Biomedical subjects

T Kawaguchi

Publications and source records attributed to T Kawaguchi.

At least 37 records · Page 2Linked to original sources

PubMed2002

Dextran-magnetite complex: temperature dependence of its NMR relaxivity.

The NMR relaxivity of proton by dextran-magnetite (DM) complex was examined at temperatures from 20 to 80 degrees C. The decrease in T1 relaxivity with increasing temperature is due to the thermal activation of motion of water molecules in and/or surrounding DM particle. The decrease in magnetization of magnetite core is the secondary effect. The temperature dependence of T1 relaxivity was found to depend on molecular weight of dextran. The motion of dextran chains binding to core may affect the thermal activation of "heavy water" interacted with dextran. The Arrhenius plots of T1 relaxivity showed different slopes at 20-40 degrees C and 50-80 degrees C, while, no change in slope was observed for Fe(NO3)3, CuSO4 and Gd-DTPA solutions.

Journal Article↗

PubMed2002

Association of platelet hyper-aggregability with leukoaraiosis.

OBJECTIVES: To investigate whether there is any relationship between leukoaraiosis and platelet hyper-aggregability of the systemic blood. METHODS: Platelet aggregability, leukoaraiosis, hypertension and hematocrit were assessed in 175 consecutive out-patients attending a regular clinic. Platelet aggregability was estimated by an optical analytical method using two different concentrations each of ADP and collagen (the double ADP method). Hyper-aggregability and non hyper-aggregability were defined with this method. RESULTS: Patients with leukoaraiosis (73 cases) showed a significantly higher incidence of platelet hyper-aggregability than patients with no leukoaraiosis (102 cases) (90.4 vs 56.9%, P=0.000001). Leukoaraiosis was also significantly related to age. Hypertension was a less significant risk factor (P=0.023). CONCLUSIONS: Platelet hyper-aggregability is a significant feature in leukoaraiosis, and appears to be a more important risk factor than hypertension. Normalization of platelet hyper-aggregability might offer an alternative strategy for the prevention of leukoaraiosis in patients with platelet hyper-aggregability, although an interventional study is essential.

Adult↗

PubMed2002

Dual adrenergic control of in vivo choline levels in the mouse major salivary glands.

1. The purpose of this study was to demonstrate that the adrenergic nervous system regulates the in vivo choline levels in the mouse major salivary glands. 2. Methoxamine (alpha1-adrenoceptor agonist, 2.5-20 mg kg-1, s.c.) elevated choline levels dose-dependently and the effect of methoxamine (10 mg kg-1) was completely inhibited by the alpha-adrenoceptor antagonist phentolamine (5 mg kg-1, i.p.) but not by the beta-adrenoceptor antagonist propranolol (3 mg kg-1, i.p.). 3. In contrast, isoprenaline (beta-adrenoceptor agonist 0.25-20 mg kg-1, s.c.) lowered choline levels and the effect of isoprenaline (2 mg kg-1) was inhibited by propranolol, but not by phentolamine. 4 Noradrenaline (1-4 mg kg-1, s.c.) manifested both the alpha- and beta-adrenergic actions depending on its dose. Noradrenaline at 1-2 mg kg-1, lowered choline levels and the effect of noradrenaline (1 mg kg-1) was inhibited by propranolol, but not by phentolamine. On the other hand, noradrenaline (4 mg kg-1) elevated choline levels and the effect was blocked by phentolamine, but not by propranolol. 5. Tyramine (5-80 mg kg-1, s.c.) elicited the release of noradrenaline from sympathetic nerve terminals and induced essentially the same effects on the choline levels as noradrenaline. Tyramine (10 mg kg-1) lowered choline levels and the effect was inhibited by propranolol, but not by phentolamine. However, tyramine (80 mg kg-1) elevated choline levels and the effect was inhibited by phentolamine, but not by propranolol. 6. These results suggest that choline levels in the salivary glands may be under separate alpha- and beta-adrenergic control and suggest a possibility that the neurotransmitter noradrenaline released for sympathetic nerve terminals can manage the dual control of choline levels in some autonomic organs in a characteristic dose-dependent manner.

Adrenergic Agonists↗

PubMed2001

Glucose and cAMP regulate the L-type pyruvate kinase gene by phosphorylation/dephosphorylation of the carbohydrate response element binding protein.

Recently we purified and identified a previously uncharacterized transcription factor from rat liver binding to the carbohydrate responsive element of the L-type pyruvate kinase (L-PK) gene. This factor was named carbohydrate responsive element binding protein (ChREBP). ChREBP, essential for L-PK gene transcription, is activated by high glucose and inhibited by cAMP. Here, we demonstrated that (i) nuclear localization signal and basic helix-loop-helix/leucine-zipper domains of ChREBP were essential for the transcription, and (ii) these domains were the targets of regulation by cAMP and glucose. Among three cAMP-dependent protein kinase phosphorylation sites, Ser(196) and Thr(666) were the target sites. Phosphorylation of the former resulted in inactivation of nuclear import, and that of the latter resulted in loss of the DNA-binding activity and L-PK transcription. On the other hand, glucose activated the nuclear import by dephosphorylation of Ser(196) in the cytoplasm and also stimulated the DNA-binding activity by dephosphorylation of Thr(666) in the nucleus. These results thus reveal mechanisms for regulation of ChREBP and the L-PK transcription by excess carbohydrate and cAMP.

Amino Acid Sequence↗

PubMed2001

Regulation of energy metabolism in macrophages during hypoxia. Roles of fructose 2,6-bisphosphate and ribose 1,5-bisphosphate.

Macrophages can adapt to the absence of oxygen by switching to anaerobic glycolysis. In this study, we investigated (a) the roles of fructose 2,6-bisphosphate (Fru-2,6-P2) and ribose 1,5-bisphosphate (Rib-1,5-P2), potent activators of phosphofructokinase, (b) the enzymes responsible for the synthesis of Rib-1,5-P2, and (c) the mechanisms of regulation of these enzymes in H36.12j macrophages during the initial phase of hypoxia. Within 1 min after initiating hypoxia, glycolysis was activated through activation of phosphofructokinase. Over the same period, Fru-2,6-P2 decreased 50% and recovered completely upon reoxygenation. Similar changes in cAMP levels were observed. In contrast, the Rib-1,5-P2 concentration rapidly increased to a maximum level of 8.0 +/- 0.9 nmol/g cell 30 s after hypoxia. Thus, Rib-1,5-P2 was the major factor increasing the rate of glycolysis during the initial phase of hypoxia. Moreover, we found that Rib-1,5-P2 was synthesized by two steps: the ribose-phosphate pyrophosphokinase (5-phosphoribosyl-1-pyrophosphate synthetase; PRPP synthetase) reaction (EC ) catalyzing the reaction, Rib-5-P + ATP --> PRPP + AMP and a new enzyme, "PRPP pyrophosphatase" catalyzing the reaction, PRPP --> Rib-1,5-P2 + P(i). Both PRPP synthetase and PRPP pyrophosphatase were significantly activated 30 s after hypoxia. Pretreatment with 1-octadecyl-2-methyl-rac-glycero-3-phosphocholine and calphostin C prevented the activation of ribose PRPP synthetase and PRPP pyrophosphatase as well as increase in Rib-1,5-P2 and activation of phosphofructokinase 30 s after hypoxia. These data suggest that the activation of the above enzymes was mediated by protein kinase C acting via activation of phosphatidylinositol specific phospholipase C in the macrophages during hypoxia.

Adenosine Monophosphate↗

PubMed2001

Endotoxin increases paracellular permeability of isolated rat hepatocyte couplets.

Hyperbilirubinemia is frequently associated with endotoxemia. Regurgitation of bile constituents including bilirubin into the sinusoidal space is prevented by tight junctions which maintain paracellular permeability between hepatocytes. To investigate the mechanism of endotoxin-associated hyperbilirubinemia, we have studied the changes in paracellular permeability of primary hepatocyte couplets treated with endotoxin. In addition, we examined the effects of ursodeoxycholic acid (UDCA), which has been widely used for various liver diseases, on endotoxin-associated changes in paracellular permeability. The paracellular permeability of hepatocyte couplets was evaluated by paracellular penetration of fluorescein isothiocyanate (FITC)-dextran with molecular weights of 3, 10 and 70K using confocal laser scanning microscopy. Endotoxin increased the paracellular penetration of FITC-dextran 3 and 10K. These changes were prevented by treatment with UDCA. There was little paracellular penetration of FITC-dextran 70K under any conditions. These results suggested that endotoxin increased the paracellular permeability of hepatocyte couplets and these changes were prevented by treatment with UDCA. Furthermore, bile regurgitation through the paracellular route is involved in endotoxin-associated hyperbilirubinemia, and UDCA might be a potential therapeutic agent for endotoxin-associated hyperbilirubinemia.

Journal Article↗

PubMed2001

Somatic mutations of the PTEN/NMAC1 gene associated with frequent chromosomal loss detected using comparative genomic hybridization in endometrial cancer.

OBJECTIVES: We analyzed the mutational status of the transforming growth factor-beta type II receptor (TGF beta RII), BAX, and PTEN/MMAC1 genes as well as microsatellite instability (MI) in 29 consecutive cases of endometrial carcinoma operated on at the Cancer Institute Hospital (Tokyo, Japan). To identify chromosomal loss associated with significant somatic mutations, we conducted comparative genomic hybridization (CGH) analysis. METHODS: We conducted a direct sequence for mutational analysis of these genes. To examine copy number loss at the chromosomal regions bearing these genes, we used CGH analysis. CGH analysis may provides a genome-wide overview about tumor-associated genomic imbalances. RESULTS: Among nine tumors that showed the MI+ phenotype, four (44%) demonstrated a significant mutation with a definite amino acid change in the PTEN/MMAC1 gene. CGH analysis demonstrated that all four tumors (100%) showed chromosomal copy number loss around the locus of this gene, whereas four (57%) of seven tumors with PTEN/MMAC1 mutations showed chromosomal loss or double mutations in MI- carcinomas. The role of TGF beta RII and BAX genes is limited as a target gene of MI+ phenotype in endometrial cancer, because several mutations of these genes were detected but a chromosomal loss was demonstrated by CGH in only one tumor in MI+ endometrial cancers with mutation. CONCLUSIONS: This report reveals, by using CGH, that most MI+ endometrial cancers with PTEN/MMAC1 mutations as well as MI- tumors showed inactivation of both alleles of this gene, which strongly suggested the involvement of this gene in carcinogenesis.

Adenocarcinoma↗

PubMed2001

Lung volume reduction surgery and nutritional status in patients with severe emphysema.

OBJECTIVE: We studied the short-term effect of lung volume reduction surgery on nutritional status including body composition and the relationship between preoperative nutritional status and postoperative morbidity. METHODS: Subjects were 28 patients with emphysema who underwent bilateral thoracoscopic lung volume reduction surgery (23 simultaneously, 5 staged). Functional tests, body weight, and body composition were measured before and 6 months after surgery. Fat-free mass and fat mass were assessed by bioelectrical impedance analysis. RESULTS: FEV1.0 improved 35.2% following surgery and maximal oxygen uptake 23.8%. Body weight and fat-free mass increased significantly after surgery, while fat mass was unchanged. Of the 23 undergoing simultaneous bilateral lung volume reduction surgery, 8 had major complications-3 required additional surgery to close air leaks, 3 required mechanical ventilation (> 72 hrs), and 2 developed postoperative infection. The preoperative percentage of ideal body weight and fat-free mass was significantly higher among patients without major complications. CONCLUSIONS: Bilateral lung volume reduction surgery increases fat-free mass and provides functional improvement for underweight patients with severe emphysema. We found fat-free mass and body weight to be good predictors of unacceptable postoperative complications following bilateral lung volume reduction surgery.

Aged↗

PubMed2001

Treatment of chronic aortic dissection by transluminal endovascular stent-graft placement: preliminary results.

PURPOSE: To investigate efficacy of stent-graft repair for the treatment of patients with chronic aortic dissection. MATERIALS AND METHODS: Fifteen patients with chronic aortic dissection were treated with endovascular stent-grafts. Entry tears were located in the descending thoracic aorta in all patients. The mean maximum diameter of the descending thoracic aorta was 47 mm +/- 8. The mean diameter of the true lumen at the same level was 20 mm +/- 5. The mean interval between diagnosis and stent-graft procedure was 32 months +/- 91. Stent-grafts were fabricated from expanded polytetrafluoroethylene and Z-stents. RESULTS: Stent-grafts were placed successfully in all patients. Two stent-grafts were required in one patient. Entry closure and thrombosis of the false lumen of the descending thoracic aorta were also achieved in all patients. No procedure-related complications were observed except for postimplantation syndrome, including fever and leukocytosis. The diameter of the true lumen was significantly increased (mean, 31 mm +/- 6) at the level of the descending thoracic aorta (P <.01) and the diameter of the aorta was significantly decreased (mean, 44 mm +/- 8) at the same level (P <.01). There were no deaths and no instances of aortic rupture during the subsequent average follow-up period of 24 months. Secondary stent-graft procedures were required to treat the abdominal component of dissection during follow-up in one patient. CONCLUSIONS: Stent-graft repair of chronic aortic dissection is a safe and effective method and may be an alternative to surgical graft replacement in selected patients. However, further evaluation is mandatory before this method is widely employed.

Adult↗

PubMed2001

Dextran-magnetite complex: conformation of dextran chains and stability of solution.

Three kinds of dextran-magnetite (DM) complexes were prepared using alkali-treated dextrans with molecular weights of 1900, 4200 and 9600, respectively. The number of dextrans binding to a magnetite core was determined. The number was proportional to the area of core surface and the area occupied by a dextran was 2.5 nm2 for molecular weight of 1900, 2.8 for 4200 and 3.8 for 9600. The binding of dextrans to core may be conditioned by the conformation of dextran chains in water (possibly by the steric hindrance between dextrans covering core). Stability of the DM solution was examined at 80 degrees C. Aggregation and/or precipitation of DM particles were observed within two weeks. The stability of DM solution was found to increase with increasing molecular weight of dextran. The dissociation of dextran from the core may cause the aggregation and subsequent precipitation of DM particles (the dissociation constant at 20 degrees C, 3.7 x 10(-6) for a molecular weight of 1900 and 5.4 x 10(-7) for 9600).

Journal Article↗

PubMed2001

A mutation of the Wilson disease protein, ATP7B, is degraded in the proteasomes and forms protein aggregates.

BACKGROUND & AIMS: Wilson disease is a genetic disorder characterized by the accumulation of copper in the body as a result of a defect of copper excretion from hepatocytes. The intracellular localization of the Wilson disease gene product, ATP7B, was recently identified as the late endosomes. Various mutations have been documented in patients with Wilson disease. The clinical manifestations vary greatly among the patients; however, there is little information on the genotype-phenotype correlation. METHODS: We investigated the distribution of a common ATP7B mutant His1069Gln and a mutant Asp1270Ser by expressing the mutants tagged with green fluorescent protein in Huh7 and HEK293 cells. Intracellular organelles were visualized by fluorescence microscopy. RESULTS: Although the wild-type ATP7B and Asp1270Ser mutant localized in the late endosomes, His1069Gln mutant did not locate in the late endosomes and was degraded by the proteasomes in the cytoplasm. Furthermore, His1069Gln formed aggresomes composed of the degradates and intermediate filaments at the microtubule-organizing center. These aggresomes were similar to Mallory bodies on electron microscopy. CONCLUSIONS: The different protein properties of ATP7B mutants may explain the variety of clinical spectrums in patients with Wilson disease.

Acetylcysteine↗

PubMed2001

Involvement of p21(WAF1/Cip1), p27(Kip1), and p18(INK4c) in troglitazone-induced cell-cycle arrest in human hepatoma cell lines.

Peroxisome proliferator-activated receptor gamma (PPARgamma) regulates cell growth and differentiation. Recent evidence has suggested that PPARgamma ligands had anti-tumor effects through inhibiting cell growth and inducing cell differentiation in several types of malignant neoplasm. In the present study, we investigated: 1) the expression of PPARgamma in both human hepatoma cell lines and 5 resected human hepatocellular carcinoma (HCC) tissues; 2) the growth-inhibitory effect of troglitazone, a PPARgamma ligand, on those hepatoma cells; and 3) the molecular mechanisms of troglitazone-induced cell-cycle arrest. Five hepatoma cell lines, HLF, HuH-7, HAK-1A, HAK-1B, and HAK-5, were used. The mRNA expression levels of PPARgamma, p21(WAF1/Cip1), and p27(Kip1) were determined by real-time quantitative reverse transcription-polymerase chain reaction. The expression of cell cycle-regulating proteins, such as p21, p27, p18(INK4c), cyclin E, and pRb, was examined using Western blotting. PPARgamma was constitutively expressed in all the cell lines and the HCC tissues used in this study. A cytostatic effect of troglitazone was found in those cell lines, and this inhibition of cell growth was dosage-dependent. G0/G1 arrest was apparently demonstrated in flow cytometric analysis in HLF, HAK-1A, HAK-1B, and HAK-5, all of which showed an increased expression of p21 protein. However, HuH-7, lacking p21 protein expression, did not demonstrate clear arrest in the cell-cycle analysis. HLF, which was deficient in the protein product of the retinoblastoma tumor-suppressor gene (pRb), responded most profoundly to troglitazone, showing an increased expression in not only p21, but also in p27 and in p18. These findings suggested that p21, p27, and p18 might be involved in troglitazone-induced cell-cycle arrest in human hepatoma cells.

CDC2-CDC28 Kinases↗

PubMed2001

Alterations in tight junctions differ between primary biliary cirrhosis and primary sclerosing cholangitis.

Tight junctions (TJ) of biliary epithelial cells (BEC) and hepatocytes prevent bile regurgitation from the biliary tract. Alterations in these TJs may participate in chronic cholestatic liver diseases such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). We examined the localization of 2 TJ proteins, ZO-1 and 7H6, in these diseases. Frozen sections from livers of PBC, PSC, extrahepatic cholestasis (Ex-C), and hepatitis C-associated cirrhosis (LC-C), as well as histologically normal livers, were processed for double-fluorescence immunohistochemistry. In controls and cirrhosis, 7H6 and ZO-1 colocalized surrounding the luminal space of the bile ducts and outlined the bile canalicular spaces between hepatocytes. In untreated PBC, immunostaining for ZO-1 in BEC of bile ducts 40 to 80 microm in diameter was preserved, but that for 7H6 was diminished to absent. In PBC treated with ursodeoxycholic acid (UDCA), immunostaining for 7H6 was well preserved. In PSC as well as in Ex-C, immunostaining for both 7H6 and ZO-1 was well preserved in bile ducts. In hepatocytes, ZO-1 showed preserved immunoreactivity, but immunostaining for 7H6 frequently disappeared. The percentage of bile ducts with immunostaining for 7H6 in all bile ducts with immunostaining for ZO-1 was significantly reduced in PBC compared with that in control, LC-C, Ex-C, and PSC (all P <.0001). Substantial alteration in the TJ protein occurs predominantly in bile ducts in PBC and in hepatocytes in PSC, suggesting increased paracellular permeability along different paracellular routes for bile regurgitation in these chronic cholestatic liver diseases.

Adolescent↗

PubMed2001

Autocrine motility factor enhances hepatoma cell invasion across the basement membrane through activation of beta1 integrins.

Autocrine motility factor/phosphohexose isomerase (AMF/PHI) is a cytokine that is linked to tumor invasion and metastasis. In hepatocellular carcinoma (HCC) tissues, hepatoma cells produce AMF/PHI and its receptor, Mr 78,000 glycoprotein (gp78), is strongly detected in hepatoma cells invading into the stroma and tumor thrombi in the portal vein. Here, we investigated the mechanism of hepatoma cell invasion through Matrigel induced by AMF/PHI using 3 hepatoma cell lines. Production of AMF/PHI, phosphorylation of MEK1/2, and Rho activity were investigated by immunoblotting. Expression of AMF/PHI and gp78 was observed by confocal fluorescence microscopy. The influence of AMF/PHI on activated integrin beta1 subunit expression was evaluated by flow cytometry. Changes in invasion, adhesion, and motility induced by AMF/PHI were evaluated using chemoinvasion, adhesion, and phagokinetic track motility assays. The effect of AMF/PHI on matrix metalloproteinase (MMP) secretion was evaluated by gelatin zymography. Hepatoma cells produced AMF/PHI and expressed gp78. Although AMF/PHI was ubiquitously detected, gp78 was strongly expressed in migrating cells. AMF/PHI induced up-regulation of activated integrin beta1 subunit expression. AMF/PHI stimulated hepatoma cell invasion through Matrigel, and stimulated the adhesion, motility, and MMP-2 secretion of hepatoma cells. The latter effects were suppressed by the function-blocking antibody for integrin beta1 subunit. AMF/PHI also enhanced Rho activity and the phosphorylation of MEK1 and MEK 2. Our results indicate that AMF/PHI enhances hepatoma cell invasion through Matrigel in an autocrine manner by stimulating the adhesion, motility, and MMP-2 secretion of these cells through activation of beta1 integrins.

Basement Membrane↗

PubMed2001

Classification of venous ischaemia with MRI.

PURPOSE: Venous ischaemia is diagnosed by angiography and estimated with SPECT and PET. But venous ischaemia presents different features due to aetiology, type of onset, time course and collateral circulation. The purpose of this study was to analyse and to classify VI with MRI. METHODS: An analysis of 12 cases of dural arteriovenous fistula (DAVF) with venous ischaemia, 4 cases of sinus thrombosis, and a case of cortical venous thrombosis was performed. Venous ischaemia is classified with MRI as Type 1: no abnormality, Type 2: T2WI showed high signal intensity area and Gd-MRI showed no enhancement, Type 3: T2WI showed high signal intensity area and Gd-MRI showed enhancement, Type 4: venous infarction or haemorrhage. RESULTS: Type 1 was 8 cases. Type 2 was 3 cases and indicated cytotoxic oedema. Type 3 was 2 cases and indicated vasogenic oedema because of the destruction of blood brain barrier. Type 4 was 4 cases. CONCLUSIONS: The classification may be a useful indicator of severity of venous ischaemia and treatment.

Adult↗

PubMed2001

The effect of nutritional status on morbidity in COPD patients undergoing bilateral lung reduction surgery.

BACKGROUND: Although candidates for lung reduction surgery (LRS) include malnourished patients with severe chronic obstructive pulmonary disease (COPD), the impact of preoperative nutritional status on surgical outcome has not been clearly elucidated. METHODS: We investigated the relationship between preoperative nutritional status and postoperative morbidity in 23 consecutive patients undergoing LRS. The percentage of ideal body weight (%IBW) and body mass index (BMI) were calculated, and fat-free mass (FFM) and fat mass (FM) were measured using a bioelectrical impedance analyzer. FFM and FM were expressed as height-normalized indices, FFM index [FFM (kg)/height (m)(2), or FFMI] and FM index [FM (kg)/height (m)(2), or FMI]. Serum levels of total protein and albumin were also determined. RESULTS: 8 patients had major complications. Preoperative %IBW and FFMI were significantly lower among patients with major complications, while no significant differences were observed in pulmonary function, FMI or serum protein. The complication rate was significantly higher among patients with low FFMI (FFMI < or = 16) but not with low %IBW or BMI. CONCLUSION: These results suggest that FFM depletion is an excellent predictor of unacceptable postoperative complication following LRS.

Aged↗

PubMed2001

Aneurysmal degeneration of the aorta after stent-graft repair of acute aortic dissection.

PURPOSE: Stent-graft repair of acute aortic dissection has only recently begun, and the true efficacy and safety of this technique have not yet been clarified. In this report, we describe a significant, previously unreported complication following stent-graft repair of acute aortic dissection. MATERIALS AND METHODS: Fourteen patients with acute aortic dissection underwent stent-graft repair. All of the entry tears were located in the descending thoracic aorta. Five patients had type A aortic dissection, and nine patients had type B aortic dissection. The entry tears were closed with stent-grafts, which were fabricated from expanded polytetrafluoroethylene and Z-stents. RESULTS: Stent-graft placement was successfully performed without any complications in all patients. Entry closure was achieved in 13 (93%) of 14 patients. The mean follow-up period was 18 months (range, 9 days to 36 months). During this period, four patients had saccular aneurysms in the proximal descending thoracic aorta. A saccular aneurysm was noted during a mean follow-up period of 63 days (range, 38-99 days). Two of these patients were treated with stent-grafts. Conventional surgical repair is planned in one patient. The other patient is being treated with conservative management. CONCLUSIONS: Stent-graft repair is a technically feasible and effective method for the treatment of acute aortic dissection in selected patients. However, careful follow-up is mandatory to check for the development of saccular aneurysms.

Aged↗

PubMed2001

Orthostatic hypotension in elderly persons during passive standing: a comparison with young persons.

BACKGROUND: The present study was aimed at clarifying the mechanism of orthostatic hypotension (OH) that occurs in elderly persons and at investigating assisting methods to prevent OH by evaluating changes in autonomic nervous system (ANS) activity and cerebral circulation of elderly persons when engaged in passive standing. METHODS: Eight elderly volunteers and 9 young volunteers gave informed consent to participate in the study. Two experimental conditions were established: (i) "active standing," in which the subjects stood on their own with guidance from an assistant, and (ii) "passive standing," in which the subjects were placed in a standing position completely by an assistant. ANS was determined before and after standing by measuring the heart rate variability. The reaction of the ANS was evaluated on the basis of low-frequency power (LF: 0.05--0.15 Hz) and high-frequency power (HF: 0.15--0.4 Hz), which were separated from the R-R interval data by power spectral analysis using the fast Fourier transformation. Cerebral perfusion was measured over the right frontal region using a near-infrared spectroscopy cerebral oxygen monitor. RESULTS: The main findings were: (i) Transient decreases in blood pressure occurred immediately after standing in both the young and elderly subjects. (ii) The LF:HF ratio increased significantly ( p <.05) immediately after active standing in the young subjects, whereas this ratio increased in the elderly subjects after some delay. (iii) The LF:HF ratio increased significantly ( p <.01) immediately after passive standing in the young subjects, whereas this ratio decreased significantly ( p <.05) in the elderly subjects. (iv) In the elderly subjects, the total hemoglobin (HbT) and oxyhemoglobin showed the greatest decrease during the 15-second period after standing. The maximum changes in the HbT with passive standing differed significantly ( p <.01) from those observed during active standing. CONCLUSIONS: Our findings emphasize the need to devise bioengineered means that allow elderly persons to exert themselves, to maintain or improve muscle contractility and ANS function, while providing minimum assistance for standing.

Adult↗