showed a positive immunostaining for Cu, Zn-SOD and Mn-SOD throughout the entire menstrual cycle and in early pregnancy. In the stroma, weak immunostaining for Cu,Zn-SOD and moderate immunostaining for Mn-SOD were observed in the predecidual cells in the late secretory phase. Decidual cells in early pregnancy showed strong immunostaining for Cu,Zn-SOD and Mn-SOD. Total SOD activity in the endometrium increased from early proliferative phase to mid-late proliferative phase and further increased in the mid-secretory phase, and decreased in the late secretory phase. The total SOD activity in the endometrium of of early pregnancy was the same level as that in the mid-secretory phase. Cu,Zn-SOD and Mn-SOD activities changed in a similar manner to total SOD activity throughout the menstrual cycle and in early pregnancy. Lipid peroxide concentration in the endometrium increased from early proliferative phase to mid-late proliferative phase and further increased in the late secretory phase. However, lipid peroxide concentration in the endometrium of early pregnancy was the same as that in the mid-secretory phase. These results suggested that the superoxide radical and its scavenging system may play an important role in the regulation of human endometrial function.

Adult↗
PubMed1996

Catecholamines, renin-angiotensin-aldosterone system, and atrial natriuretic peptide at rest and during submaximal exercise in patients with congestive heart failure.

The aim of this study was to determine the responses of plasma catecholamines, renin-angiotensin-aldosterone (RAA) activity, and plasma atrial natriuretic peptide (ANP) to exercise in patients with congestive heart failure (CHF). Cardiac and neurohormonal responses were assessed during submaximal treadmill exercise testing in 23 patients with CHF (New York Heart Association classes I-III) and 13 control subjects (without CHF). Plasma norepinephrine, epinephrine, renin activity (PRA), angiotensin II (ATII), aldosterone, and ANP were measured at rest and immediately after exercise. Exercise duration was shorter in patients with CHF (control, 10.4 +/- 0.9 minute; CHF, 6.2 +/- 0.7 minute; P < 0.01). Heart rate and blood pressure responses were similar except for the smaller peak heart rate (control, 145 +/- 5 beats per minute; CHF, 129 +/- 4 beats per minute; P < 0.05) and higher systolic blood pressure at recovery stage (control, 122 +/- 4 mm Hg; CHF, 142 +/- 4 mm Hg; P < 0.01) in patients with CHF. At rest, plasma norepinephrine levels were insignificantly higher in patients with CHF (control, 110 +/- 10 pg/mL; CHF, 170 +/- 26 pg/mL; P = 0.09), and ANP levels (control, 40 +/- 5 pg/mL; CHF, 94 +/- 17 pg/mL; P < 0.05) and PRA levels (control, 0.77 +/- 0.11 ng/mL/hr; CHF, 4.33 +/- 1.25 ng/mL/hr; P < 0.05) were significantly higher. There were no differences in peak norepinephrine, epinephrine, or ANP between the two groups. Angiotensin II and aldosterone levels were similar between the two groups, although, in patients with CHF, there was a trend toward higher levels of ATII while at rest (control, 12.4 +/- 1.4 pg/mL; CHF, 20.3 +/- 3.3 pg/mL; P = 0.08) and at peak (control, 20.5 +/- 1.8 pg/mL; CHF, 41.0 +/- 9.4 pg/mL; P = 0.10). Peak values of PRA, ATII, and aldosterone positively correlated with respective resting values of PRA (r = 0.88 ng/mL/hr, P < 0.01), ATII (r = 0.63 pg/mL, P < 0.01), and aldosterone (r = 0.99, P < 0.01). Peak norepinephrine and peak ANP also positively correlated with respective resting values of norepinephrine (r = 0.58 pg/mL, P < 0.05) and ANP (r = 0.94, P < 0.01). Analysis of these results showed that patients with CHF had significantly higher levels of PRA and ANP at rest, and a trend toward augmentation in RAA system activity during exercise with less exercise workload. Basal level of neurohormones seemed to be an important determinant for the degree of exercise-induced neurohormonal activation in patients with CHF.

Atrial Natriuretic Factor↗
PubMed1996

Family history-related risk of gastric cancer in Japan: a hospital-based case-control study.

In Japan, there have been a few reports on the familiar factors of gastric cancer (GC) and on the GC risk related to family history (FH) at other cancer sites. We analyzed the association between GC occurrence and a positive FH of cancer of the stomach and of other sites in a hospital-based case-control study. The subjects included cases histologically confirmed as incident cancer of the stomach (n = 136; 86 male and 50 female patients) and sex and age (+/- 1 year)-matched controls. GC risk was high when a subject had a parental history of GC [Mantel-Haenszel odds ratio adjusted for sex and age (OR)=2.3; 95% confidence interval (95% CI):1.1-5.0]. GC risk was almost unity for a cancer FH of any other cancer site, even among closer relatives, suggesting little or no contribution to GC occurrence. The familial occurrence of GC found in this study suggests the existence of a genetic susceptibility to cancer of the stomach. Further, females tended to show higher GC risks than males, when reporting an affected mother (OR=6.0; 95% CI:1.1-31.4 and OR= 1.4; 95% CI:0.4-4.8, respectively), whereas males showed a slightly higher risk than females when reporting an affected father (OR=2.4; 95% CI:0.8-7.5 and OR=2.3; 95% CI:0.4-15.6, respectively). This suggests a possible gender difference in how environmental factors influence GC occurrence. The development of gastric tumors seems to be due to a complex and unknown interaction between environmental and genetic factors.

Aged↗
PubMed1996

Ammonia response to exercise in patients with congestive heart failure.

OBJECTIVE: To assess energy depletion in skeletal muscle in patients with congestive heart failure by measuring blood purine metabolites during exercise and, at the same time, determine the implications of the ammonia response to exercise in these patients. SETTING: Tottori University Hospital, Yonago, Japan. PATIENTS: 49 heart failure patients (New York Heart Association (NYHA) grades I-III) and 16 normal subjects. MAIN OUTCOME MEASURES: Blood lactate, ammonia, and hypoxanthine levels were measured during exercise with expired gas analysis. RESULTS: In normal exercising subjects as well as in each heart failure subgroup, the ammonia threshold was significantly higher than both the lactate threshold [control: 21.8 (SD 5.3) v 17.4 (3.3) ml/kg/min; NYHA class I: 18.9 (3.8) v 15.5 (2.6); class II: 14.8 (2.5) v 12.7 (2.4); class III: 13.5 (2.6) v 11.8 (2.5)] and the ventilatory threshold (P < 0.01). The difference between the ammonia and lactate thresholds was noted in all normal subjects and in all heart failure patients. The ammonia threshold, however, was significantly lower in heart failure patients than in normal subjects and it decreased with increasing NYHA class (P < 0.01). Maximum ammonia levels were lower in the heart failure group and decreased further with higher NYHA classifications [control: 198 (52) mg/dl; NYHA class I: 170 (74); class II: 134 (58); class III: 72 (15); P < 0.01]. There were significant correlations between maximum ammonia values and maximum lactate, oxygen consumption, and hypoxanthine levels (r = 0.74, 0.48, and 0.87, respectively; P < 0.001). CONCLUSIONS: The ammonia threshold may reflect the onset of ATP depletion in exercising skeletal muscles, as opposed to the onset of anaerobic respiration. It seems therefore that energy depletion in skeletal muscles during exercise occurs after attaining the anaerobic threshold. Both aerobic and anaerobic capacities of skeletal muscle are reduced in patients with congestive heart failure.

Adenosine Triphosphate↗
PubMed1996

Length-dependent activation in intact ferret hearts: study of steady-state Ca(2+)-stress-strain interrelations.

We examined the steady-state stress-strain relationships and the steady-state stress-intracellular calcium concentration ([Ca2+]i) relationship in intact ferret hearts and compared these to previously published analogous relationships in skinned and intact muscle. Langendorff-perfused ferret hearts were treated with ryanodine and tetanized by rapid stimulation to create steady-state conditions. [Ca2+]i was measured concurrently by macroinjected aequorin. Over a range of volumes corresponding to strains between 1.0 and 0.75, steady-state stress decreased by 33% when saturating levels of perfusate calcium were used, indicating the degree to which physical factors contribute to the Frank-Starling relationship. The steady-state stress-[Ca2+]i relationship was sigmoidal with a mean Hill coefficient (nH) of 4.91 +/- 0.29 at a strain of 1.0, and the [Ca2+]i required for half-maximal activation (K1/2) was 0.41 +/- 0.03 microM. K1/2 increased and nH decreased with decreasing strains. These results are similar to those observed in intact muscle but differ quantitatively from results obtained in isolated, skinned preparations. Based on these results, we suggest that whole heart function can be related to average sarcomere function without the need for complex models of ventricular structure.

Aequorin↗
PubMed1996

Progesterone inhibits superoxide radical production by mononuclear phagocytes in pseudopregnant rats.

This study investigated the changes in superoxide radical production by mononuclear phagocytes in the corpus luteum (CL) during pseudopregnancy in rats. Activity of superoxide radical production was determined by the conversion of nitro blue tetrazolium (NBT) to blue formazan deposit. Rats received 10 mg NBT via the abdominal aorta on day 3, 7, or 13 of pseudopregnancy and were autopsied 1 min later to prepare the histological sections. The cells with blue formazan deposits (NBT-positive cells) in the CL were scarce on days 3 and 7 of pseudopregnancy and significantly increased on day 13 of pseudo-pregnancy. On the other hand, simultaneous administration of 100 micrograms phorbol 12-myristate 13-acetate, which activates mononuclear phagocytes to produce superoxide radical, significantly increased the numbers of NBT-positive cells in the CL on day 7 of pseudopregnancy, but not in the CL on day 3 or 13 of pseudopregnancy. To study the possibility that superoxide radical production by mononuclear phagocytes is inhibited by progesterone on day 7 of pseudopregnancy, peritoneal mononuclear phagocytes prepared on day 7 or 13 of pseudopregnancy were preincubated with 10, 50, or 100 ng/ml progesterone for 6 h and then stimulated with phorbol 12-myristate 13-acetate. Superoxide radical production was measured by the cytochrome c reduction method. One hundred nanograms per ml progesterone significantly inhibited superoxide radical production by mononuclear phagocytes, and this inhibitory effect of progesterone was significantly blocked by the simultaneous addition of RU486 (10(-7) M). These results suggested that progesterone inhibited superoxide radical production by the mononuclear phagocytes in the CL during midpseudopregnancy in rats.

Animals↗
PubMed1996

Augmented response in plasma atrial natriuretic peptide to dynamic exercise in patients with congestive heart failure.

Neurohormonal activation is present and neurohormonal responses to dynamic exercise are altered in patients with congestive heart failure (CHF). The aim of this study was to determine if the responses of atrial natriuretic peptide (ANP) normalized for peak oxygen consumption (peak VO2) to exercise are augmented in patients with CHF. Ventilatory and ANP responses were assessed in 28 patients with CHF (NYHA classes II: 16, III: 12), 17 patients in NYHA class I, and 14 normal subjects during symptom-limited cardiopulmonary exercise testing. Plasma ANP was measured at rest and immediately after peak exercise. The increase in ANP was divided by peak VO2 and this ratio [ANP-Exercise Ratio: (peak ANP-rest ANP)/peak VO2] was compared among the 3 groups. Peak VO2 (Normal, NYHA I, CHF: 29.9 +/- 1.7, 24.0 +/- 1.3, 17.4 +/- 0.8 ml/min per kg), anaerobic threshold and peak work rate were lower in patients with CHF. The resting ANP level was significantly higher in patients with CHF (Normal, NYHA I, CHF: 35.4 +/- 4.6, 42.9 +/- 5.8, 80.8 +/- 12.9 pg/ml). The ANP level increased during exercise in all 3 groups, and patients with CHF had a significantly higher ANP level than normal subjects and NYHA class I patients (Normal, NYHA I, CHF: 65.3 +/- 10.7, 75.9 +/- 14.4, 141.6 +/- 20.1 pg/ml). The ANP-Exercise Ratio in patients with CHF was significantly higher than those in normal subjects and NYHA class I patients (Normal, NYHA I, CHF: 0.96 +/- 0.26, 1.32 +/- 0.38, 3.59 +/- 0.72). These data suggest that patients with CHF but not those in NYHA class I have an augmented ANP response, as reflected by both absolute ANP levels and by the exercise ratio, which was normalized by the peak exercise level.

Atrial Natriuretic Factor↗
PubMed1996

[Vitrectomy in Coats' disease].

Four eyes of four patients with Coats' disease underwent vitrectomy because of exudative or tractional detachments involving the macula or premacular fibrosis. All cases had gelatinous vitreous and had no complete posterior vitreous detachment. The exudates decreased and the retina reattached after removing vitreous traction and coagulating abnormal vessels with endodiathermy and not removing subretinal fluid in 3 eyes with retinal detachment. In one eye with tractional detachment, retinal breaks were found beneath the proliferative membrane during the initial vitrectomy procedure. This eye needed multiple operations because of recurrent traction by the remaining peripheral vitreous. Exudation into the vitreous and vitreous traction may cause mutual progression in these eyes, and vitrectomy is an effective treatment, although there are difficulties in removing vitreous traction completely.

Adolescent↗
PubMed1995

Role of Kupffer cells in rat liver injury induced by diethyldithiocarbamate.

The hepatotoxicity of diethyldithiocarbamate was examined using an in vitro rat liver slice system. Concentration- and time-dependent losses of intracellular K+ and adenosine triphosphate (ATP) levels were observed in rat liver slices incubated with diethyldithiocarbamate at concentrations between 1 and 10 mM over a 4-h period. Histological study revealed perivenous hepatocyte damage. To examine the involvement of Kupffer cells in diethyldithiocarbamate-induced cytotoxicity, rats were injected intravenously with 10 mg/kg of gadolinium chloride (GdCl3) which diminishes Kupffer cell function. Incubation of liver slice preparations from the GdCl3-treated rats with diethyldithiocarbamate showed marked inhibition of the cytotoxicity induced by diethyldithiocarbamate. Moreover, in vitro addition of manganese-superoxide dismutase, a superoxide anion scavenger, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, also showed potent inhibition. However, dexamethasone, an inhibitor of tumor necrosis factor, and N,N'-diphenyl-p-phenylenediamine (DPPD), an antioxidant, showed partial prevention of cytotoxicity. Formazan deposits formed as a result of nitro blue tetrazolium reduction were found in Kupffer cells at an early stage after diethyldithiocarbamate treatment, while lipid peroxidation occurred after 3 h. Both pretreatment with GdCl3 in vivo and addition of DMSO in vitro prevented the increase in lipid peroxidation within the liver slice preparations induced by diethyldithiocarbamate. These findings suggest that Kupffer cell function may be involved in the pathogenesis of diethyldithiocarbamate hepatotoxicity.

Adenosine Triphosphate↗
PubMed1995

The determination of nitrite and nitrate in human blood plasma by capillary zone electrophoresis.

The determination of nitrite and nitrate in human blood plasma by capillary zone electrophoresis (CZE) is described. Electrophoresis was carried out in a 65 cm long, 75 microns wide silica capillary, using 750 mM sodium chloride containing 5% NICE-Pak OFM Anion-BT (an additive reversing the electroosmotic flow) as running buffer, at a potential of 20 kV, with on-column UV detection at 214 nm. Under these conditions, the two anions migrated in the order of nitrite and nitrate, completely resolved from each other. Forty-one samples of ultrafiltered blood plasma of healthy volunteers were analyzed. The concentrations of nitrite and nitrate were 0.15 +/- 0.07 mg/L and 3.2 +/- 1.6 mg/L (mean +/- SD), respectively, with a linear correlation in the range of 0.1-50 mg/L. The within-day and between-day coefficients of variation (CVs) for nitrite and nitrate were lower than 5% and 8%, respectively. The recovery was 97-114%. The estimated plasma volume needed for each determination was 108 nL.

Electrophoresis, Capillary↗
PubMed1995

Mechanisms of the Frank-Starling phenomena studied in intact hearts.

The impact of ventricular volume on the relationship between intracellular calcium and ventricular pressure under steady-state conditions was determined in intact ferret hearts. The results reveal major quantitative differences and minor qualitative differences between these relations and those previously measured in isolated intact and skinned cardiac muscle. The importance of these differences is discussed within the context of developing a comprehensive mechanistic theory to describe load-dependence of the intact ventricle.

Animals↗