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N Shimoyama

Publications and source records attributed to N Shimoyama.

At least 37 records · Page 2Linked to original sources

Role of nitric oxide in the development of thermal hyperesthesia induced by sciatic nerve constriction injury in the rat.

BACKGROUND: Nitric oxide (NO) has been shown to be involved in mediating nociceptive information transmission in the spinal cord. It is known that the N-methyl-D-aspartate receptor plays an important role in the development of the spinal facilitation evoked by a protracted small afferent input and that this effect is mediated at least in part by NO. Recently, it has been found that N-methyl-D-aspartate receptor-mediated spinal facilitation is crucial in the development of thermal hyperesthesia evoked by a nerve constriction injury. In the current study, we investigated the role of NO in the development of thermal hyperesthesia after a nerve constriction injury. METHODS: The Bennett and Xie model (four loose chromic gut ligations around the rat sciatic nerve) was used to examine the development of thermal hyperesthesia. An NO synthase inhibitor (N omega-nitro-L-arginine or N omega-nitro-L-arginine methyl ester hydrochloride), rat hemoglobin, or L-arginine was administered intrathecally 10 min before the nerve injury (pretreatment study) or 15 min after the nerve injury (posttreatment study). RESULTS: Pretreatment but not posttreatment administration of NO synthase inhibitor significantly delayed the development of thermal hyperesthesia. The effect of NO synthase inhibitor was reversed by the coadministration of L-arginine but not by the coadministration of D-arginine. Pretreatment with rat hemoglobin also delayed the development of thermal hyperesthesia. L-Arginine itself had no effect on the development of thermal hyperesthesia. CONCLUSIONS: NO may play an important role in the development of N-methyl-D-aspartate receptor-mediated spinal facilitation after a nerve constriction injury.

Animals↗

Plasma plasminogen activator inhibitor-1, tissue plasminogen activator and serum lipoprotein(a) after reperfusion therapy in acute myocardial infarction: comparison between sequential and direct percutaneous transluminal coronary angioplasty.

To determine which reperfusion therapy for acute myocardial infarction (AMI) is advantageous to avoid subsequent thrombotic coronary occlusion, 8 patients with AMI were studied. Four of them (group S) underwent sequential PTCA following unsuccessful intracoronary thrombolysis and the others (group D) direct PTCA. Serial changes in plasma plasminogen activator inhibitor-1 (PAI-1), plasma tissue plasminogen activator (t-PA) antigen and serum lipoprotein(a) levels were compared between the two groups. In group S, plasma PAI-1 levels showed no significant serial change after PTCA. However, in group D, plasma PAI-1 levels increased significantly 4-24 h after PTCA. We suggest that more attention should be focused on the prevention of thrombotic coronary closure as well as mechanical abrupt occlusion after direct PTCA.

Angioplasty, Balloon, Coronary↗

Electrocardiographic abnormalities in patients with Cushing's syndrome.

The electrocardiograms in 8 patients with Cushing's syndrome and 4 with Cushing's disease were studied. The patients were divided into group A with electrocardiographic abnormalities and group B without. The mean age was significantly higher in group B than in group A. However, blood pressure, mean heart rate and the plasma adrenocorticotropic hormone level showed no significant differences between the two groups. In group A, the plasma concentration of cortisol had a tendency to be higher than in group B (A vs. B: 281 +/- 100 ng/ml, 188 +/- 9 ng/ml, respectively). Echocardiography performed on three of four patients in group A revealed cardiac hypertrophy. While, in group B, echocardiography performed on two patients showed no hypertrophic findings. As a result, it seems that the electrocardiographic changes are correlated with the plasma level of cortisol via myocardial hypertrophy.

Adrenocorticotropic Hormone↗

Time-dependent effect of morphine and time-independent effect of MK-801, an NMDA antagonist, on the thermal hyperesthesia induced by unilateral constriction injury to the sciatic nerve in the rat.

BACKGROUND: It is known that peripheral nerve injury induces time-dependent changes in dorsal horn function. The current study investigated the time dependency of the effects of intrathecal morphine and MK-801, an N-methyl-D-aspartate antagonist, on the thermal hyperesthesia evoked by unilateral constriction injury to the sciatic nerve in the rat. METHODS: In rats with a unilateral constriction injury to the sciatic nerve, paw withdrawal latency against thermal stimulation for the injured paw was typically 3 s less than that for the uninjured paw during the first 5 weeks after the injury. Drugs were administered intrathecally 1 or 5 weeks after the nerve injury. RESULTS: Intrathecal morphine increased the paw withdrawal latencies of both the injured paw and the uninjured paw in an equally dose dependent manner in the 1-week study. In the 5-week study, morphine increased the paw withdrawal latency of the uninjured paw in a dose-dependent manner, but not that of the injured paw. Intrathecal MK-801 increased the paw withdrawal latency of the injured paw to the level of the uninjured paw in a dose-dependent manner in both the 1- and 5-week studies. CONCLUSIONS: These data indicate that (1) an N-methyl-D-aspartate receptor-mediated spinal facilitation may be the common mechanism maintaining the thermal hyperesthesia evoked by the constriction injury, and (2) the effects of intrathecal morphine on this thermal hyperesthesia are time-dependent.

Animals↗

Analysis of the role of endothelin-A and endothelin-B receptors on nociceptive information transmission in the spinal cord with FR139317, an endothelin-A receptor antagonist, and sarafotoxin S6c, an endothelin-B receptor agonist.

Endothelin (ET)-A and ET-B receptors have been reported to exist in the spinal cord but the roles of ET-A and ET-B receptors in the spinal cord are poorly understood. To gain a better understanding of the roles of ET-A and ET-B receptors in nociceptive information transmission in the spinal cord, this study evaluated the effects of ET-1, ET-3, Sarafotoxin S6c (an ET-B receptor-selective agonist) and (R)2-[(R)-2-[(S)-2-[[1- (hexahydro-1H-azepinyl)]carbonyl]amino-4-methyl-pentanoyl]amino-3- [3-(1-methyl-1H-indolyl)]propionyl]amino-3-(2-pyridyl)propionic acid (FR139317, an ET-A receptor-selective antagonist) on the agitation behavior evoked by formaldehyde solution injection and on the thermal nociceptive test. The s.c. injection of formaldehyde solution into the hind paw evoked a biphasic flinching (phase 1, 0-9 min; phase 2, 10-60 min) of the injected paw. For the purpose of data analysis, phase 2 was further divided into two phases (phase 2a, 10-34 min; phase 2b, 35-60 min). Intrathecal injection of ET-1 depressed the phase 1 and 2 flinching behavior in a dose-dependent manner and this ET-1 effect was antagonized by FR139317. Intrathecal injection of either ET-3 or Sarafotoxin S6c enhanced the phase 2a flinching behavior in a dose-dependent manner. Intrathecal injection of the highest doses of ET-1, ET-3 and Sarafotoxin S6c had no effect on the thermal nociceptive test. These data indicate that ET-A and ET-B receptors have a powerful effect on spinal nociceptive processing evoked by formaldehyde solution injection but not that evoked by thermal stimulation.

Animals↗

Effects of intrathecal FK888, a novel dipeptide NK1 receptor antagonist, on the formalin test in the rat.

This study investigates the effects of intrathecally administered FK888, a novel dipeptide NK1 receptor antagonist, on the formalin test in the rat. Subcutaneous formalin induces biphasic episodes of flinching behavior at 0-5 min (Phase 1) and 10-60 min (Phase 2) after treatment. FK888 administered intrathecally 10 min before the formalin injection depresses the Phase 2 flinching behavior in a dose-dependent manner, but not the Phase 1 flinching behavior. FK888 has no effect on the Phase 2 flinching behavior when administered intrathecally 60 min before or 9 min after the formalin injection. Intrathecally administered FK888 has no effect on the motor function. These results suggest that FK888 is good drug to study the role of the NK1 receptor in the spinal cord of the rat.

Animals↗

Effect of low-power He-Ne laser on deformability of stored human erythrocytes.

This study was designed to investigate the effect of the He-Ne laser (continuous wave, lambda = 632.8 nm, 8.5 mW in power) irradiation on human erythrocyte deformability. Blood samples were obtained from hematologically normal adult donors by venipuncture. Red cells were washed and adjusted to 30% Ht with 0.9% NaCl solution (pH 7.00). Red cell solution samples were assigned to three groups. Each sample was divided into seven 3-ml working aliquots. The aliquots in Group I were irradiated for 0 (control), 1, 3, 5, 10, 15, and 30 min within 2 hr after sampling. The aliquots in Group 2 and Group 3 were stored at 5 degrees C for 24 and 36 hr, respectively, and received similar irradiations after 12 hr (in both groups), 24 hr (in Group 2), and 36 hr (in Group 3) from sampling. Red cell deformability was measured by the Nuclepore filter filtration and presented as the filter filtration rate (FFR). The deformability shown as FFR was unchanged in Group 1 (fresh cell group) from the control value, but improved significantly in Groups 2 and 3 (damaged cell groups) after the irradiation. These results suggested that the irradiation of low-powered He-Ne lasers improved cytoskeletal protein activities in damaged erythrocytes.

Cytoskeletal Proteins↗

Do low-power lasers change phase transition temperature of dipalmitoyl phosphatidylcholine (DPPC) membrane?

This study was designed to investigate the effects of the He-Ne laser (632.8 nm of wavelength, 8.5 mW in power, Senko Med. Co. Ltd., Tokyo, Japan) on the phase transition temperature of dipalmitoyl phosphatidylcholine (DPPC) membranes. Liposomal bilayers of DPPC (12.5 mM) were obtained with ultrasonification for 45 min at 40 degrees C and refrigerated for 2-3 days at 5 degrees C. The bilayers vesicle solution was divided into 3-ml working aliquots, which were assigned to three groups. The aliquots in Group 1 were used as controls without irradiation and the aliquots in Groups 2 and 3 were irradiated in 37 degrees C baths for 15 to 30 min, respectively. To determine phase transition temperature, optical density (%T; percent of permittance) of each aliquot was measured spectrophotomechanically at a wavelength of 440 nm while increasing its temperature at a rate of 0.5 degrees C every minute. Main phase transition temperatures in Groups 1, 2, and 3 were 41.54 +/- 0.23 degrees C (n = 10), 41.50 +/- 0.27 degrees C (n = 10), and 41.30 +/- 0.36 degrees C (n = 10), respectively. No significant difference between the nonirradiation and irradiation groups was established. These results suggest that irradiations of low-power He-Ne lasers up to 30 min do not change important physical characteristics of artificial DPPC membranes.

1,2-Dipalmitoylphosphatidylcholine↗

The effects of morphine, MK-801, an NMDA antagonist, and CP-96,345, an NK1 antagonist, on the hyperesthesia evoked by carageenan injection in the rat paw.

BACKGROUND: The spinal mechanisms underlying the hyperesthetic state during inflammation are little understood. To gain a better understanding of these mechanisms, this study evaluated the effects of intrathecal morphine; MK-801, an N-methyl-D aspartic (NMDA) antagonist; and CP-96,345, an NK1 antagonist, on the hyperesthesia observed after carageenan injection of the rat paw. METHODS: In rats injected with 2 mg carageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carageenan injection. Drugs were administered 2 h after the carageenan injection. The magnitude of hyperesthesia was evaluated with the difference score (DS), which was calculated by subtracting the PWL of the untreated paw from the PWL of the injected paw. RESULTS: Intrathecal morphine increased PWLs of both the injected and the untreated paws equally in a dose-dependent manner, but intrathecal morphine did not affect the level of DS. Intrathecal MK-801 increased PWLs of the injected paw to the level of the untreated paw in a dose-dependent manner and increased the DS levels. Intrathecal CP-96,345 had no effect on PWLs of either the injected or the untreated paw. Coadministration of MK-801 with morphine reduced the DS for each dose of morphine. CONCLUSIONS: These data indicate that (1) an NMDA receptor, but not an NK1 receptor, plays an important role in maintaining the hyperesthesia after carageenan injection; and (2) NMDA antagonism has a simple additive interaction with morphine in the carageenan model of inflammatory hyperesthesia.

Animals↗

Role of the injury discharge in the development of thermal hyperesthesia after sciatic nerve constriction injury in the rat.

BACKGROUND: Usually, a barrage of impulses ("injury discharge") is evoked following sensory nerve damage. It has been suggested that injury discharge may produce the hyperexcitatory state in the spinal cord, and this hyperexcitability may cause neurogenic pain. In the present study, the authors examined the role of injury discharge in developing the hyperesthetic state following nerve constriction injury. METHODS: A model of thermal hyperesthesia caused by a constriction injury created by making four loose ligations around the rat sciatic nerve was examined. To block the injury discharge, 0.5% bupivacaine was applied to the sciatic nerve before constriction injury. To block the hyperexcitatory state, (+)-MK-801, an N-methyl-D-aspartate antagonist, was administered intrathecally 15 min before the nerve lesion. RESULTS: Blocking injury discharge significantly delayed the development of hyperesthesia. Bupivacaine had no effect on the development of hyperesthesia when bupivacaine was applied to the sciatic nerve 15 min after the nerve constriction injury. Systemic bupivacaine had no effect on the development of thermal hyperesthesia. Intrathecal (+)-MK-801 also delayed the development of hyperesthesia when (+)-MK-801 was administered intrathecally 15 min before the nerve injury. When (+)-MK-801 was administered 15 min after the nerve injury, (+)-MK-801 had no effect on the development of hyperesthesia. CONCLUSION: These results suggest that injury discharge may induce facilitation of spinal dorsal horn neurons, and this spinal facilitation may play an important role in developing thermal hyperesthesia following sciatic nerve constriction injury.

Animals↗

Effects of FK224, a novel cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist, on development and maintenance of thermal hyperesthesia evoked by carrageenan injection in the rat paw.

BACKGROUND: The role of tachykinins, such as substance P and neurokinin A, in the development or maintenance of thermal hyperesthesia during inflammation is unclear. In the current study, the authors examined the role of NK1 and NK2 receptors on the thermal hyperesthesia evoked by injection of carrageenan into the rat paw using FK224, a cyclopeptide NK1 and NK2 antagonist, and CP-96,345, a nonpeptide NK1 antagonist. METHODS: In rats injected with 2 mg carrageenan, the paw withdrawal latency (PWL) for the injected paw was typically 5-6 s less than that for the untreated paw, at 2 h after the carrageenan injection. In the pretreatment study, drugs were administered intravenously or intrathecally 10 min before the carrageenan injection. In the posttreatment study, drugs were administered intravenously or intrathecally 2 h after the carrageenan injection. RESULTS: In the pretreatment study, both intravenous CP-96,345 and intravenous FK224 blocked the development of thermal hyperesthesia and reduced paw edema in a dose-dependent manner 2 h after the carrageenan injection. The effect of CP-96,345 on thermal hyperesthesia was stereospecific, but that on paw edema was not. Posttreatment with intravenous CP-96,345 and intravenous FK224 failed to reduce the level of thermal hyperesthesia or paw edema, and intrathecal injections, either pre- or posttreatment, had no effect on thermal hyperesthesia or paw edema. CONCLUSIONS: These data indicate that: 1) spinal NK1 and NK2 receptors do not play an important role in development and maintenance of thermal hyperesthesia evoked by paw carrageenan, and 2) the peripheral NK1 receptor may play an important role in the development of thermal hyperesthesia, but not of paw edema.

Animals↗

Nitric oxide synthase inhibitor blocks spinal sensitization induced by formalin injection into the rat paw.

This study evaluated the role of nitric oxide (NO) in spinal cord nociceptive transmission during peripheral inflammation evoked by formalin injection into the rat paw, using N omega-nitro-L-arginine (N-Arg), an NO synthase inhibitor. Male rats were prepared with intrathecal (IT) catheters. To quantify the formalin response, the instances of "flinching behavior" were counted at 5-min intervals for 60 min. IT N-Arg depressed the flinching behavior in a dose-dependent manner when N-Arg was administered 10 min before the formalin injection. This N-Arg effect was reversed with L-arginine but not D-arginine. We conclude that NO plays an important role in nociceptive transmission in the spinal cord during the formalin test.

Amino Acid Oxidoreductases↗

Suppression of ventricular premature contractions continues after the washout of antiarrhythmic drugs.

The effects of the washout of antiarrhythmic drugs on the frequency of ventricular premature contraction (VPC) were investigated in 64 patients (VPCs > 2000/day). Included were patients on mexiletine (300-600 mg/day; 23 patients), disopyramide (300-600 mg/day; 19 patients) and atenolol (50 mg/day; 22 patients). Holter monitoring was repeated before, during and after the treatment with the above 3 drugs and the efficacies of the drugs were evaluated based on the spontaneous variability before the treatment. VPC reduction exceeding the calculated spontaneous variability during drugs therapy (drug-responders) and after the washout of the drugs (wash-responders) was noted in 17 (63%) and 3 (13%) of the mexiletine group; 11 (58%) and 5 (26%) of the disopyramide group; and 13 (59%) and 8 (36%) of the atenolol group, respectively. For the entire group of 64 patients, wash-responders were noted significantly (p < 0.05) more among drug-responders (14 of 41 patients; 34%) than drug-nonresponders (2 of 23 patients; 9%). Therefore, the antiarrhythmic effects of drugs observed during drugs therapy seem to continue even after the discontinuation of antiarrhythmic drugs in 34% of patients those whose VPC reduction exceeded the spontaneous variability (drug-responders).

Adult↗

The relationship between serum lipoprotein(a) and restenosis after initial elective percutaneous transluminal coronary angioplasty.

The purpose of this study was to elucidate the possible link between lipoprotein(a) (Lp(a)) and the occurrence of restenosis after initial elective percutaneous transluminal coronary angioplasty (PTCA). Serum lipids, including Lp(a), total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-I (Apo A-I), and apolipoprotein B (Apo B), and the Apo B/Apo A-I ratio were examined in 63 consecutive patients (41 men and 22 women, average age 63 +/- 8 years) who underwent initial elective PTCA in our department. Forty two target lesions were in left anterior descending, 10 were in left circumflex and 11 were in right coronary branches. Restenosis was observed in 22 patients (35%) 6.4 +/- 2.6 months after PTCA. The serum Lp(a) level was significantly higher in the restenosis group than in the non-restenosis group (38.0 vs 19.9 mg/dl, p < 0.05). A significant correlation was observed between serum Lp(a) levels and the degree of % restenosis after PTCA (r = 0.557, p < 0.001). However, other lipids showed no significant relationship to restenosis. In addition, the % stenosis before PTCA was found to be related to the occurrence of restenosis after successful PTCA. We conclude that the serum Lp(a) level has a close correlation with the degree of % restenosis after PTCA, and may be a useful index for predicting the possibility of restenosis after PTCA, especially in patients with an Lp(a) level above 30 mg/dl.

Aged↗

[Serial changes in QT interval during acute myocardial infarction: comparison of QT interval changes of reperfused cases and non-reperfused cases].

The serial changes in QT intervals during the course of acute myocardial infarction are of interest from the standpoint of the electrocardiogram itself, the development of ventricular tachyarrhythmias, residual cardiac function, and the prognosis of the patients. However, only sparse literature has dealt with this issue because it is difficult to obtain ECGs for analysis, and multiple factors influence the QT interval including the degree of reperfusion, electrolyte imbalance, hemodynamic changes and drugs which alter the QT interval. The ECGs of patients with acute myocardial infarction who underwent reperfusion therapy were analyzed: Sixteen consecutive patients were enrolled in this study, 9 with TIMI grade II and III (TIMI: the thrombolysis in myocardial infarction study group criteria) and 7 with TIMI grade 0, myocardial infarction with (9) and without (7) reperfusion. Patients with collaterals, TIMI grade I, hypertrophic cardiomyopathy, electrolyte imbalance, Ia antiarrhythmic drugs, beta adrenoreceptor blockades, atrial fibrillation, and intraventricular conduction disturbances were excluded from the study. Serial ECG recordings were performed at 3, 6, 9, 12, 24, 48, and 72 hours after the onset of myocardial infarction. One week after and one month after the onset, the ECGs were recorded. Patients who exhibited reocclusion on their arteriograms in the chronic phase were also excluded from the study. Measurements of the QT intervals were performed at the ischemic lead (II in the standard limb lead in inferior infarction and V2 in anteroseptal infarction), and values were averaged from 5 consecutive QRS complexes according to Lepeschkin's method and corrected using Bazett's method. The left ventricular ejection fraction (LVEF) and percent fractional shortening (FS) in segments 2, 3, 4 or 5 were calculated from the ventriculogram in the chronic phase. The QT interval revealed a lengthening with its peak within 12 hours after the onset and it became shorter thereafter in reperfused patients. In patients without reperfusion, the QT interval became progressively prolonged without showing a peak point, up to one month. LVEF and FS were significantly higher values in patients with reperfusion than in those without reperfusion. In conclusion, in patients with reperfusion, the QT interval was transiently prolonged and later shortened with improved LVEF and FS than in patients without reperfusion.

Adult↗

[Serum thyroid hormone levels correlate with cardiac function and ventricular tachyarrhythmia in patients with chronic heart failure].

The relationship between cardiac function and serum thyroid hormone levels was investigated in 41 patients with chronic heart failure (25 men and 16 women, mean age 63.7 +/- 11.1 years) and 15 normal subjects (5 men and 10 women, mean age 55.5 +/- 12.2 years). Patients with apparent thyroid disease were excluded from the study. All patients were evaluated according to the New York Heart Association (NYHA) classification using echocardiography, cardiothoracic ratios, mean daily heart rates calculated from ambulatory electrocardiograms (ECG), and ventricular tachyarrhythmias greater than triplets based on either Holter or ECG monitoring. The serum free triiodothyronine (FT3), free thyroxine (FT4), and reverse triiodothyronine (rT3) levels were measured. Decreased FT3 levels and FT3/FT4 ratios, and increased rT3 levels were associated with worse NYHA class. FT3/FT4 was positively and rT3 was negatively correlated with echocardiographical fractional shortening. FT3 and rT3 were negatively and positively correlated with mean daily heart rates, in contrast to known hypothyroid patients. Patients with ventricular tachycardia demonstrated significantly lower serum values of FT3 and FT3/FT4, and significantly higher values of rT3. Serum thyroid hormone levels can provide a quantitative index for evaluating the severity of chronic heart failure and predicting ventricular tachycardia.

Echocardiography↗

[Ganglioneuroma in the cervical ganglion with neurofibromatosis-2: a case report].

The authors report a case of a 20 year old male with ganglioneuroma in the cervical ganglion. The patient was complaining of a mass in the neck on his right-hand side, and neurological examination revealed hypesthesia on the C5 area of the same side. Computed tomography and magnetic resonance imaging scan showed extradural dumbbell-shaped tumor from C3 to C5 levels. A two-staged operation was performed to remove the tumor totally, and a ganglioneuroma was diagnosed. After surgery, he complained of facial weakness and hearing disturbance on the left side. As MRI scan revealed bilateral cerebro-pontine angle tumors, he was diagnosed as having neurofibromatosis-2. This report may represent a rare case of ganglioneuroma with neurofibromatosis-2.

Adult↗

QT interval shortening and ST elevation in intracoronary ECG during PTCA.

Percutaneous transluminal coronary angioplasty (PTCA) can provide a unique model of transient and reversible myocardial ischemia. The aim of this study was to assess the serial changes in QT interval during elective PTCA-induced transient ischemia. The serial changes in QT interval before, during, and after PTCA of the left anterior descending artery (LAD) were measured in patients who showed ST elevation in intracoronary electrocardiogram. Twelve consecutive patients who showed ST-segment elevation during PTCA-induced ischemia anterior precordial leads of the electrocardiogram (ECG) were enrolled in the present study. Target lesions for PTCA were all in the LAD. There were six patients with angina pectoris, two with non-Q-wave infarction, and four with Q-wave myocardial infarction. During balloon inflation, QTc interval shortened in both intracoronary ECG (ic-ECG) (0.472 +/- 0.013 vs 0.436 +/- 0.014) and surface ECG (0.462 +/- 0.012 vs 0.438 +/- 0.011). However, a significant shortening of the QT interval was more rapidly observed in the ic-ECG (20 s) than in the surface ECG (40 s). We conclude that the QT interval in both ic-ECG and surface ECG becomes shortened in PTCA-induced myocardial ischemia, and that the ic-ECG might be a good probe for detecting survived viable myocardium in the infarcted zone.

Aged↗