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Biomedical subjects

M Tagami

Publications and source records attributed to M Tagami.

At least 19 recordsLinked to original sources
PubMed1999

[Dorsal root identification using spinal endoscopy and electro-physiology].

We aimed to develop a method of accurately identifying the dorsal root for the corresponding peripheral afferent nerve under endoscopic observation. We developed an endoscope with an external diameter of 1.8 mm. After small laminectomy on the lower thoracic vertebrae, we inserted this endoscope carefully into the epidural and then subarachnoid spaces. We observed structures in these spaces with the endoscope. We tried to determine the spatial relationship between these electrodes and dorsal root. After identifying each space, we inserted two electrodes into the visualized space to record evoked potentials; a bipolar electrode (protocol 1) and a catheter-type eight polar electrode (protocol 2). Each pole could be distinguished by marks. To stimulate peripheral nerves, we inserted needle-type electrodes into Th 10, 11 and 12 intercostal nerves. We attempted to record potentials from dorsal surface of the cord generated by intercostal nerve stimulus. Protocol 1: We moved the position of the bipolar recording electrodes between Th 9 and L 1 by 1 cm increment, and obtained evoked potentials correspondingly. Protocol 2: We chose the neighboring pairs of poles sequentially from the tip of the catheter for bipolar recording. At the end of each experiment, we dissected the animal and checked the intercostal nerve originating from the root. With the endoscope, we could clearly observe structures in the epidural and subarachnoid spaces. We could record evoked potentials from the dorsal spinal cord with the electrodes located either in epidural or in subarachnoid spaces. Shapes of evoked potentials changed characteristically according to the relative position between the root and the electrode. The largest potentials were obtained when the electrode was nearest to the dorsal root, of which the peripheral nerve was being stimulated. By combining endoscopy with the electrophysiological technique, we could accurately identify the dorsal roots for the corresponding peripheral afferent nerves. This method may be used for the selective dorsal root blockade under the visual field.

Animals↗
PubMed1998

Measurement of serum and synovial fluid keratan sulphate and antibody to collagen type II in equine osteoarthritis.

Keratan sulphate (KS) concentration and anticollagen type II antibody levels were measured in the serum and synovial fluid (SF) of clinically normal horses and horses with osteoarthritis (OA). Serum KS in OA was significantly higher than that in normal horses, while no significant difference was found in KS levels of SF between normal and OA. Assays of antibody to collagen type II showed no significant increase in sera and SF of OA. It was suggested that levels of serum KS would be of value in the pathological detection of OA in the joint, although there was no evidence that the measurable autoimmunity to collagen antigens would reflect the process of OA.

Animals↗
PubMed1998

Zonal differences in effects of HGF/SF and EGF on DNA synthesis in hepatocytes under fed or starved conditions.

Zonal differences of DNA synthesis in hepatocytes induced by hepatocyte growth factor and/or scatter factor (HGF/SF) and epidermal growth factor (EGF) were investigated using male Wistar rats under fed or starved conditions. Overall, DNA synthesis was greater in fed rats than in starved rats. The predominance of EGF in periportal hepatocytes (PPH) on zonal DNA synthesis was reversed by starved conditions, but the predominance of HGF/SF on zonal DNA synthesis in perivenous hepatocytes (PVH) was not influenced by nutritional conditions. 125I-labeled EGF and 125I-labeled HGF/SF-receptor binding studies revealed no significant difference between PPH and PVH in starved or fed rats. To investigate the mechanism of the signal transduction pathway, we used genistein, an inhibitor of tyrosine kinase. Genistein had different effects on zonal difference in EGF and HGF/SF. In EGF, 1 microgram/ml genistein abolished zonal differences, but in HGF/SF 1 microgram/ml genistein did not abolish zonal differences. These data suggest that, in contrast to HGF/SF, zonal difference of DNA synthesis by EGF was dependent on nutritional conditions and DNA synthesis induced by HGF/SF and EGF might be related to tyrosine kinase, but the influence of tyrosine kinase on DNA synthesis was different between HGF/SF and EGF.

Animals↗
PubMed1998

Serum copper and ceruloplasmin activity at the early growing stage in foals.

Serum concentrations of copper (Cu), zinc (Zn), manganese (Mn), calcium (Ca) and inorganic phosphorus (P), as well as antigenic ceruloplasmin (Cp) and oxidase activity as a functional index for copper metabolism, were measured in 10 foals (5 males and 5 females) and their dams. Samples were harvested from the foals within 1 wk after birth and monthly from 1 to 17 mo of age. Samples were collected from their dams in the perinatal period (monthly from 2 mo before delivery to 5 mo postpartum). Serum oxidase activity, antigenic Cp and Cu in foals were extremely low at 1 wk. Serum Cp had the lowest value of 17.0 +/- 8.0 (mean +/- SD) mg/dL within the 1st wk, then increased rapidly up to 43.7 +/- 5.8 mg/dL at 1 mo, and maintained this level until the 17th mo. Serum Zn in foals had the highest value of 73.2 +/- 13.1 micrograms/dL within 1 wk, then decreased to 38.3 +/- 5.9 micrograms/dL by 17 mo. Serum Mn, Ca and P in mares were almost stable and within established reference ranges for our laboratory in the perinatal period, and these values in foals were also in the normal range. Even on appropriate feeding, serum Cu, Cp and oxidase activity were quite low a few weeks after birth, while a higher proportion of Cp-binding copper was found in the foals. This might be caused by the limited synthesis of ceruloplasmin in this period. These data suggest that newborn foals are in a critical situation of marginal copper status in the early stage of growth.

Aging↗
PubMed1998

Vitamin E prevents apoptosis in cortical neurons during hypoxia and oxygen reperfusion.

Cerebral ischemia followed by oxygen reperfusion induces apoptosis in hippocampal neurons in stroke-prone spontaneously hypertensive rats (SHRSP) but not in Wistar Kyoto rats (WKY). The overproduction of oxygen-free radicals that occurs in the tissues of SHRSP is implicated in reoxygenation injury after hypoxia. Antioxidants inhibit reoxygenation injury in hippocampal slices, and temporal cortices in Alzheimer's disease increase sensitivity to oxygen-free radicals. Because this sensitivity may contribute to the development of the disease, we have studied hypoxia and oxygen reperfusion using cortical neurons isolated from WKY and SHRSP (at 15 days of gestation). We have tried to determine whether cortical neurons are damaged under these conditions, and whether neurons from SHRSP are more vulnerable than those from WKY. We have tried also to verify whether neuronal damage is minimized by vitamin E using the following techniques: (a) Trypan blue staining, (b) in situ staining of apoptosis, (c) ultrastructural examination, and (d) measurement of lactic dehydrogenase (LDH) activity in the bathing medium. Furthermore, we have examined the mechanisms involved in the development of neuronal damage and have studied ways of minimizing it. We demonstrated that 36 hours of hypoxia significantly increased the rate of cell death in SHRSP (p < 0.01), although 12 to 24 hours of hypoxia did not increase cell death in either WKY or SHRSP. In addition, 6 to 36 hours of hypoxia and 1.5 to 5 hours of oxygen reperfusion heavily damaged cells of both WKY and SHRSP, and most became apoptotic or necrotic. In contrast, cells incubated with 50 to 300 microg/ml of vitamin E remained intact, although 10 to 20 microg/ml of vitamin E did not totally preserve the cells. Moreover, vitamin E protected the neurons from high concentrations of sodium nitroprusside (nitric oxide donor) in a dose-dependent manner. Vitamin E, when added to the cells, increased in concentration in a time-dependent manner over a 24-hour period and in a dose-dependent manner below 200 microg/ml, and it was detected mostly in the mitochondria. We also demonstrated that serial treatments with allopurinol (a xanthine oxidase inhibitor) or superoxide dismutase preserved neurons during hypoxia and oxygen reperfusion. These data indicate that SHRSP neurons are weaker than WKY neurons in long-term hypoxia; oxygen radical generation occurs in the early minutes after reperfusion, and then the oxygen-free radicals cause heavy damage to the cells; and antioxidants including vitamin E react with the radicals, thereby preventing apoptosis and necrosis. Therefore, antioxidants appear to be the most important agents in lowering oxygen-free radical damage in cortical neurons.

Animals↗
PubMed1997

Nitric oxide deficiency induces myocardial infarction in hypercholesterolaemic stroke-prone spontaneously hypertensive rats.

1. To observe the effect of nitric oxide (NO) on the myocardium, the NO synthesis inhibitor NG-nitro-L-arginine (L-NNA) was administered to hypercholesterolaemic stroke-prone spontaneously hypertensive (SHRSP) rats. 2. Hypercholesterolaemic SHRSP were produced by feeding SHRSP a high fat and high cholesterol diet (HFC) for 2 weeks. The rats were then divided into three groups: (i) the N group, which were fed the HFC diet containing 0.023% L-NNA and 1% NaCl in their drinking water (n = 10); (ii) the NH group, which were fed the HFC diet containing 0.023% L-NNA and 1% NaCl in their drinking water which also contained 80 mg/L hydralazine (n = 10); and (iii) the C group, which were fed the HFC diet and 1% NaCl in their drinking water (n = 10). 3. All rats in the N and NH groups died within 35 days of the initiation of L-NNA administration. Rats in the N and NH groups had significantly increased serum creatine phosphokinase, lactate dehydrogenase, glutamic oxaloacetic transaminase and serum total cholesterol levels compared with rats in the C group. 4. Fibrosis in response to necrosis was histopathologically observed in the hearts of all rats in the N and NH groups without exception. Occlusion or intimal thickening in the arteries adjacent to the necrotic regions was also observed. 5. These results suggest that nitric oxide deficiency induces myocardial infarction in hypercholesterolaemic SHRSP. These NO-deficient hypercholesterolaemic SHRSP offer a new model of myocardial infarction in rats.

Animals↗
PubMed1997

[Aspiration pneumonia during the endotracheal intubation on the occasion of bladder perforation by TUR].

We report on two cases of aspiration pneumonia which developed during the endotracheal intubation after bladder perforation during TUR. The first case was a 79 y.o. male, who underwent TUR-P and lithotripsy under spinal and epidural anesthesia. The second case was a 69 y.o. male, who had undergone TUR-Bt under nitrous oxide-oxygen-enflurane anesthesia. General anesthesia was selected to perform an laparotomy when the diagnosis was made. They vomited a considerable amount of gastric content just after giving the drugs for induction. The chest X-rays revealed signs of aspiration pneumonia. These X-ray findings improved in a week using antibiotic therapy. Although TUR is performed as scheduled, vomiting may occur in the case of unexpected bladder perforation, which can cause aspiration pneumonia. In such emergency, we should insert a nasal tube before induction, press the cricoid (crush induction), or intubate with the patient awake.

Aged↗
PubMed1997

Insulin-like growth factors prevent apoptosis in cortical neurons isolated from stroke-prone spontaneously hypertensive rats.

Cerebral ischemia induces a massive efflux of glutamate causing delayed neuronal death in stroke-prone spontaneously hypertensive rats (SHRSP) but not in Wistar Kyoto rats (WKY). It is obvious that L-N-nitroarginine (L-NNA; NO synthase (NOS) inhibitor), benzamide (poly(ADP-ribose) synthetase inhibitor), and growth factors are involved in reducing neuronal cell death due to toxic conditions, especially phosphatidylinositol 3 (PI3)-kinase activity; however, no studies have clarified whether genetic vulnerability to neurotoxic states is present in cortical neurons isolated from SHRSP. For this purpose, we prepared cortical neurons from WKY and SHRSP (15 weeks of gestation) to test the genetic vulnerability involved in the pathogenesis of stroke as well as apoptosis of cortical neurons isolated from SHRSP. We also examined the mechanisms necessary to reduce apoptosis under neurotoxic states using ultrastructural and biochemical techniques. Cortical neurons from SHRSP were in fact found to be more vulnerable than neurons from WKY and resulted in apoptosis when treated with nitric oxide (NO)- and N-methyl-D-aspartate (NMDA)-mediated neurotoxic agents. Growth factors, especially insulin-like growth factor (IGF), rescued neurons from NO- and NMDA-mediated neurotoxicity, particularly those from SHRSP. Conversely, benzamide and L-NNA reduced NMDA-mediated neurotoxicity but not NO-mediated toxicity. The ability to protect neurons from neurotoxicity was as follows: IGF-->nerve growth factor epidermal growth factor-->L-NNA-->benzamide. In addition, it was demonstrated that wortmannin, a PI3-kinase inhibitor, lessened the protective effects of these growth factors against NO-mediated toxicity. The data thus indicate that genetic factors related to neuronal vulnerability to apoptosis are involved in the pathogenesis of stroke lesions in SHRSP. PI3-kinase activity, which is stimulated by growth factors, is closely related to protective effects against NO- and NMDA-mediated toxicity in cortical neurons, especially those isolated from SHRSP. Moreover, the genetic vulnerability observed in SHRSP neurons is possibly linked to the inadequate activation of signaling pathways in the downstream of protein tyrosine kinases.

Animals↗
PubMed1997

Insulin-like growth factor-1 attenuates apoptosis in hippocampal neurons caused by cerebral ischemia and reperfusion in stroke-prone spontaneously hypertensive rats.

Cerebral ischemia followed by reperfusion induced apoptosis in stroke-prone spontaneously hypertensive rats (SHRSP) but not in Wistar Kyoto rats (WKY). Our in vitro studies revealed that IGF-1 prevented apoptosis caused by nitric oxide- and N-methyl-D-aspartate-mediated toxic agents in cortical neurons isolated from SHRSP. In addition, it was reported that IGF-1 given 1 hour before ischemia significantly attenuated the incidence of myocyte apoptosis after myocardial ischemia and reperfusion. IGF-1 (20 micrograms/rat) was administered ip 1 hour before the clipping of both common carotid arteries in WKY and SHRSP. Rats underwent cerebral ischemia for 20 minutes and reperfusion for 6 days before they were killed. We cut the brain coronally, removed sections from the hippocampal CA1 region, and examined the neurons in these samples using an electron microscope. We tried to clarify whether pretreatment using IGF-1 decreases the number of apoptotic neurons in SHRSP with cerebral ischemia followed by reperfusion. SHRSP with normal cerebral circulation had 30.4 +/- 8.0 apoptotic neurons per 1000 neurons. Cerebral ischemia followed by reperfusion significantly (p < 0.01) increased the number of apoptotic neurons (235.2 +/- 25.2/1000 neurons) in SHRSP. In contrast, pretreatment with IGF-1 reduced the number of apoptotic neurons in SHRSP (82.8 +/- 11.2/1000 neurons; p < 0.01) under otherwise identical conditions. We concluded that the genetic vulnerability to apoptosis in SHRSP neurons was involved in the pathogenesis of stroke lesions and that this vulnerability was attenuated by the IGF-1 pretreatment.

Animals↗
PubMed1997

Evaluation of the catabolic activity of cartilage by measurement of serum keratan sulfate concentration in foals.

OBJECTIVES: To determine keratan sulfate (KS) concentration in the serum of foals at the early stage of growing, and to evaluate the role of serum KS as a cartilage catabolic marker, comparing its values with the fluctuation of serum alkaline phosphatase (ALP) activity as a measurement of osteoblastic activity. ANIMALS: 12 foals with normal growth and 3 foals with joint abnormalities within 18 months after birth. PROCEDURE: Measurement of KS concentration and ALP activity in serum and radiographic and physical examinations were done. RESULTS: In all foals, serum KS concentration was high from 1 week after birth to 3 months of age, while serum ALP decreased with aging. The value started to decrease rapidly from 3 to 5 months of age, then gradually reached adult values. During the first 3 months, KS concentration in male foals was significantly higher than that in female foals. In 3 foals which had joint problems, KS concentration was higher than that in normally growing foals at 1 week, and at 1, 2, and 3 months of age. CONCLUSIONS: Cartilage catabolic activity is higher in developing foals up to 3 months of age, suggesting that the immature joint at this time could be easily affected by any factor of loading. Moreover, though only 3 diseased foals were examined, higher serum KS concentration in these foals suggest that this variable might be a useful measure of joint diseases, even at an early stage of life in foals.

Aging↗
PubMed1996

Ultrastructural analysis of survival in cultured smooth muscle cells isolated from stroke-prone spontaneously hypertensive rats: effect of growth factors.

Our previous study in vivo suggested that vascular smooth muscle cells (VSMCs) in stroke-prone spontaneously hypertensive rats (SHRSP) were vulnerable when plasma components were deficient. Therefore, we cultured VSMCs isolated from normotensive and hypertensive rats to clarify the weakness of VSMCs isolated from hypertensive rats and maintained in plasma-deficient conditions by employing ultrastructural and biochemical analyses. VSMCs, obtained from normotensive rats and cultured without fetal bovine serum (FBS) for 1 week, were intact and well differentiated; without FBS for 2 weeks retained their original structures except for several degenerative changes. VSMCs, obtained from hypertensive rats and cultured without FBS for 2 weeks, were extensively damaged and lost their cell organelles. Apoptotic bodies were frequently observed. We also cultured VSMCs in medium containing a variety of growth factors. VSMCs obtained from normotensive rats and cultured with epidermal growth factor or insulin-like growth factor-1 for 2 weeks were almost intact, as were VSMCs from hypertensive rats, although some degenerative changes of cell organelles were observed. VSMCs from hypertensive rats, maintained with platelet-derived growth factor-BB or basic fibroblast growth factor, were generally in poor condition. Thus VSMCs from hypertensive rats have hereditary weaknesses in cell survival including apoptosis and require specific growth factors for their maintenance.

Animals↗
PubMed1996

[Usefulness of NODSS (nasal/oral discriminate sampling system) in end-tidal carbon dioxide gas monitoring].

We investigated the usefulness of nasal/oral discriminate sampling system (NODSS) that had been developed recently in order to obtain the accurate end-tidal carbon dioxide (PET(CO2)) from a spontaneously breathing patient through a nomal airway. Fifty patients were monitored using a capnograph with NODSS following extubation in the postanesthesia unit. PET(CO2) data were collected by means of nasal, oral or nasal/oral sampling. The levels of arterial carbon dioxide (PaCO2) were determined simultaneously. In addition to examining the correlation between PET(CO2) and PaCO2, we investigated the influence of method of anesthesia, age and respiratory rate on the (PaCO2 - PET(CO2)) gradient. In most patients without nasal obstruction breathing through the nostril, PET(CO2) determined by selective nasal sampling was closer to PaCO2 than those by oral or nasal/oral sampling. Furthermore, the mean (PaCO2 - PET(CO2)) gradient was 4.98 mmHg in patients aged over 60, while it was 2.02 mmHg in patients aged under 60, suggesting that PET(CO2) could not be a good index in elderly people. There was no significant difference in the mean (PaCO2 - PET(CO2)) gradient among different methods of anesthesia. In conclusion, NODSS was useful in determining PET(CO2) more accurately and estimating PaCO2 precisely when used in relatively young people by selective nasal or oral sampling.

Adolescent↗
PubMed1995

Intravenous midazolam suppresses noxiously evoked activity of spinal wide dynamic range neurons in cats.

The effects of intravenously (i.v.) administered midazolam on noxiously evoked activity of spinal wide dynamic range (WDR) neurons were investigated in decerebrate, spinal-cord-transected cats. Extracellular, single-unit recordings were measured during stimulation by pinching the receptive field on the hind paw and the effect of midazolam at doses of 0.25, 0.5, 1, 2, and 4 mg/kg were measured. Two series of experiments were performed to characterize the analgesic effects of midazolam. In the first, dose-response experiments (n = 59) demonstrated a dose-dependent suppression of the noxiously evoked activity of spinal WDR neurons after midazolam administration. This effect of midazolam was maximal at a dose of 1 mg/kg i.v.. The second series of experiments (n = 14) demonstrated that a benzodiazepine antagonist, flumazenil (n = 8), promptly reversed the effect of midazolam, while an opioid antagonist, naloxone (n = 6), had no effect on the effect of midazolam. The present study demonstrates that i.v. administered midazolam suppresses noxiously evoked activity of spinal WDR neurons that is reversible by a benzodiazepine antagonist. This is consistent with an analgesic action of midazolam.

Animals↗
PubMed1995

Demonstration of hereditarily accelerated proliferation in astrocytes derived from spontaneously hypertensive rats.

1. We examined the proliferative rates of cultured astrocytes isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and stroke-resistant spontaneously hypertensive rats (SHRSR). Wistar-Kyoto rats (WKY) were used as a control for SHRSP and SHRSR. 2. In the presence of 10% fetal bovine serum (FBS), the doubling time for astrocytes from SHRSP and SHRSR was significantly shorter than WKY. 3. When quiescent astrocytes derived from SHRSP or SHRSR were released from serum-deprivation, the DNA synthesis was stimulated 13.3-fold and 12.5-fold, respectively, whereas only a 7.76-fold increase was observed in WKY astrocytes. 4. Further we studied the effects of two growth factors, epidermal growth factor (EGF) and fibroblast growth factor (FGF) on astrocytes proliferation. EGF induced greater DNA synthesis in SHRSP and SHRSR astrocytes compared with WKY astrocytes, although FGF had little or no effect. 5. Total cholesterol levels in SHRSP astrocytes and SHRSR astrocytes were significantly lower than that of WKY astrocytes, which was consistent with our previous observations in cultured vascular smooth muscle cells. 6. There was no difference in morphology among the cultured astrocytes from the three strains. 7. The abnormality of growth rate and cell membranes composition of astrocytes might be closely related to the genetic phenotypes (acute death of neurons and oedema of astrocytes) of SHRSP or SHRSR.

Animals↗
PubMed1995

Detailed examination of vascular lesions triggered by an inhibitor of endothelium-derived relaxing factor.

BACKGROUND: Inhibition of an endothelium-derived relaxing factor (EDRF) may contribute to the pathogenesis of thrombotic arterial occlusions. EXPERIMENTAL DESIGN: We measured the blood pressure and urinary excretion of protein, sodium, and potassium and histologically examined the brains, hearts, and kidneys in normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) fed on a diet containing: (a) EDRF inhibitor (L-N-nitroarginine:L-NNA); (b) L-arginine, which reverses the effect of L-NNA; or (c) both L-NNA and L-arginine for 1 to 8 weeks. In addition, we examined L-NNA-treated SHRSP, the blood pressures of which were lowered using hydralazine. Furthermore, we produced and examined Goldblatt's renal hypertensive rats, which are of a different type from those resulting from the L-NNA treatment. RESULTS: Both WKY and SHRSP rats fed on a diet containing L-NNA suffered from hypertension and cerebral infarctions in a dose-dependent manner. Cerebral infarctions occurred whether or not SHRSP rats were treated with an antihypertensive agent when they were fed a high dosage of L-NNA. In contrast, SHRSP rats, treated simultaneously with both L-NNA and L-arginine, suffered few cerebral infarctions, although they were severely hypertensive. In addition, there were no cerebral infarctions in Goldblatt's renal hypertensive rats, although they suffered from advanced hypertension. CONCLUSIONS: The data indicate that the inhibition of EDRF injures the vessel walls and encourages platelet adhesion to the damaged areas. The adhering platelets narrow the lumen with resultant thrombotic arterial occlusions. Pathophysiologic conditions that decrease EDRF synthesis appear to play an important role in cerebral, renal, and myocardial infarctions.

Animals↗
PubMed1994

[Effects of hyperventilation upon the spinal pain modulating system (third report)].

The purpose of this study is to investigate the mechanisms of the effect of hyperventilation on the spinal pain modulating system by using phentolamine. Under enflurane anaesthesia, cats received mid-collicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was changed to induce hypocapnia of PCO2 20-25 mmHg. After activities were well suppressed, phentolamine 0.5 mg with normal saline 1.0 ml was injected on the spinal cord. Changes of firings were investigated. When normocapnia was resumed, recovery followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Phentolamine significantly antagonized the suppressive effects of hyperventilation upon the activities of WDR cells. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to adrenergic pain modulating system.

Action Potentials↗
PubMed1994

[The effects of hyperventilation upon the spinal pain modulating system (second report)].

The purpose of this study is to investigate the effect of hyperventilation on the spinal pain modulating system by using naloxone. Under enflurane anaesthesia, cats were prepared with midcollicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was adjusted to produce hypocapnia of PCO2 20-25 mmHg. After activities of WDR cells were well suppressed, naloxone 0.1 mg.kg-1 was given intravenously. Changes of firings of WDR cells were investigated. Returning to normocapnia, recovery of firings was followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Naloxone significantly antagonized the suppressive effects of hyperventilation upon the activity of WDR cell. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to pain modulating system by endogenous opiates.

Action Potentials↗