Biomedical subjects

Takefumi Sakabe

Publications and source records attributed to Takefumi Sakabe.

26 records · Page 2Linked to original sources

PubMed2003

Lack of evidence for apoptosis as a cause of delayed onset paraplegia after spinal cord ischemia in rabbits.

UNLABELLED: The mechanisms for delayed onset paraplegia after transient spinal cord ischemia are not fully understood. We investigated whether apoptotic motor neuron death is involved in its development. Spinal cord ischemia was induced for 15 min by occlusion of the abdominal aorta in rabbits. At 8, 24, or 48 h after reperfusion, hind limb motor function was assessed, and the lumbar spinal cord was examined morphologically (hematoxylin-eosin and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling staining) and biochemically (breakdown products of alpha-fodrin and patterns of DNA changes). At each time point, 14 rabbits were studied (7 for histopathology and 7 for biochemical analysis). Six rabbits served as sham controls. Delayed motor dysfunction developed in two thirds of the rabbits. The motor neurons in the rabbits with motor dysfunction (not paraplegia) showed swelling and a finely granular dispersed Nissl substance. In paraplegic rabbits, destruction of the gray matter and prominent inflammatory cell infiltration were observed. No apoptotic motor neuron was found in any rabbit. There was neither detectable increase in a caspase-3-mediated breakdown product of alpha-fodrin, nor DNA laddering in any rabbit. The results suggest that apoptosis has a negligible role in the pathophysiology of delayed paraplegia in the spinal cord ischemia model examined. IMPLICATIONS: Although the possibility of apoptotic motor neuron death cannot be completely excluded, delayed onset paraplegia after transient spinal cord ischemia is largely associated with necrotic cell death.

Anesthesia↗

PubMed2003

The temporal profile of the reaction of microglia, astrocytes, and macrophages in the delayed onset paraplegia after transient spinal cord ischemia in rabbits.

UNLABELLED: In the present study, we sought to elucidate the temporal profile of the reaction of microglia, astrocytes, and macrophages in the progression of delayed onset motor dysfunction after spinal cord ischemia (15 min) in rabbits. At 2, 4, 8, 12, 24, and 48 h after reperfusion (9 animals in each), hind limb motor function was assessed, and the lumbar spinal cord was histologically examined. Delayed motor dysfunction was observed in most animals at 48 h after ischemia, which could be predicted by a poor recovery of segmental spinal cord evoked potentials at 15 min of reperfusion. In the gray matter of the lumbar spinal cord, both microglia and astrocytes were activated early (2 h) after reperfusion. Microglia were diffusely activated and engulfed motor neurons irrespective of the recovery of segmental spinal cord evoked potentials. In contrast, early astrocytic activation was confined to the area where neurons started to show degeneration. Macrophages were first detected at 8 h after reperfusion and mainly surrounded the infarction area later. Although the precise roles of the activation of microglia, astrocytes, and macrophages are to be further determined, the results indicate that understanding functional changes of astrocytes may be important in the mechanism of delayed onset motor dysfunction including paraplegia. IMPLICATIONS: Microglia and macrophages play a role in removing tissue debris after transient spinal cord ischemia. Disturbance of astrocytic defense mechanism, breakdown of the blood-spinal cord barrier, or both seemed to be involved in the development of delayed motor dysfunction.

Anesthesia↗

PubMed2003

A comparison of the neurotoxic effects on the spinal cord of tetracaine, lidocaine, bupivacaine, and ropivacaine administered intrathecally in rabbits.

UNLABELLED: We have reported that increased glutamate concentrations in microdialysate of the cerebrospinal fluid (CSF) may be clue phenomena to elucidate mechanisms of neurotoxicity of intrathecal tetracaine. However, little is known about whether this is true for other local anesthetics. In this study, we compared the effects of local anesthetics on glutamate concentrations in CSF microdialysate and neurologic and histopathologic outcome. Rabbits were assigned into 5 groups (n = 6 in each) and intrathecally received 0.3 mL of NaCl solution (control), 2% tetracaine, 10% lidocaine, 2% bupivacaine, or 2% ropivacaine. Neurologic and histopathologic assessments were performed 1 wk after the administration. Intrathecal local anesthetics significantly increased glutamate concentrations with no significant differences among the four local anesthetics. The sensory and motor functions in the lidocaine group were significantly worse than in the other groups. Characteristic histopathologic changes were vacuolation in the dorsal funiculus and chromatolytic damage of motor neurons. The extent of vacuolation of the dorsal funiculus was in the order of lidocaine = tetracaine > bupivacaine > ropivacaine. Although the differences among the local anesthetics cannot be explained by glutamate concentrations, the results suggest that the margin of safety may be smallest with lidocaine. IMPLICATIONS: Large concentrations of local anesthetics administered intrathecally increased glutamate concentrations in the cerebrospinal fluid. The margin of safety may be smallest with lidocaine.

Amides↗

PubMed2003

[Effect of body fat percentage on estimated propofol concentrations at awakening from anesthesia using target controlled infusion].

BACKGROUND: Target controlled infusion (TCI) for propofol allows anesthesiologists to target constant blood concentrations of propofol. However, the pharmacokinetic parameters in TCI system do not take account of the patient's age, make up and gender. We evaluated the relationship between body fat percentage and the estimated effect site propofol concentrations at awakening. METHODS: Anesthesia was induced in 37 patients with fentanyl and propofol by TCI. Patients's percentage of fat was evaluated by measuring the thickness of the three parts of the skin fat with Skyndex (Caldwell Justiss, USA). After surgery and discontinuation of anesthesia, the estimated effect site propofol concentrations (EPEC) were determined when the patient could respond to verbal command. RESULTS: The EPECs at awakening were 1.5 +/- 0.2 micrograms.ml-1 in male and 1.5 +/- 0.3 micrograms.ml-1 in female. In male, the percentage of fat and body mass index (BMI) correlated significantly with EPEC (r = 0.79 and 0.49 respectively). In female, the percentage of fat and BMI did not correlate with EPEC. The estimated fentanyl effect site concentrations at awakening did not correlate with the EPEC. CONCLUSIONS: Male patients who have high percentage of fat have a tendency to delayed of awakening from propofol anesthesia. In female, however, no correlation was seen between percentage of fat and awakening time from propofol anesthesia. Measuring the percentage of fat might bring a new insight into pharmacokinetics of propofol.

Anesthesia Recovery Period↗

PubMed2002

Preconditioning with hyperbaric oxygen and hyperoxia induces tolerance against spinal cord ischemia in rabbits.

BACKGROUND: The aim of this study was to determine if the ischemic tolerance could be induced in the spinal cord by pretreatment with hyperbaric oxygen (HBO) and what components of HBO (hyperoxia, hyperbaricity, and combination of these two) were critical in the induction of tolerance against ischemic injury. METHODS: In experiment 1, 21 rabbits were randomly assigned to one of three groups (n = 7 each): animals in the control group received no HBO before spinal cord ischemia; animals in the HBO-1 and HBO-2 groups received HBO (2.5 atmosphere absolute [ATA], 100% O2) pretreatment 1 h/day for 3 and 5 days before ischemia, respectively. In experiment 2, 48 rabbits were randomly assigned to one of four groups (n = 12 each): the control group received no HBO (21% O2, 1 ATA, 1 h/day, 5 days) before spinal cord ischemia; the HB group received 1-h treatment in 21% O2 at 2.5 ATA each day for 5 days; the HO group received 1-h treatment in 100% oxygen at 1 ATA each day for 5 days; and the HBO group received HBO (2.5 ATA, 100% O2) treatment 1 h/day for 5 days. Twenty-four hours after the last treatment, spinal cord ischemia was induced by an infrarenal aorta clamping for 20 min. Forty-eight hours after reperfusion, hind-limb motor function and histopathology of the spinal cord were examined in a blinded fashion. RESULTS: In experiment 1, the neurologic outcome in the HBO-2 group was better than that of the control group (P = 0.004). The number of normal neurons in the anterior spinal cord in the HBO-2 group was more than that of the control group (P = 0.021). In experiment 2, the neurologic and histopathologic outcomes in the HBO group were better than that of the control group (P < 0.01). The histopathologic outcome in the HO group was better than that in the control group (P < 0.05). CONCLUSIONS: Serial exposure to high oxygen tension induced ischemic tolerance in spinal cord of rabbits. Simple hyperbaricity (2.5 ATA, 21% O2) did not induce ischemic tolerance.

Animals↗

PubMed2002

Rapid tolerance to focal cerebral ischemia in rats is attenuated by adenosine A1 receptor antagonist.

Two types of ischemic tolerance in the brain, rapid and delayed, have been reported in terms of the interval between the conditioning and test insults. Although many reports showed that delayed-phase neuroprotection evoked by preconditioning is evident after 1 week or longer, there have been a few investigations about rapidly induced tolerance, and the reported neuroprotective effects become ambiguous 7 days after the insults. The authors examined whether this rapid ischemic tolerance exists after 7 days of reperfusion in a rat focal ischemic model, and investigated modulating effects of the adenosine A 1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine). Preconditioning with 30 minutes of middle cerebral artery occlusion reduced infarct volume 7 days after 180 minutes of subsequent focal ischemia given after 1-hour reperfusion. The rapid preconditioning also improved neurologic outcome. These beneficial effects were attenuated by pretreatment of 0.1 mg/kg DPCPX, which did not influence the infarct volume after conditioning (30 minutes) or test (180 minutes) ischemia when given alone. The results show that preconditioning with a brief focal ischemia induces rapid tolerance to a subsequent severe ischemic insult, the effect of which is still present after 7 days of reperfusion, and that the rapid ischemic tolerance is possibly mediated through an adenosine A 1 receptor-related mechanism.

Adaptation, Physiological↗

PubMed2002

[Transient complete atrioventricular block during renal transplantation].

A 25-year-old female underwent renal transplantation. The patient had no complication preoperatively except hypertension. Preoperative electrocardiogram revealed no abnormality. Anesthesia was maintained with sevoflurane. Donor kidney was perfused with University of Wisconsin (UW)'s solution (4 degrees C) after removal. Transient complete atrioventricular block appeared twice after reperfusion of the transplanted kidney. Adenosine in the UW's solution was considered the major cause of atrioventricular block in this patient. Attention must be paid to the occurrence of atrioventricular block and bradycardia shortly after reperfusion in the case where UW's solution was used for donor kidney perfusion.

Adenosine↗

PubMed2002

[Efficacy of bispectral index monitoring in improving anesthetic management, economics, and use of the operating theater].

This study was designed to assess the efficacy of bispectral index (BIS) monitoring in reducing the amount of volatile anesthetics used and improving recovery profiles. Sixty patients (ASA physical status 1 or 2) undergoing various surgical procedures under sevoflurane/nitrous oxide anesthesia were studied. The patients were randomly assigned to two groups of which anesthesia was carried out with (BIS group) or without (control group) monitoring BIS, and in the latter, anesthesiologist was blinded to the BIS values. In the BIS group, sevoflurane concentration was adjusted to achieve target BIS values between 40-60 during surgery and 60-75 during the final 15 min of the surgery. Drug usage, incidence of intraoperative complications, and recovery parameters were recorded. Demographics were similar between the groups. The BIS values in the BIS group were significantly higher compared with those of control group in which BIS values were blinded during anesthesia. The sevoflurane consumption in the BIS group (17 +/- 3 ml.h-1) was lower than control group (22 +/- 3 ml.h-1). Compared with control group, the patients in BIS group were extubated earlier and became eligible for discharge earlier from recovery room than control group. There was no significant difference in the incidence of intraoperative complications between the groups. Titrating sevoflurane concentration with BIS monitoring during anesthesia decreased anesthetic consumption and improved recovery compared with standard clinical practice.

Adult↗