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Biomedical subjects

Fumio Goto

Publications and source records attributed to Fumio Goto.

At least 19 recordsLinked to original sources
PubMed2003

Fluvoxamine modulates pain sensation and affective processing of pain in human brain.

To better understand the antinociceptive effect of fluvoxamine, we measured regional cerebral blood flow during laser-evoked pain and hot sensations using H(2)15O positron emission tomography and also subjective pain and hot sensations before and after fluvoxamine or placebo administration for 7 days to 12 healthy volunteers. The subjectively rated pain score was significantly reduced by fluvoxamine administration. Painful stimuli activated multiple brain regions. After fluvoxamine administration the ipsilateral anterior cingulate cortex (ACC), contralateral insular cortex (IC), and contralateral secondary somatosensory cortex (SII) activations were reduced. The bilateral IC activation was also reduced in the placebo group. These results suggest that fluvoxamine specifically reduced activation of the ACC and SII, which are areas concerned with the affective and integrative components of pain.

Adult↗
PubMed2003

Interactions of 5-HT2 receptor agonists with acetylcholine in spinal analgesic mechanisms in rats with neuropathic pain.

Serotonin type 2 (5-HT(2)) receptors reportedly inhibit neuropathic pain in the spinal cord, but little is known about how spinal 5-HT(2) receptors might act against such abnormal sensitivity. We examined whether the cholinergic and tachykinin systems were involved in the antiallodynic effect of intrathecally administered 5-HT(2) receptor agonists in rats with nerve injury. Allodynia was produced by tight ligation of the left L5 and L6 spinal nerves, and determined by applying von Frey hairs to the left hindpaw. Effects of intrathecal pretreatment with 5-HT(2) receptor antagonists (ketanserin and RS-102221), muscarinic receptor antagonists (atropine and scopolamine), a choline uptake blocker (hemicholium-3), and an NK(1) receptor antagonist (L-706336) were assessed in rats subsequently given a 100- micro g intrathecal dose of a 5-HT(2) receptor agonist either alpha-methyl-5-HT or iododimethoxy aminopropane (DOI). Antiallodynic effects of 5-HT(2) receptor agonists were attenuated by the 5-HT(2A) receptor antagonist ketanserin (30 micro g), but not by the 5-HT(2C) receptor antagonist RS-102221 (40 micro g). Muscarinic receptor antagonists (30 micro g each), the choline uptake blocker (10 micro g), and the NK(1) receptor antagonist (30 micro g) also inhibited the antiallodynic effects of 5-HT(2) receptor agonists. Antiallodynic effects of intrathecally administered 5-HT(2) receptor agonists may be mediated by spinal release of acetylcholine induced via 5-HT(2A) and NK(1) receptors.

Acetylcholine↗
PubMed2003

Transfer of NMDAR2 cDNAs increases endogenous NMDAR1 protein and induces expression of functional NMDA receptors in PC12 cells.

The pheochromocytoma cell line (PC12) has been used as a model system for the study of regulation of expression of NMDA receptors. PC12 cells express a substantial amount of NMDAR1 subunit (NR1) mRNA, whereas they express only a small amount of NR1 protein. The level of functional NMDA receptor expression is almost negligible. To test the possibility that NMDAR2 subunits (NR2) control expression of functional NMDA receptors as well as NR1 protein, we transferred NR2A-D cDNAs into PC12 cells using adenovirus vectors. Prominent NMDA receptor-mediated currents were recorded in PC12 cells to which NR2A or NR2B cDNA was delivered without NR1 cDNA. The amplitudes of these responses were similar to those in PC12 cells to which NR1 cDNA was delivered together with NR2A or NR2B cDNA. In cells to which either NR2C or NR2D cDNA alone was delivered, NMDA receptor-mediated currents were also detected, although to a much lesser extent. These results showed that NR2 proteins produced by gene transfer are co-assembled with the endogenous NR1 protein to form functional heteromeric receptors. The delivery of NR2A-D cDNAs also increased the amount of NR1 protein but not that of NR1 mRNA, suggesting that this protein increase is due to post-transcriptional mechanisms. The effects of NR2A-B gene transfer on expression of NR1 protein were much more efficient than those of NR2C-D gene transfer.

Adenoviridae↗
PubMed2003

Epidural abscess in a patient with dorsal hyperhidrosis.

PURPOSE: To report the management of a patient who developed a lumbar epidural abscess when an epidural catheter was placed three years after a thoracic sympathectomy. The possible contribution of hyperhidrosis is discussed. CLINICAL FEATURES: A 62-yr-old male had compensatory hyperhidrosis in his back after thoracic sympathectomy. The patient, who suffered from thromboangeitis obliterans, underwent lumbar (L2-3) epidural catheterization in order to improve arterial circulation and ameliorate resting pain in his left leg. On the third day after catheterization, the patient complained of a dull pain in his back. Emergency magnetic resonance imaging revealed a 12-mm abscess in the epidural space. On the tenth day after catheterization, laminotomy at the 3-4 lumbar vertebrae and local drainage were performed. A 14-mm abscess was removed from the epidural space. The patient was discharged on day 21 after catheterization without any disability. CONCLUSION: Special precautions against infection may be necessary in patients with hyperhidrosis in the area where continuous epidural catheterization is attempted.

Anesthesia, Epidural↗
PubMed2003

Comparative effects of propofol versus fentanyl on cerebral oxygenation state during normothermic cardiopulmonary bypass and postoperative cognitive dysfunction.

BACKGROUND: The purpose of this study was to examine the comparative effects of propofol and fentanyl on cerebral oxygenation during normothermic cardiopulmonary bypass and postoperative cognitive dysfunction. METHODS: One hundred eighty patients scheduled for elective coronary artery bypass grafting were randomly divided into two groups: propofol group (n = 90) and fentanyl group (n = 90). After induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor jugular venous oxygen hemoglobin saturation continuously. Hemodynamic measurements and arterial and jugular venous blood gases were measured at seven time points. All patients underwent a battery of neurologic and neuropsychological tests on the day before the operation and at 6 months after the operation. RESULTS: Cerebral desaturation (defined as a jugular venous oxygen hemoglobin saturation value less than 50%) during cardiopulmonary bypass was more frequent in the fentanyl group than in the propofol group. Cerebral desaturation time (duration when jugular venous oxygen hemoglobin saturation was less than 50%) and the ratio of cerebral desaturation time to total cardiopulmonary bypass time in the fentanyl group differed significantly from those in the propofol group (fentanyl group: 27 +/- 14 minutes, 20% +/- 9%; propofol group: 18 +/- 11 minutes, 14% +/- 7%, respectively, p < 0.05). There was no significant difference in postoperative cognitive dysfunction at 6 months after operation between the two groups (propofol group: 5 of 77, 6%; fentanyl group: 5 of 75, 7%). CONCLUSIONS: Propofol preserved cerebral oxygenation state estimated by jugular venous oxygenation during cardiopulmonary bypass compared with the fentanyl group. However, propofol did not affect postoperative cognitive dysfunction.

Aged↗
PubMed2003

The effects of volatile anesthetics on nonadrenergic, noncholinergic depressor responses in rats.

UNLABELLED: The effects of volatile anesthetics on nonadrenergic, noncholinergic (NANC) transmission mediated by calcitonin gene-related peptide (CGRP) are unclear. We studied the effects of isoflurane, halothane, and sevoflurane on NANC depressor responses to electrical spinal cord stimulation in pithed rats whose mean arterial blood pressure was maintained near 120 mm Hg by continuous infusion of methoxamine. Autonomic outflow was blocked by hexamethonium. After 30 min of inhalation of different concentrations of anesthetics, spinal cord stimulation at the lower thoracic level (10 V at 4 Hz; duration, 1 ms) was applied for 30 s to induce a NANC depressor response. Isoflurane at 2% and halothane at 1.5% attenuated NANC depressor responses significantly, whereas isoflurane at 1%, halothane at 0.75%, and sevoflurane at 2% or 4% did not. Volatile anesthetics did not attenuate the release of CGRP after spinal cord stimulation, whereas isoflurane at 2% and halothane at 1.5% significantly inhibited depressor responses to exogenously administered CGRP. Sevoflurane at 4% did not significantly affect CGRP-induced depressor responses. Thus, isoflurane and halothane at large concentrations attenuate NANC depressor responses by attenuating the depressor action of CGRP, not CGRP release. IMPLICATIONS: The anesthetics isoflurane and halothane attenuate nonadrenergic, noncholinergic depressor responses mediated by calcitonin gene-related peptide in the rat without affecting the release of the peptide.

Anesthetics, Inhalation↗
PubMed2003

Anesthetic management for clipping a giant basilar artery aneurysm with moderate hypothermia, extracorporeal circulation assistance, and propofol infusion.

A 65-year-old female patient underwent surgery to clip a giant basilar artery aneurysm with closed-chest extracorporeal circulation using femorofemoral bypass. Moderate hypothermia (27 degrees C-30 degrees C), retention of spontaneous circulation, and propofol infusion (3-5 mg. kg(-1). h(-1)) were used under general anesthesia. Blood outflow via femoral vein was sufficient to maintain cardiopulmonary bypass and to induce hypothermia. Hemodynamics were controlled with dopamine and noradrenaline. In this case, extracorporeal circulation under moderate hypothermia was used to assist rather than substitute for spontaneous circulation, and spontaneous circulation was maintained at all times. We think that this method had advantages over deep hypothermic circulatory arrest with regard to intraoperative risks and postoperative complications.

Aged↗
PubMed2003

End-tidal carbon dioxide monitoring stabilized hemodynamic changes during ECT.

Accumulation of carbon dioxide (CO2) can disturb systemic and cerebral hemodynamics in patients receiving electroconvulsive therapy (ECT). The purpose of this study was to identify the effects of end-tidal CO2 monitoring on hemodynamic changes in patients who received ECT under propofol anesthesia. ECT was prescribed to 40 patients under propofol anesthesia. Ventilation was assisted using a face mask and 100% oxygen, with or without end-tidal CO2 monitoring. Heart rate was significantly increased in patients without end-tidal CO2 monitoring at 1 to 5 minutes after electrical stimulation (p < 0.01). Mean arterial blood pressure and middle cerebral artery blood flow velocity in the group without end-tidal CO2 monitoring were significantly larger than the values in the group with the monitor at 1 to 5 minutes after electrical stimulation. Arterial CO2 tension in the group without end-tidal CO2 monitoring was larger than the value in the group with the monitoring at 1 minute (45+/-5 mm Hg with the monitor and 56+/-8 without the monitor) and 5 minutes (37+/-4 mm Hg with the monitor and 51+/-8 without the monitor) after electrical stimulation (p < 0.01). Application of end-tidal CO2 monitoring is considered beneficial for safe and effective anesthesia management of patients undergoing ECT, especially patients with an intracranial disorder or ischemic heart disease.

Adult↗
PubMed2003

Antinociception with intrathecal alpha-methyl-5-hydroxytryptamine, a 5-hydroxytryptamine 2A/2C receptor agonist, in two rat models of sustained pain.

UNLABELLED: Type 2 serotonin (5-hydroxytryptamine [5-HT](2)) receptors in the spinal cord have been reported to mediate antinociception using pain threshold tests, but little is known about the actions of spinal 5-HT(2) receptors in sustained pain. In rats, we examined antinociceptive effects of the intrathecal administration of a 5-HT(2A/2C) receptor agonist, alpha-methyl-5-HT maleate (alpha-m-5-HT), using the formalin test and the chronic constriction injury (CCI) model. An intrathecal catheter was implanted for injection of drugs. In the formalin test, flinches were counted from Minute 1 to 2 and Minute 5 to 6 (Phase 1) and then for 1-min periods at 5-min intervals from 10 to 60 min (Phase 2). In rats with CCI, hind paw withdrawal latency after thermal stimulation was measured. In the formalin test, intrathecal administration of alpha-m-5-HT (1 to 100 microg) dose-dependently suppressed the number of flinches in both Phases 1 and 2. In the CCI model, intrathecally administered alpha-m-5-HT (10 to 100 microg) attenuated thermal hyperalgesia in a dose-dependent manner. These effects were reversed by intrathecal pretreatment with a 5-HT(2A/2C) antagonist, ketanserin (30 microg), or a muscarinic receptor antagonist, atropine (30 microg). These findings suggest that spinal 5-HT(2A/2C) receptors mediate antinociception in inflammatory pain and neuropathic pain, and the muscarinic receptors contribute to this action. IMPLICATIONS: Activation of spinal 5-hydroxytryptamine(2A/2C) receptors mediate antinociception in rat-sustained pain models such as inflammatory pain and neuropathic pain, and spinal muscarinic receptors are involved in this action.

Animals↗
PubMed2003

Neurotrophic factors can partially reverse morphological changes induced by mepivacaine and bupivacaine in developing sensory neurons.

UNLABELLED: Both bupivacaine and mepivacaine induce morphological changes in growing neurons. We designed this study to investigate the role of some neurotrophic factors (NTFs) in supporting developing neurons exposed to the deleterious effects of these drugs. Dorsal root ganglia were isolated from chick embryos and exposed to either bupivacaine or mepivacaine. After 60 min of exposure, the culture media were replaced with fresh culture media free from local anesthetics. NTFs-brain-derived NTF, glial-derived NTF, or neurotrophin-3-were added to the replacement media, and the cells were examined up to 48 h after the washout. The growth cone collapse assay was applied by a quantitative method of assessment. When the replacement media were not supported by any NTF, the growth cone collapse values were significantly larger than the control values at 20 h after the washout of mepivacaine and 48 h after the washout of either bupivacaine or mepivacaine (P < 0.05). However, when any of the NTFs were used, the collapsing activity was significantly attenuated, and growth cone collapse values showed no statistically significant differences in comparison with the control values at these time points (P > 0.05). We conclude that several NTFs support the recovery of neurons after exposure to local anesthetics. The supporting effects of NTFs on the reversibility of mepivacaine-induced collapse tended to be more obvious than those seen after the bupivacaine washout. IMPLICATIONS: Three neurotrophic factors (NTFs) can partially support the reversibility of mepivacaine- and bupivacaine-induced growth cone collapse in growing primary cultured sensory neurons. The effect of NTFs is more apparent after mepivacaine than after bupivacaine washout.

Anesthetics, Local↗
PubMed2002

Possible involvement of a muscarinic receptor in the anti-allodynic action of a 5-HT2 receptor agonist in rats with nerve ligation injury.

Intrathecal administration of 5-HT(2) receptor agonists produces an anti-allodynic effect in a rat model of neuropathic pain. Several non-serotonergic neurotransmitters have been implicated these anti-nociceptive effects. In the present study, intrathecal pre-treatment with the muscarinic receptor antagonist atropine (10 and 30 microg) and pirenzepine (10 microg) reversed the anti-allodynic effect of the 5-HT(2) receptor agonist alpha-methyl-5-hydroxytryptamine, unlike various other antagonists. Thus, muscarinic receptors may be involved in the anti-allodynic action of intrathecally injected 5-HT(2) receptor agonist.

Analgesics↗
PubMed2002

G-protein coupled receptor kinase 2 is altered during septic shock in rats.

BACKGROUND: One of the key mechanisms leading to beta-adrenergic receptor-specific desensitization is the phosphorylation of agonist-occupied receptors by the specific beta-adrenergic receptor kinase (GRK2). The present study examines whether GRK2 is altered during septic shock in rats. MATERIALS AND METHODS: Male Wistar rats (7 weeks) weighing between 250 and 300 g were anesthetized with pentobarbital (10 mg/kg ip). Escherichia coli endotoxin (10 mg/kg in 0.3 mL of saline) or saline (0.3 ml) was injected intravenously via the dorsal vein. Hemodynamic parameters and humoral mediators were measured at 2 h after the administration of endotoxin. The hearts were immediately excised to examine beta-adrenergic receptor density and GRK2 level. We also studied the inotropic response to isoproterenol at the same time in other animals. RESULTS: Myocardial beta-adrenergic receptor density in the membrane fraction was decreased after an intravenous administration of 10 mg/kg LPS (LPS group: baseline value; 82 +/- 11 fmol/mg protein; 120 min after LPS; 58 +/- 11 fmol/mg protein, P < 0.05). GRK2 levels in the membrane and cytosolic fraction of the control group did not change. In the LPS group, GRK2 levels in the membrane fraction were increased at 60 and 120 min after the treatment (60 min; control, 4.5 +/- 0.4; pithed control, 4.4 +/- 0.6; LPS group, 6.2 +/- 0.3; pithed LPS group, 5.5 +/- 0.4; 120 min: control, 4.4 +/- 0.3; pithed control, 4.9 +/- 0.7; LPS group, 7.1 +/- 0.3; pithed LPS group, 5.9 +/- 0.4; densitometric unit, respectively: P < 0.05). CONCLUSIONS: GRK2 levels in the membrane fraction are increased during septic shock in rats. GRK2 might play a role in the impairment of the beta-adrenergic receptor signal transduction system.

Adrenergic beta-Agonists↗
PubMed2002

The neurotoxicity of local anesthetics on growing neurons: a comparative study of lidocaine, bupivacaine, mepivacaine, and ropivacaine.

UNLABELLED: Local anesthetics can be neurotoxic. To test the hypothesis that exposure to local anesthetics produces morphological changes in growing neurons and to compare this neurotoxic potential between different local anesthetics, we performed in vitro cell biological experiments with isolated dorsal root ganglion neurons from chick embryos. The effects of lidocaine, bupivacaine, mepivacaine, and ropivacaine were examined microscopically and quantitatively assessed using the growth cone collapse assay. We observed that all local anesthetics produced growth cone collapse and neurite degeneration. However, they showed significant differences in the dose response. The IC(50) values were approximately, 10(-2.8) M for lidocaine, 10(-2.6) M for bupivacaine, 10(-1.6) M for mepivacaine, and 10(-2.5) M for ropivacaine at 15 min exposure. Some reversibility was observed after replacement of the media. At 20 h after washout, bupivacaine and ropivacaine showed insignificant percentage growth cone collapse in comparison to their control values whereas those for lidocaine and mepivacaine were significantly higher than the control values. Larger concentrations of the nerve growth factor (NGF) did not improve this reversibility. In conclusion, local anesthetics produced morphological changes in growing neurons with significantly different IC(50). The reversibility of these changes differed among the four drugs and was not influenced by the NGF concentration. IMPLICATIONS: Local anesthetics induce growth cone collapse and neurite degeneration in the growing neurons. Mepivacaine was safer than lidocaine, bupivacaine, and ropivacaine for the primary cultured chick neurons.

Amides↗
PubMed2002

Slow rewarming has no effects on the decrease in jugular venous oxygen hemoglobin saturation and long-term cognitive outcome in diabetic patients.

UNLABELLED: The purpose of this study was to examine the effects of rewarming rate on internal jugular venous oxygen hemoglobin saturation (SjvO(2)) during the rewarming period, and long-term cognitive outcome in diabetic patients. We studied 30 diabetic patients scheduled for elective coronary artery bypass graft surgery. As a control, 30 age-matched nondiabetic patients were identified. The diabetic patients were randomly divided into two groups: the Slow Rewarming group (n = 15) (mean rewarming speed: 0.22 degrees +/- 0.07 degrees C/min, mean +/- SD) or the Standard Rewarming group (Standard group) (n = 15) (mean rewarming speed: 0.46 degrees +/- 0.09 degrees C/min, mean +/- SD). After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor SjvO(2) continuously. Hemodynamic variables and arterial and jugular venous blood gases were measured at nine time points. All patients underwent a battery of neurologic and neuropsychologic tests on the day before the operation and at 4 mo after surgery. The SjvO(2) values in the Standard group were decreased during the rewarming period compared with at the induction of anesthesia (P < 0.05). There was a significant difference in the SjvO(2) value in the Control group between standard rewarming and slow rewarming during rewarming periods (Standard Control group: 51% +/- 8%, Slow Control groups: 58% +/- 5%) (P < 0.05). However, there was no difference in the SjvO(2) value in diabetic patients between standard rewarming and slow rewarming during the rewarming period. The rewarming rates (odds ratio: 0.8; 95% confidence interval: 0.5-1.3; P = 0.6) had no correlation with cognitive impairment at 4 mo after the surgery. Diabetes (odds ratio: 1.6; 95% confidence interval: 0.9-2.6; P = 0.04) was a factor in relation to cognitive impairment at 4 mo after the surgery. We concluded that a slow rewarming rate had no effects on the reduction in SjvO(2) value and long-term cognitive outcome in diabetic patients. IMPLICATIONS: We examined the effects of rewarming rate on internal jugular venous oxygen hemoglobin saturation in diabetic and nondiabetic patients during the rewarming period and long-term cognitive outcome. Slow rewarming could not prevent the frequency of the reduction in internal jugular venous oxygen hemoglobin saturation and adverse cognitive outcome in diabetic patients.

Aged↗
PubMed2002

Increasing mean arterial blood pressure has no effect on jugular venous oxygen saturation in insulin-dependent patients during tepid cardiopulmonary bypass.

UNLABELLED: Preexisting diabetes mellitus is one of the major factors related to adverse postoperative neurological disorders after cardiac surgery. In previous reports, we found that diabetic patients more often experienced cerebral desaturation than nondiabetic patients during normothermic cardiopulmonary bypass (CPB). The purpose of this study was to examine the effects of increasing mean arterial blood pressure (MAP) by the administration of phenylephrine on internal jugular venous oxygen hemoglobin saturation (SjvO2) during tepid CPB in diabetic patients. We studied 20 diabetic patients scheduled for elective coronary artery bypass graft surgery and, as a control, 20 age-matched nondiabetic patients. After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor SjvO2. After measuring the baseline partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values, MAP was increased by the repeated administration of a 10-microg bolus of phenylephrine until it reached 100% of baseline values. There was a significant difference in SjvO2 value between the Diabetic and CONTROL GROUPs after the administration of phenylephrine (Diabetic group, 56% +/- 6%; CONTROL GROUP: 60% +/- 4%) (P < 0.05). There was a significant difference in the arterial-jugular oxygen content difference value between the Diabetic and CONTROL GROUPs after the administration of phenylephrine (diabetic group, 4.9% +/- 0.6%; CONTROL GROUP, 4.5% +/- 0.4%) (P < 0.05). We subdivided the Diabetic group into three groups (Diet Therapy group [n = 4], Glibenclamide group [n = 10], and Insulin-Dependent group [n = 6]). There was a significant difference in the mean slopes of SjvO2 versus cerebral perfusion pressure for increasing cerebral perfusion pressure between the Insulin-Dependent group and the other groups (Dunnett test: P = 0.04). Increasing MAP had no effects on the SjvO2 value in insulin-dependent patients during tepid CPB. IMPLICATIONS: We examined the effects of increasing mean arterial blood pressure (MAP) by the administration of phenylephrine on internal jugular venous oxygen saturation (SjvO2) during tepid cardiopulmonary bypass in diabetic patients and found that increasing MAP had no effect on the SjvO2 value in insulin-dependent patients.

Adrenergic alpha-Agonists↗
PubMed2002

Impairment of hepatosplanchnic oxygenation and increase of serum hyaluronate during normothermic and mild hypothermic cardiopulmonary bypass.

UNLABELLED: Hepatic sinusoidal endothelial cells (SECs) are more vulnerable to hypoxia or hypothermia than hepatocytes. To test the hypothesis that hepatic venous desaturation during cardiopulmonary bypass (CPB) leads to impairment of SEC function, we studied the plasma kinetics of endogenous hyaluronate (HA), a sensitive indicator of SEC function, and hepatosplanchnic oxygenation during and after CPB. Twenty-five consecutive patients scheduled for elective coronary artery bypass graft surgery, who underwent normothermic (>35 degrees C; n = 15) or mild hypothermic (32 degrees C; n = 10) CPB participated in this study. A hepatic venous catheter was inserted into each patient to monitor hepatosplanchnic oxygenation and serum levels of HA concentration. Hepatic venous oxygen saturation decreased essentially to a similar degree during normothermic and mild hypothermic CPB. Hepatosplanchnic oxygen consumption and extraction increased during normothermic (P < 0.05), but not mild hypothermic, CPB. Both arterial and hepatic venous HA concentrations showed threefold increases during and after CPB in both groups. A positive correlation was found between hepatosplanchnic oxygen consumption and arterial HA concentrations during CPB, suggesting a role of changes in hepatosplanchnic oxygen metabolism in the mechanisms of increases in serum HA concentrations. The failure of the liver to increase HA extraction to a great degree suggests that a functional impairment of the SEC may contribute to the observed increase of serum HA. IMPLICATIONS: Hepatic sinusoidal endothelial cells (SECs) are pivotal in the regulation of sinusoidal blood flow. This study showed that SEC function might be impaired during and after cardiopulmonary bypass, irrespective of the temperature management.

Aged↗