Prediction of pathological response to preoperative chemotherapy for pancreatic ductal adenocarcinoma using 2-[18F]-fluoro-2-deoxy-d-glucose positron-emission tomography.

AIM: To determine whether the pathological response to preoperative chemotherapy for pancreatic ductal adenocarcinoma (PDAC) can be predicted using 2-[18F]-fluoro-2-deoxy-d-glucose positron-emission tomography (F-18 FDG-PET). MATERIALS AND METHODS: Twenty-eight patients with PDAC who underwent only neoadjuvant chemotherapy (NAC) before surgery were enrolled in the study. All patients had F-18 FDG-PET examinations before NAC. The resected specimen was pathologically evaluated according to the Classification of Pancreatic Carcinoma (7th edn). Patients were categorised into a non-response group and a response group based on the pathological findings. The non-response group (Grades 1a and 1b) showed ≤50% necrosis in the specimen, while the specimens of the response group (Grades 2-3) showed >50% necrosis. The maximum standardised uptake values (SUVmax) of the tumours on F-18 FDG-PET were measured. The mean values of SUVmax were compared between the two groups. The diagnostic performance of SUVmax in distinguishing the two groups was also evaluated using receiver operating characteristic analysis. RESULTS: The mean SUVmax of the response group was higher than that of the non-response group (9.00 ± 1.78 versus 4.26 ± 2.35; p<0.001). The optimal cut-off value of SUVmax was 9.28 for distinguishing the two groups. The sensitivity, specificity, and accuracy for the prediction in the response group were 80%, 95.7%, and 92.9%, respectively. CONCLUSIONS: SUVmax on F-18 FDG-PET may be useful as a biomarker to predict the pathological response to NAC in patients with PDAC.

Spectroscopy of surface-induced noise using shallow spins in diamond.

We report on the noise spectrum experienced by few nanometer deep nitrogen-vacancy centers in diamond as a function of depth, surface coating, magnetic field and temperature. Analysis reveals a double-Lorentzian noise spectrum consistent with a surface electronic spin bath in the low frequency regime, along with a faster noise source attributed to surface-modified phononic coupling. These results shed new light on the mechanisms responsible for surface noise affecting shallow spins at semiconductor interfaces, and suggests possible directions for further studies. We demonstrate dynamical decoupling from the surface noise, paving the way to applications ranging from nanoscale NMR to quantum networks.

Involvement of adhesion molecule in in vitro plaque-like formation of macrophages stimulated with Aggregatibacter actinomycetemcomitans lipopolysaccharide.

BACKGROUND AND OBJECTIVE: Inflammatory agents, such as lipopolysaccharide (LPS), in periodontal pockets may promote atherogenesis by activating leukocytes. In our previous study, we developed a microchannel chip to observe the cell adhesion process in a fluid system. The objective of this investigation was to examine the mechanism by which periodontopathic bacterial LPS enhances plaque-like formation on a microchannel chip. MATERIAL AND METHODS: To evaluate the effect of Aggregatibacter actinomycetemcomitans LPS on the expression of adhesion molecules, e.g. intercellular adhesion molecule 1 (ICAM-1), lymphocyte function-associated antigen 1 (LFA-1) and L-selectin, on the surface of murine macrophage RAW264.7 cells, the expression of each adhesion molecule was examined by flow cytometry and western blot analysis. Moreover, a flow test on the microchannel chip involving anti-adhesion molecule antibodies was conducted to clarify which adhesion molecule is related to plaque-like formation of RAW264.7 cells. RESULTS: The expressions of ICAM-1 and LFA-1 on the surface of RAW 264.7 cells increased following 12 h culture with LPS; L-selectin expression was unaffected. An increase in ICAM-1 expression was also confirmed by western blot analysis. The flow test revealed that anti-ICAM-1 antibody inhibited plaque-like formation of LPS-stimulated macrophages on the micropillars of the microchannel chip. CONCLUSION: These findings indicate that ICAM-1 plays an important role in plaque-like formation of LPS-stimulated macrophages. Our microchannel chip is a suitable tool for the investigation of etiological factors of atherosclerosis, including periodontitis, in vitro.

Measurement of plaque-forming macrophages activated by lipopolysaccharide in a micro-channel chip.

BACKGROUND AND OBJECTIVE: In the present study, micro-channel arrays were fabricated on the surface of plastic-based disposable chips. The cell adhesion process and the detection of plaque-forming macrophages were observed. Further, we evaluated cell adhesion in a fluid system in vitro. MATERIAL AND METHODS: Features of the micro-channel (1.4 mm wide and 10 mm long) included twenty micro-pillars (with a projection of 200 microm diameter and 250 microm high) coated in a 50 microm thick silicon rubber layer, which were regularly arranged at the bottom of each channel. The efficiency of cell capture was expected to increase by arrangement of micro-pillars in a micro-channel. Mouse macrophage RAW264.7 cells, stimulated for 24 h with lipopolysaccharide (LPS) derived from periodontopathic bacteria, were circulated continuously for 2 h at room temperature by the pump in a chip. RESULTS: Control cells had not formed plaques on micro-pillars 20 min into the experiment. By contrast, LPS-activated macrophages produced plaques at the side walls of micro-pillars after 20 min. The plaques grew during the flow test, and image shading became clearer with increasing flow time for 120 min. The maximal adhesion rate per unit area appeared at 20% for control cells, whereas the peak was shifted to 30% for LPS-activated macrophages (n = 20). The average adhesion rate was 3.0 +/- 2.0% for control cells and 5.0 +/- 3.9% for LPS-activated macrophages (n = 100). CONCLUSION: These findings indicate that LPS-activated macrophages accumulate in micro-channel arrays, and suggest that macrophage plaque formation is a two-step procedure: (1) LPS-activated macrophages adhere physically to the silicon rubber layer on micro-pillars; and (2) consequently, the cells adhere to the activated macrophage layer.

Hematopoietic stem cell transplantation for 30 patients with primary immunodeficiency diseases: 20 years experience of a single team.

We retrospectively analyzed our results of 30 patients with three distinctive primary immunodeficiency diseases (PIDs)--severe combined immunodeficiency (SCID, n = 11), Wiskott-Aldrich syndrome (WAS, n = 11) and X-linked hyper-immunoglobulin M (IgM) syndrome (XHIM, n = 8)--who underwent hematopoietic SCT (HSCT) during the past 20 years. Until 1995, all donors were HLA-haploidentical relatives with T-cell depletion (TCD) (n = 8). Since 1996, the donors have been HLA-matched related donors (MRD) (n = 8), unrelated BM (UR-BM) (n = 7) and unrelated cord blood (UR-CB) (n = 7). Twenty-seven of 30 patients had various pre-existing infections with or without organ damages before HSCT. Conditioning regimen and GVHD prophylaxis were determined according to disease, donor and pretransplant status. Although one of eight patients transplanted with TCD is alive with full engraftment, the other seven died. On the other hand, 18 of 22 patients transplanted without TCD are alive and well, including six of eight transplanted from MRD, seven of seven from UR-BM and five of seven from UR-CB. All 19 survivors did not require Ig supplementation after HSCT. These results indicate that UR-CBT as well as UR-BMT provides good results for PID comparable to MRD-SCT, and that early diagnosis, HSCT at early stage, careful supportive therapy and monitoring for various pathogens are important for the successful HSCT.

Role of calcium-sensitive K(+) channels and nitric oxide in in vivo coronary vasodilation from enhanced perfusion pulsatility.

BACKGROUND: In vitro studies support K(+)(Ca) channel-induced smooth muscle hyperpolarization as underlying acetylcholine-mediated (or bradykinin-mediated) vasodilation that persists despite combined nitric oxide (NO) and PGI(2) inhibition. We tested the hypothesis that these channels are activated by enhanced pulsatile perfusion in vivo and contribute substantially to vasodilation from this stimulus. METHODS AND RESULTS: The canine left descending coronary artery was perfused with whole blood at constant mean pressure, and physiological flow pulsatility was set at 40 or 100 mm Hg by computer servo-pump. Cyclooxygenase was inhibited by indomethacin. Mean flow increased +18+/-2% (P:<0.0001) with enhanced pulsatility. This response declined approximately 50% by blocking NO synthase (L-NMMA) or K(+)(Ca) [charybdotoxin (CbTX)+apamin (AP)]. Combining both inhibitors virtually eliminated the flow rise. Inhibiting either or both pathways minimally altered basal coronary flow, whereas agonist-stimulated flow was blocked. Bradykinin-induced dilation declined more with CbTX+AP than with L-NMMA (-66% versus -46%, P:=0.03) and was fully blocked by their combination. In contrast, acetylcholine-induced dilation was more blunted by L-NMMA than by CbTX+AP (-71% versus -44%, P:<0.002) and was not fully prevented by the combination. Substituting iberiotoxin (IbTX) for CbTX greatly diminished inhibition of pulse pressure and agonist flow responses (with or without NOS inhibition). Furthermore, blockade by IbTX+AP was identical to that by AP alone, supporting a minimal role of IbTX-sensitive large-conductance K(+)(Ca) channels. CONCLUSIONS: K(+)(Ca) activation and NO comodulate in vivo pulsatility-stimulated coronary flow, supporting an important role of a hyperpolarization pathway in enhanced mechanovascular signaling. Small- and intermediate-conductance K(+)(Ca) channels are the dominant species involved in modulating both pulse pressure- and bradykinin-induced in vivo coronary dilation.

Improved mechanoenergetics and cardiac rest and reserve function of in vivo failing heart by calcium sensitizer EMD-57033.

BACKGROUND: Myofilament Ca(2+) sensitizers enhance contractility but can adversely alter diastolic function through sensitization to low intracellular Ca(2+) concentration. Concomitant phosphodiesterase III inhibition (PDE3I) may offset diastolic changes but limit the mechanoenergetic benefits. We tested whether selective Ca(2+) sensitization in vivo with the use of EMD-57033 enhances both systolic and diastolic function in failing hearts at minimal energetic cost. METHODS AND RESULTS: Pressure-dimension data were measured with sonomicrometry/micromanometry in conscious dogs before (CON, n=9) and after tachycardia-induced heart failure (HF, n=11). In contrast to blunted dobutamine (DOB) responses in HF, low-dose EMD-57033 (0.4 mg. kg(-1). min(-1) for 20 minutes) markedly enhanced contractility, doubling end-systolic elastance and raising fractional shortening similarly in CON-treated and HF hearts. EMD-57033 effects were achieved at a reduced heart rate, without vasodilation. EMD-57033 augmented blunted heart rate-dependent contractility responses in HF at a rate of twice that of DOB, despite matched basal inotropic responses. EMD-57033 also improved diastolic function, lowering left ventricular end-diastolic pressure and increasing the filling rate. At equipotent inotropic doses and matched preload, EMD-57033 lowered the oxygen cost of contractility by -11.4+/-5.8%, whereas it rose 64+/-18% with DOB (P=0.001) and 28+/-11% with milrinone. Doubling EMD-57033 dose further augmented positive inotropy in CON and HF, accompanied by vasodilation, increased heart rate, and other changes consistent with PDE3I coactivity, but the oxygen cost of contractility remained improved compared with the use of DOB. CONCLUSIONS: Selective Ca(2+) sensitization with minimal PDE3I in vivo is achieved with the use of EMD-57033, improving basal and rate-stimulated contractility and mechanoenergetics of HF without compromising diastolic function. Despite PDE3I activity at higher doses, energetic benefits persist.

Reversal of glibenclamide-induced coronary vasoconstriction by enhanced perfusion pulsatility: possible role for nitric oxide.

OBJECTIVES: ATP-sensitive potassium channels (K+ATP) prominently contribute to basal coronary tone; however, flow reserve during exercise remains unchanged despite channel blockade with glibenclamide (GLI). We hypothesized that increasing perfusion pulsatility, as accompanies exercise, offsets vasoconstriction from K+ATP-channel blockade, and that this effect is blunted by nitric oxide synthase (NOS) inhibition. METHODS: In 31 anaesthetized dogs the left anterior descending artery was blood-perfused by computer-controlled servo-pump, with real-time arterial perfusion pulse pressure (PP) varied from 40 and 100 mm Hg at a constant mean pressure and cardiac workload. RESULTS: At control PP (40 mm Hg), GLI (50 micrograms/min/kg, i.c.) lowered mean regional coronary flow from 37 +/- 5 to 25 +/- 4 ml/min (P < 0.001). However, this was not observed at 100 mm Hg PP (41 +/- 2 vs. 45 +/- 4). NOS inhibition by NG-monomethyl-L-arginine (L-NMMA) did not alter basal flow at 40 mm Hg PP, but modestly lowered flow (-5%, P < 0.001) at higher PP (100 mm Hg), reducing PP-flow augmentation by -36%, and acetylcholine (ACh) induced flow elevation by -39%. Co-infusion of L-NMMA with GLI resulted in net vasoconstriction at both PP levels (-60% and -40% at 40 and 100 mm Hg PP, respectively). Unlike GLI, vasoconstriction by vasopressin (-43 +/- 3% flow reduction at 40 mm Hg PP) or quinacrine (-23 +/- 7%) was not offset at higher pulsatility (-44 +/- 4 and -23 +/- 6%, respectively). Neither of the latter agents inhibited ACh- or PP-induced flow responses, nor did they modify the effect of L-NMMA on these responses. CONCLUSIONS: Increased coronary flow pulsatility offsets vasoconstriction from K+ATP blockade by likely enhancing NO release. This mechanism may assist exercise-mediated dilation in settings where K+ATP opening is partially compromised.

Usefulness of pulsatile bidirectional cavopulmonary shunt in high-risk Fontan patients.

BACKGROUND: A bidirectional cavopulmonary shunt has been performed for the high-risk Fontan patient. It is well known that in the presence of the bidirectional cavopulmonary shunt alone to secure pulmonary blood flow, the central pulmonary artery size decreases over time. We have performed pulsatile bidirectional cavopulmonary shunt (PBCPS), keeping pulmonary blood flow from the ventricle through the stenotic pulmonary valve, or a Blalock-Taussig shunt in patients who do not meet the criteria for the Fontan operation. METHODS: Eleven patients who underwent PBCPS between 1989 and 1993 were reviewed. We compared the results of cardiac catheterization immediately before PBCPS and during the postoperative observation period (310 +/- 257 days). RESULTS: Pulmonary blood flow and arterial oxygen saturation increased significantly after PBCPS (p = 0.01). Pulmonary artery area index showed a tendency to increase (p = 0.11). The mean number of risk factors for the Fontan procedure decreased significantly for 1.8 +/- 1.1 to 0.7 +/- 0.8 after PBCPS (p < 0.05). Overall, 5 of the 11 patients (45.5%) met the criteria for the Fontan procedure, and a fenestrated Fontan procedure was carried out in 4 of them. CONCLUSIONS: The PBCPS is useful for high-risk Fontan patients not only in the staged Fontan operation, but also as definitive palliation.

Pulmonary atresia with intact ventricular septum: long-term results of "one and a half ventricular repair".

BACKGROUND: Between 1982 and 1984, we successfully performed "one and a half ventricular repair" using a Glenn shunt for 3 patients with pulmonary atresia with intact ventricular septum. Here we review the 10-year follow-up results. METHODS: In these patients, the preoperative Z scores of the tricuspid valve diameters ranged from -5.2 to -6.5. Right ventricular outflow tract reconstruction combined with a Glenn shunt were performed in all patients. Cardiac catheterization was done at least 10 years post-operatively. RESULTS: All 3 patients have maintained New York Heart Association functional class I status for more than 10 years. Angiography in 2 patients confirms sufficient left pulmonary artery pressure with pulsatile blood flow and good right ventricular contraction. A pulmonary arteriovenous fistula has developed in 1 patient. CONCLUSIONS: Although the lower limits of the tricuspid valve diameter for "one and a half ventricular repair" using a cavopulmonary shunt have not yet been determined, we successfully performed this procedure in 3 patients with severely hypoplastic right ventricles and tricuspid valve diameter Z scores of less than -5.0. The results up to 10 years postoperatively are acceptable.

Management of prenatally diagnosed congenital cystic adenomatoid malformation of the lung.

We have treated four prenatally diagnosed cases of extensive congenital cystic adenomatoid malformation (CCAM) of the lung. The first case in 1982 was associated with severe fetal hydrops. After thoracentesis at 31 weeks of gestation abruptio placentae occurred, and a female baby was delivered by cesarean section. She underwent a right lower lobectomy, but soon died. The second baby without hydrops, diagnosed as having CCAM at 26 weeks of gestation, was followed conservatively until full term. After birth, it was necessary to treat the baby boy with extracorporeal membrane oxygenation (ECMO), but he survived. The third baby with fetal hydrops had an indwelling drainage catheter inserted into the CCAM at 27 weeks of gestation. The hydrops subsided and the baby was delivered at 37 weeks of gestation. He was allowed to breathe spontaneously, but was intubated 16 hours after birth. A right lower lobectomy was successfully performed 24 hours after delivery. The fourth baby without fetal hydrops was followed conservatively until delivery. He underwent left lower lobectomy successfully on the 4th day of life. Although management of prenatally diagnosed CCAM varies among patients, insertion of an indwelling catheter into the cyst appears to be the treatment of choice if indicated; the catheter can be maintained for as long as 10 weeks, as shown in Case 3. Cases of CCAM without fetal hydrops should also be treated carefully, because persistent fetal circulation may occur postnatally.

[Superior vena cava-right atrial appendage direct anastomosis for repair of partial anomalous pulmonary venous connection to superior vena cava].

Successful repair was performed for a 7-year-old male with a diagnosis of partial anomalous pulmonary venous connection (PAPVC) to superior vena cava (SVC) and superior sinus venosus atrial septal defect (ASD). The SVC was divided above the orifice of the anomalous pulmonary vein and the cephalad end of the SVC was anastomosed directly to the right atrial appendage. A patch was used to divert pulmonary venous flow from the orifice of the SVC through superior sinus venosus ASD into the left atrium. Postoperative course was uneventful with normal sinus rhythm. There was no evidence of vena caval or pulmonary venous obstruction. At 3-month after surgery, sinus node function was confirmed to be normal by electrophysiological study. This is useful alternative method for repair of PAPVC to high or middle SVC.

[Autogenous pericardial patch augmentation of the anastomotic orifice of Blalock-Taussig shunt].

Our recent experiences of the autogenous pericardial patch augmentation of Blalock-Taussig anastomotic orifice are reported. In Case 1, the direct suture between the left subclavian artery and the left pulmonary artery was difficult on the anterior wall because of the shortness of the left subclavian artery. Therefore, a piece of the patient's own pericardium was excised and sutured anteriorly between the two vessels by interrupted 7-0 polypropylene sutures. A 19 months postoperative angiogram showed so-called parrot-beaking of the subclavian artery probably due to tension, but there was no distortion or stenosis of the pulmonary artery. In Case 2, the right subclavian artery distal to the bifurcation of the vertebral artery was longitudinally split measuring approximately 2.5 cm in length, and widened by a piece of the autogenous pericardium in a wedge shape. Then, it was anastomosed to the right pulmonary artery without undue tension. Seven months postoperatively the patient died from severe AV valve regurgitation. The autopsy showed widely patent anastomosis and good healing as well as slight expansion of the pericardial patch but without aneurysm formation. In Case 3, the same operation as in Case 2 was performed. A 6 months postoperative angiogram showed no stenosis or distortion of either the subclavian or the pulmonary artery. Although it is premature to draw any conclusion, the use of the autogenous pericardium may be indicated to widen the anastomotic orifice of Blalock-Taussig shunt without sacrificing the length of the subclavian artery even in small infants or neonates.

Cord blood transplantation is associated with rapid B-cell neogenesis compared with BM transplantation.

Hematopoietic cell transplantation (HCT) is used for treatment of hematopoietic diseases. Assessment of T- and B-cell reconstitution after HCT is crucial because poor immune recovery has a major effect on the clinical course. In this study, we retrospectively analyzed T-cell receptor excision circles (TRECs) as well as signal and coding joint kappa-deleting recombination excision circles (sjKRECs and cjKRECs, respectively) as markers of newly produced lymphocytes in 133 patients (56 primary immunodeficient and 77 malignant cases, median (range): 12 (0-62) years old). We analyzed the kinetics of TREC and KREC recovery and determined the factors that contributed to better immune recovery. KRECs became positive earlier than TRECs and increased thereafter. Younger recipient age had a favorable effect on recovery of sjKRECs and cjKRECs. Compared with BM and peripheral blood, our data suggested that cord blood (CB) provided rapid B-cell recovery. CB also provided better B-cell neogenesis in adult HCT recipients. Chronic GVHD was associated with low TRECs, but not increased sjKRECs/cjKRECs. Finally, positive sjKRECs 1 month after HCT were associated with fewer infectious episodes. Monitoring of TRECs and KRECs may serve as a useful tool for assessment of immune reconstitution post HCT.

Development of an Interaction Assay between Single-Stranded Nucleic Acids Trapped with Silica Particles and Fluorescent Compounds.

Biopolymers are easily denatured by heating, a change in pH or chemical substances when they are immobilized on a substrate. To prevent denaturation of biopolymers, we developed a method to trap a polynucleotide on a substrate by hydrogen bonding using silica particles with surfaces modified by aminoalkyl chains ([A-AM silane]/SiO2). [A-AM silane]/SiO2 was synthesized by silane coupling reaction of N-2-(aminoethyl)-3-aminopropyltrimethoxysilane (A-AM silane) with SiO2 particles with a diameter of 5 µm at 100 °C for 20 min. The surface chemical structure of [A-AM silane]/SiO2 was characterized by Fourier transform infrared spectroscopy and molecular orbital calculations. The surface of the silica particles was modified with A-AM silane and primary amine groups were formed. [A-AM silane]/SiO2 was trapped with single-stranded nucleic acids [(Poly-X; X = A (adenine), G (guanine) and C (cytosine)] in PBS solution at 37 °C for 1 h. The single-stranded nucleic acids were trapped on the surface of the [A-AM silane]/SiO2 by hydrogen bonding to form conjugated materials. The resulting complexes were further conjugated by derivatives of acridine orange (AO) as fluorescent labels under the same conditions to form [AO:Poly-X:A-AM silane]/SiO2 complexes. Changes in the fluorescence intensity of these complexes originating from interactions between the single-stranded nucleic acid and aromatic compounds were also evaluated. The change in intensity displayed the order [AO: Poly-G: A-AM silane]/SiO2 > [AO:Poly-A:A-AM silane]/SiO2 >> [AO:Poly-C:A-AM silane]/SiO2. This suggests that the single-stranded nucleic acids conjugated with aminoalkyl chains on the surfaces of SiO2 particles and the change in fluorescence intensity reflected the molecular interaction between AO and the nucleic-acid base in a polynucleotide.

Reconsideration of criteria for the Fontan operation. Influence of pulmonary artery size on postoperative hemodynamics of the Fontan operation.

BACKGROUND: The outcome of the Fontan operation largely depends on the selection of patients because this procedure is a physiological correction. Among the several selection criteria for the Fontan operation, the importance of adequate size of the pulmonary artery remains controversial. In this series, in order to clarify whether the pulmonary artery size is indispensable or not as one of the selection criteria for the Fontan operation, we considered the physiological meaning of pulmonary artery size and investigated how it influenced postoperative hemodynamics of the Fontan operation. METHODS AND RESULTS: In congenital heart disease of decreasing pulmonary blood flow, 40 patients were examined for this analysis. Pulmonary artery indexes (cross-sectional area of the right and left pulmonary arteries divided by body surface area) were measured as the expression of pulmonary artery size, and the relations of pulmonary artery index (PAI) to pulmonary vascular resistance (Rp) and compliance (Cp) were studied. There was no significant correlation between PAI and Rp, whereas a significant correlation was found between PAI and Cp (r = .71, P = .001). Furthermore, Cp influenced postoperative hemodynamics of the Fontan operation by affecting the peak central venous pressure (pCVP) and total impedance, which was the afterload to the ventricle. Impedance increased abruptly when PAI was < approximately 100 mm2/m2. CONCLUSIONS: The smaller pulmonary artery size causes more disadvantageous hemodynamics after the Fontan operation, with resultant effects of the rise in pCVP and the increase in afterload to the single ventricle.

[Relationship between deep body temperature and hemodynamics in pediatric patients with congenital heart disease].

Relationship of the abdomen-sole deep body temperature difference (DBT) to the hemodynamics was examined in patients with congenital heart disease. Hemodynamic data were obtained by routine cardiac catheter examination, and DBT was measured during the catheterization. Significant positive correlation was found between DBT and systemic-pulmonary flow ratio (Qp/Qs) (r = 0.85, p = 0.001). DBT was maintained below 2 C degrees in almost every patient when the Qp/Qs was less than 2, whereas DBT rose rapidly when the Qp/Qs was more than 2. Furthermore, systemic blood flow and arterial-venous oxygen difference ranged widely within the normal values when DBT was less than 2 C degrees. On the other hand, when DBT was more than 2 C degrees, systemic blood flow and arterial-venous oxygen difference tended to show fixed values which were around the normal upper or lower limits. This means that systemic circulation is marginally adapted when the Qp/Qs is more than 2. The measurement of deep body temperature difference is noninvasive, easy and useful as a circulatory monitor in pediatric patients with congenital heart disease.