Atypical true hermaphroditism with a mosaic 45,X/46,X,dic(Y) (q11.2) karyotype.
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Adult↗
Biomedical subjects
S Satoh
Publications and source records attributed to S Satoh.
[Effects of prophylactic antibiotic agent on interleukin-6 level in open chest surgery--comparison between imipenem and flomoxef].
Cytokines are known to increase in the patients subjected to open chest surgery. Those patients are usually administered with antibiotic agents for prophylaxis, while some of antibiotic agents might yield significantly higher level of cytokines than other agents especially in patients suffering from severe infections. It is believed that imipenem may yield lower interleukin-6 (IL6) level than cephem antibiotics. To study whether such difference could be observed in the patients who show no sign of severe infections, a total of 13 patients underwent scheduled open chest surgery were allocated at random into two groups, the imipenem-group and the flomoxef-group. The cytokine levels of the patients in the two groups were compared, while the prophylactic administration of imipenem or flomoxef. In both groups, IL6 increased immediately after the operation while endotoxin remained unchanged. Thereafter IL6 decreased gradually in both groups, however, the decrease of IL6 in the imipenem-group was faster and greater than the flomoxef-group resulting in the significantly lower level of IL6 on the 4th day after operation. One week after the operation, there existed no difference in the IL6 levels between these two groups. In conclusion, it was suggested that, depending on the choice of a prophylactic antibiotic agent, some invasive burden could be added to those patients underwent open chest surgery, a certain number of whom would develop severe infection.
Adult↗
Effects of C-type natriuretic peptide on renal vasoconstriction in dogs.
Intrarenal arterial infusion of C-type natriuretic peptide (CNP, 50 ng/kg per min) increased urine flow rate without affecting glomerular filtration rate. Intrarenal arterial bolus injection of angiotensin II (25, 50 and 100 ng) or of norepinephrine (0.25, 0.5 and 1.0 microg) reduced renal blood flow. The blood flow response induced by angiotensin II was slightly attenuated but the response induced by norepinephrine was unaffected during CNP infusion. These results suggest that exogenous CNP, even at the pharmacological dose that can induce diuresis, has little effect on the canine renal vasculature.
Angiotensin II↗
Humoral injury in porcine livers perfused with human whole blood.
BACKGROUND: We investigated the influence of humoral injury during xenoperfusion of porcine livers by human blood. METHODS: The porcine livers were perfused under physiological conditions for 9 hr. The perfusates consisted of porcine whole blood in group 1, human whole blood in group 2, and human whole blood with soluble complement receptor type 1 (300 microg/ml) in group 3. RESULTS: Liver enzyme release and serum hemoglobin in group 2 increased significantly after 3 hr of xenoperfusion, compared with those in group 1 and group 3 (P<0.05). Severe histological damage with minimal cellular infiltration was observed in group 2 after 6 hr of xenoperfusion, but was present only at trace levels in group 1 and group 3. In group 2, von Willebrand factor, a possible target of natural antibodies, was induced on sinusoidal endothelial cells after 3 hr of xenoperfusion, correlating with diffuse deposition of human IgM and membrane attack complex. In group 3, von Willebrand factor, human IgM, and membrane attack complex staining in the intralobular region were present at trace levels. In group 3, the indocyanine green removal capacity, representing hepatocyte function, was significantly higher than in group 2 (P<0.05). CONCLUSIONS: Based on these results, we suggest that humoral injury is a major cause of liver damage during liver xenoperfusion. The pattern of humoral injury in xenoperfused livers may be attributed to anatomical features of the liver and unique responses of sinusoidal endothelial cells to xenoperfusion.
Animals↗
Role of insulin receptor substrate-1 and pp60 in the regulation of insulin-induced glucose transport and GLUT4 translocation in primary adipocytes.
In muscle and fat, glucose transport occurs through the translocation of GLUT4 from an intracellular pool to the cell surface. Phosphatidylinositol (PI) 3-kinase has been shown to be required in this process. Insulin is thought to activate this enzyme by stimulating its association with tyrosine-phosphorylated proteins such as insulin receptor substrate (IRS)-1, IRS-2, Grb2-associated binder-1, and pp60. To study the role of these endogenous substrates in glucose transport, we analyzed adipocytes from IRS-1 null mice that we previously generated (Tamemoto, H., Kadowaki, T., Tobe, K., Yagi, T., Sakura, H., Hayakawa, T., Terauchi, Y., Ueki, K., Kaburagi, Y., Satoh, S., Sekihara, H., Yoshioka, S., Horikoshi, H., Furuta, Y. , Ikawa, Y., Kasuga, M., Yazaki Y., and Aizawa S. (1994) Nature 372, 182-186). In adipocytes from these mice, we showed that: 1) insulin-induced PI 3-kinase activity in the antiphosphotyrosine immunoprecipitates was 54% of wild-type; 2) pp60 was the major tyrosine-phosphorylated protein that associated with PI 3-kinase, whereas tyrosine phosphorylaion of IRS-2 as well as its association with this enzyme was almost undetectable; and 3) glucose transport and GLUT4 translocation at maximal insulin stimulation were decreased to 52 and 68% of those from wild-type. These data suggest that both IRS-1 and pp60 play a major role in insulin-induced glucose transport in adipocytes, and that pp60 is predominantly involved in regulating this process in the absence of IRS-1.
Adipocytes↗
Pharmacological characterization of a novel, orally active, nonpeptide bradykinin B2 receptor antagonist, FR167344.
To investigate the pathophysiological role of bradykinin and to develop a drug for inflammatory diseases, we discovered an orally active, nonpeptide bradykinin B2 receptor antagonist, FR167344, N-[N-[3-[(3-bromo-2-methylimidazo[1,2-a]pyridin-8-yl)oxymethyl]-2, 4dichlorophenyl]-N-methylaminocarbonylmethyl]-4-(dimethyl aminocarbonyl) cinnamylamide hydrochloride. This compound competitively displaced [3H]bradykinin binding to bradykinin B2 receptors present in guinea-pig ileum membrane with an IC50 value of 6.6 X 10(-10) M. In isolated guinea-pig ileum preparations, it also antagonized bradykinin-induced contraction with a pA2 value of 9.3. In human lung fibroblast IMR-90 cells, FR167344 displaced [3H]bradykinin binding to human bradykinin B2 receptors with an IC50 value of 1.3 X 10(-8) M, but not [3H]des-Arg10-kallidin binding to human bradykinin B1 receptors. In vivo, oral administration of FR167344 inhibited bradykinin-induced bronchoconstriction in guinea pigs and the bradykinin-induced hypotensive response for 6 h in rats. These results show that FR167344 is a potent, selective, orally active and long acting bradykinin B2 receptor antagonist.
Animals↗
Anterior correction of thoracic scoliosis with Kaneda anterior spinal system. A preliminary report.
STUDY DESIGN: Analysis of the clinical results of 20 patients with thoracic scoliosis treated by anterior procedure with Kaneda anterior spinal system. OBJECTIVES: To evaluate the efficacy of the anterior surgical correction procedure with a new anterior instrumentation in thoracic scoliosis. SUMMARY OF BACKGROUND DATA: Posterior correction and fusion with posterior instrumentation has been a main component of the surgical management of thoracic scoliosis. However, to the best of the authors' knowledge, no clinical results of anterior instrumentation surgery for thoracic scoliosis have been published in the English literature. METHODS: Anterior correction and fusion using Kaneda anterior spinal system was performed in 20 patients with thoracic scoliosis (3 patients with King Type II curve, 13 with Type III, and 4 with Type IV). The average follow-up was 3 years, with a range of 2 years, 3 months to 4 years, 1 month. There were 1B patients with idiopathic scoliosis (13 adolescents and 5 adults) and 2 patients with a single thoracic curve caused by other etiologies. All patients had correction of scoliosis by fusion within the major thoracic curve. Radiographic evaluations were performed to analyze frontal, sagittal, and rotational deformities of the spine. RESULTS: The average correction rate of scoliosis was 71%. Above the instrumented levels, the correction rate was 75%. Preoperative kyphosis of the instrumented levels of 7 degrees was corrected to 14 degrees of kyphosis. The trunk shift was improved from 17 mm before surgery to 9 mm at final follow-up evaluation. The average improvement of the tilt-angle in the lower and vertebra of fusion was 81%, and was 83% in the stable vertebra. Apical vertebral rotation showed correction rate of 15% in patients without performing resection of the rib head joints and rod rotation maneuver (n = 6). However, the correction rate was improved to 58% after introduction of the technique discussed (n = 14). The angle of tangential rib deformity (rib hump) showed a correction rate of 50%. There was 1.2 degrees of frontal plane and 1.0 degree of sagittal plane correction loss within the instrumented area at final follow-up evaluation. At final follow-up, nonunion at the uppermost segment of the fusion range developed in one patient, and decompensation in the lumbar spine was observed in one patient with Type II curve. CONCLUSIONS: Anterior correction with Kaneda anterior spinal system provides excellent correction of the frontal curvature and sagittal alignment by fusing within the range of the major curve, without a significant loss of correction and implant failure. Rigid rotational deformity of the thoracic scoliosis is effectively corrected by resection of the rib head joints and rod rotation maneuver. However, too much correction of the thoracic curve should be avoided, to prevent decompensation of the lumbar curve, especially in Type II curves.
Adolescent↗
Apamin-sensitive SK(Ca) channels modulate adrenal catecholamine release in anesthetized dogs.
We investigated the role of high conductance (BK(Ca)) and small conductance Ca2(+)-activated K+ (SK(Ca)) channels in adrenal catecholamine release in response to splanchnic nerve stimulation, acetylcholine, the nicotinic receptor stimulant 1,1-dimethyl-4-phenyl-piperazinium (DMPP), and muscarine in anesthetized dogs. The selective SK(Ca) channel blocker apamin and the selective BK(Ca) channel blocker charybdotoxin were infused into the adrenal gland through the phrenicoabdominal artery, and the cholinergic agonists were injected into the same artery. Splanchnic nerve stimulation (1, 2, 3 and 10 Hz), acetylcholine (0.75, 1.5 and 3 microg), DMPP (0.1, 0.2 and 0.4 microg) and muscarine (0.5, 1 and 2 microg) produced frequency- or dose-dependent increases in catecholamine output as measured in adrenal venous blood. Apamin infusion (1, 3 and 10 ng/min) enhanced the acetylcholine-, DMPP- and muscarine-induced increases in catecholamine output in a dose-dependent manner, but it did not affect the splanchnic nerve stimulation-induced catecholamine response. Charybdotoxin infusion (10, 30 and 100 ng/min) did not affect the increases in catecholamine output induced by the agonists and splanchnic nerve stimulation. Neither apamin nor charybdotoxin affected basal catecholamine output. These results suggest that apamin-sensitive SK(Ca) channels located in adrenal medullary cells may play an inhibitory role in the regulation of adrenal catecholamine release mediated by extrasynaptic nicotinic and muscarinic receptors.
Acetylcholine↗
Can twin fetuses be numerically clustered characterizing fetal cardiovascular system function?
To clarify whether twin fetuses could be clustered quantitatively observing in utero cardiovascular system function, 71 twin-paired fetuses between 24 and 40 weeks' gestation were subjected. Cluster analysis was performed using four variables; end-diastolic dimension and fractional shortening in the right ventricle (EDD, FS), resistance index in the umbilical artery (RIUA) and urine production rate (UPR). Three different groups were revealed. In Cluster 1 (C1), larger fetuses showed a significant increase in both EDD and UPR, and a significant decrease in FS, while smaller fetuses had a significant increase in RIUA and a decrease in UPR. In Cluster 2 (C2), smaller fetuses showed a significant increase in RIUA. Cluster 3 (C3) showed no significant deviations in any variable when referring to singleton pregnancies. C1 had a higher perinatal mortality rate than either C2 or C3, with the cause of death being cardiac failure in larger fetuses and renal failure in smaller fetuses. The frequencies of discordancy, hemoglobin difference above 5 g/dl and monochorionic placenta in C1 were also higher than fetuses in C3. C2 also showed higher frequencies of discordancy and small-for-gestational age than C3 fetuses. In C2 and C3, respiratory insufficiency was found to be the cause of neonatal death. The results revealed that C1 consists of twins with both larger and smaller fetuses displaying cardiac failure with an increase in renal perfusion and a decrease in renal and placental perfusion, respectively, and C2 consists of twins with smaller fetuses having both placental insufficiency and intrauterine growth retardation. C3 consists of twins with both lager and smaller fetuses having normal circulation, when compared to singleton pregnancy.
Birth Weight↗
Renal effects of a nitric oxide donor, NOC 7, in anesthetized rabbits.
Intrarenal arterial infusion of angiotensin II (4 ng/kg per min) reduced glomerular filtration rate and urinary Na+ excretion without affecting fractional Na+ excretion. Infusion of norepinephrine (30 ng/kg per min) reduced both urinary Na+ excretion and fractional Na+ excretion with a slight hypofiltration. The angiotensin II- and the norepinephrine-induced renal responses were suppressed during simultaneous infusion of a spontaneous nitric oxide donor 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl 1-triazene (NOC 7, 30 ng/kg per min) which itself had little influence on the renal parameters. The results suggest that in the rabbit kidney in vivo NOC 7 can interfere with the angiotensin II-induced hypofiltration and norepinephrine-evoked tubular reabsorption and thereby suppresses their antinatriuretic actions.
Anesthesia↗
CSF levels of prostaglandins, especially the level of prostaglandin D2, are correlated with increasing propensity towards sleep in rats.
The concentration of PGD2, PGE2, and of PGF2 alpha was measured in the cerebrospinal fluid (CSF) collected from the cisterna magna of conscious rats (n = 29), which, chronically implanted with a catheter for the CSF sampling, underwent deprivation of daytime sleep. Significant elevation of the CSF level of PGD2 was observed following 2.5-h sleep deprivation (SD), and the elevation became more marked following 5- and 10-h SD, apparently reaching the maximum at 5-h SD (703 +/- 140 pg/ml (mean +/- S.E.M.) for baseline vs. 1734 +/- 363 pg/ml for SD, n = 10). The levels of PGE2, and PGF2 alpha also significantly increased following 5- and 10-h SD, but not following 2.5-h SD. It is unlikely that these changes were simply caused by some responses of the animals to stress stimuli, because stress stimuli derived from restraint of the animal at the supine position to a board for 1 h did not produce any acute responses in the CSF levels of prostaglandins (n = 13). In a different group of animals (n = 11) implanted with electrodes for recording electroencephalogram (EEG) and electromyogram (EMG) in addition to the catheter, the levels of the prostaglandins in CSF were determined for slow-wave sleep (SWS) and wakefulness in the day and for SWS and wakefulness in the night. The highest PGD2 value was obtained at daytime SWS, whereas the lowest was at night wakefulness; furthermore, a significant difference was observed between SWS and wakefulness rather than between day and night. The CSF level of PGE2 also showed a similar tendency. In an additional group of animals (n = 6), not only PGD2 but also PGE2 and PGF2 alpha significantly increased the sleeping time of the animal when applied into the subarachnoid space underlying the ventral surface area of the rostral basal forebrain, the previously defined site of action for the sleep-promoting effect of PGD2. The promotion of sleep by PGE2 applied to the subarachnoid space was an effect completely opposite to the well-established awaking effect of the same prostaglandin demonstrated in the hypothalamic region in a series of previous studies. Based on these results, we conclude that increases in CSF levels of prostaglandins, especially that of PGD2, are correlated in rats with heightened propensity towards sleep and further with the depth of sleep under normal as well as SD conditions.
Animals↗
Successful long-term xenoperfusion of the pig liver: continuous administration of prostaglandin E1 and insulin.
For clinical utilization of extracorporeal liver perfusion as an artificial liver assist device, we examined the possibility of long-term xenoperfusion of the pig liver by the continuous administration of prostaglandin E1 (PGE1) and insulin. After a 3-hr perfusion period, pig livers that were xenoperfused with human blood exhibited a drastic decrease in the perfusate volume, a progressive elevation of the hepatic artery pressure, a gradual deterioration of bile production, and a marked increase in the release of creatine kinase-BB component. The continuous administration of PGE1 (25 microg/hr) and insulin (1 U/hr) significantly improved these derangements (P<0.05) and allowed stable perfusion for up to 9 hr. This manipulation also inhibited leukocyte aggregation in the graft, the characteristic perfusate hemolysis, and acceleration of ketogenesis. Histological examination revealed that the interlobular edema and hemorrhage, characteristics of tissue injuries in xenogeneic hyperacute rejection, were markedly alleviated in the PGE1 and insulin-treated group. This study clarifies the finding that the combined administration of PGE1 and insulin is effective for long-term xenogeneic extracorporeal liver perfusion, with the graft viability well maintained.
Alprostadil↗
Prostaglandin E1 resuscitates hepatic organic anion transport independent of its hemodynamic effect after warm ischemia.
Prostaglandin E1 (PGE1) is a promising agent against ischemic liver damage, but direct evidence of the benefit to intrinsic hepatocyte function has been lacking. We demonstrate here that organic anion transport can be supported by treatment with PGE1 even at a lower dose which does not affect hepatic microcirculation in rabbits with liver inflow occlusion. Near-infrared spectroscopy was applied to directly measure hepatic clearance of indocyanine green (ICG), an exogenous organic anion, and to estimate microcirculation as measured by oxygen saturation and the content of hemoglobin in the sinusoid. Also, morphological changes in microtubules, the cytoskeleton which is known to be associated with organic anion transport, and energy status, as measured by adenine nucleotide levels, were observed. ICG removal rate in hepatocytes decreased significantly from 0.100 +/- 0.018 to 0.027 +/- 0.019 min-1 (mean +/- SD, P < 0.01) by 60-min warm ischemia, whereas the value increased to 0.082 +/- 0.030 min-1 (P < 0.05) when PGE1 was given at a dose of 0.05 microgram/kg/min. The treated livers also showed early reorganization of microtubules, as well as amelioration of ATP resynthesis after reperfusion. However, there were no significant differences in intraoperative changes in oxygen saturation and the content of hemoglobin in the sinusoid between PGE1-treated and untreated groups, indicating that the influence of PGE1 at this dose on hemodynamic changes is not considerable. These results indicate that PGE1 resuscitates an inherent hepatocyte function of organic anion transport on reperfusion after warm ischemia and suggest that the benefit could be attributed solely to direct action on hepatocytes.
Adenine Nucleotides↗
Risk factors and probability of vertebral body collapse in metastases of the thoracic and lumbar spine.
STUDY DESIGN: The associations between vertebral body collapse and the size or location of the metastatic lesions were analyzed statistically to estimate the critical point of collapse. OBJECTIVES: To determine risk factors for collapse, to estimate the predicted probability of collapse under various states of metastatic vertebral involvement, and to establish the criteria of impending collapse. SUMMARY OF BACKGROUND DATA: Pathologic vertebral collapse brings about severe pain and paralysis in patients with cancer. Prevention of collapse plays a significant role in maintaining or improving their quality of life. Because no previous study has clarified the critical point of vertebral collapse, however, the optimum timing for prophylactic treatment has been unclear. METHODS: The size and location of metastatic tumor from Th1 to L5 were evaluated radiologically for 100 thoracic and lumbar vertebrae with osteolytic lesions. The correlations between collapse and the following risk factors (x1-x4) were determined by means of a multivariate logistic regression model: x1, tumor size (the percentage of tumor occupancy in the vertebral body [% TO]); x2, pedicle destruction, x3, posterior element destruction; and x4, costovertebral joint destruction. RESULTS: Significant risk factors were costovertebral joint destruction (odds ratio, 10.17; P = 0.021) and tumor size (odds ratio of every 10% increment in %TO, 2.44; P = 0.032) in the thoracic region (Th1-Th10), whereas, tumor size (odds ratio of every 10% increment in %TO, 4.35; P = 0.002) and pedicle destruction (odds ratio, 297.08; P = 0.009) were main factors in the thoracolumbar and lumbar spine (Th10-L5). The criteria of impending collapse were: 50-60% involvement of the vertebral body with no destruction of other structures, or 25-30% involvement with costovertebral joint destruction in the thoracic spine; and 35-40% involvement of vertebral body, or 20-25% involvement with posterior elements destruction in thoracolumbar and lumbar spine. CONCLUSIONS: With respect to the timing and occurrence of vertebral collapse, there is a distinct discrepancy between the thoracic and thoracolumbar or lumbar spine. When a prophylactic treatment is required, the optimum timing and method of treatment should be selected according to the level and extent of the metastatic vertebral involvement.
Adult↗
Antimutagenicity of Tochu tea (an aqueous extract of Eucommia ulmoides leaves): 1. The clastogen-suppressing effects of Tochu tea in CHO cells and mice.
The suppressing effect of crude extracts of Tochu tea, an aqueous extract of Eucommia ulmoides leaves and a popular beverage in Japan, on the induction of chromosome aberrations in CHO cells and mice was studied. When CHO cells were treated with Tochu tea crude extract after MMC treatment, the frequency of chromosome aberrations was reduced. Out of 17 Tochu tea components, 5 irridoids (geniposidic acid, geniposide, asperulosidic acid, deacetyl asperulosidic acid, and asperuloside) and 3 phenols (pyrogallol, protocatechuic acid, and p-trans-coumaric acid) were found to have anticlastogenic activity. Since the anticlastogenic irridoids had an alpha-unsaturated carbonyl group, this structure was considered to play an important role in the anticlastogenicity. The anticlastogenic effect of Tochu tea extracts was examined in mice using a micronucleus assay. When mice received 1.0 ml 4% Tochu tea extract by oral gavage 6 h before intraperitoneal injection of MMC, a decrease in the frequency of micronuclei was observed. This decrease was not due to a delay in the maturation of micronucleated reticulocytes.
Animals↗
FMLP actions and its binding sites in isolated human coronary arteries.
The chemoattractant f-Met-Leu-Phe (FMLP) can modulate human coronary arterial tone without the involvement of peripheral leukocytes. We investigated the actions of FMLP and its cellular mechanism in human coronary arteries isolated 2-3 h after death. A single dose of FMLP (0.01-10 microM) produced transient contraction (or, followed by relaxation) responses in most human coronary rings examined. These responses to FMLP were in large part mediated by the generation of cyclooxygenase products, mainly thromboxane A2 (TXA2) and prostaglandin I2 (PGI2). Radiolabeled N-formyl hexapeptide. 125I-f-Nle-Leu-Phe-Nle-Tyr-Lys bound densely to intimal and adventitial sites that accumulated macrophages (CD68-positive) with a Kd of 14-29 nM and, further, weakly to the media with a Kd of 2.4-3.6 microM. Several cell types including macrophages, endothelial cells and smooth muscle cells were positively immunostained for both TXA2 synthase and PGI2 synthase. However, there was no significant relation between the magnitude of the responses to FMLP and dense macrophage accumulation in the intimal plaques or the adventitia. A reverse transcription-polymerase chain reaction showed predominant expression of FMLP receptor homologues, FPRH1 and FPRH2 mRNA, in human coronary medial tissues relative to that in leukocytes. In conclusion. FMLP produced transient tension changes in human coronary arteries, mainly via the generation of TXA2 and PGI2. This effect of FMLP did not appear to be mediated by the activation of densely accumulated intimal and/or adventitial macrophages, but by the activation of unidentified medial tissue cells which might have functional FMLP receptor homologues.
Adolescent↗
The protective effects of prostaglandin E1 on sinusoidal endothelial cells in xenogeneic pig liver perfusion.
The effects of prostaglandin E1 (PGE1) on hepatic sinusoidal endothelial cells (SEC) in the xenogeneic immunoreaction were investigated. Porcine livers were perfused with fresh human blood via the portal vein (PV) and the hepatic artery (HA) either with the administration of PGE1 (Group PG) or without PGE1 (Group C). The creatine kinase-BB component (CK-BB) in the perfusate was measured to assess SEC damage. SEC activation and complement activation were evaluated immunohistochemically by the expression of von Willebrand factor (vWF) and by the deposition of membrane attack complex (MAC), respectively. Xenoperfusion in Group C was discontinued between 4 and 6 hr due to the rapid elevation of HA pressures and the massive loss of perfusate. In Group PG, both PV and HA pressures were kept stable for up to 9 hr. In Group C, severe interlobular bleeding and diffuse extrasinusoidal hemorrhage were observed at 4 hr histologically, while in Group PG, the hepatic architecture was maintained without hemorrhage at 6 hr. MAC was markedly deposited on SEC and parenchymal cells at 3 hr in both groups. The amount of vWF, however, was expressed on SEC in large amounts at 1 hr in Group C, while small amounts were expressed at 1 hr in Group PG. In Group PG, CK-BB release was significantly lower than in Group C (P < 0.01). These results suggest that PGE1 suppressed SEC activation and protected the impairment of hepatic SEC during xenoperfusion without suppressing complement activation, resulting in the prolongation of xenogeneic liver perfusion.
Alprostadil↗
New technique for time series analysis combining the maximum entropy method and non-linear least squares method: its value in heart rate variability analysis.
A new technique for time series analysis, which is a combination of the maximum entropy method (MEM) for spectral analysis and the non-linear least squares method (LSM) for fitting analysis, is described. In this technique, the MEM power spectral density (MEMPSD) is calculated using a very large lag that could diminish the lag dependence of dominant periods estimated by the MEM analysis. The validity of this large lag is confirmed by the LSM, given that the ten dominant MEM periods are known quantities. To validate the MEM plus LSM technique, it is compared with autoregressive (AR) modelling, by analysing heart rate variability under pharmacological interventions (phenylephrine and trinitroglycerine), using 16 young males. The results indicate that the MEMPSD, when compared with the ARPSD, has numerous periods that could reproduce the original time series much more accurately, as revealed by the LSM analysis. However, both the low- and high-frequency powers with MEMPSD and ARPSDs shift in the expected directions in accordance with the pharmacological effects on the cardiovascular system. The implications of these results are discussed from the theoretical and practical standpoints of the MEM plus LSM technique, compared with AR modelling.
Adolescent↗