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Biomedical subjects

M Satoh

Publications and source records attributed to M Satoh.

At least 217 records · Page 12Linked to original sources

Enzyme-linked immunosorbent assay detection of prostate-specific antigen messenger ribonucleic acid in prostate cancer.

OBJECTIVES: To develop a rapid, sensitive, reverse transcriptase-polymerase chain reaction (RT-PCR) prostate-specific antigen (PSA) messenger ribonucleic acid (mRNA) detection method by applying colorimetric enzyme-linked immunosorbent assay (ELISA). METHODS: Total RNA was extracted from 16 urogenital cancer cells (including PSA-producing LNCaP cells) from pelvic and inguinal lymph node aspiration biopsy samples from patients with prostate, bladder, and penile cancer, as well as from blood samples of 500 patients with urogenital cancer. We used rTth polymerase for RT and PCR. The RNA target was amplified by RT-PCR with dinitrophenyl-labeled primer. The PCR product was denatured and hybridized on a PSA-specific probe-coated microwell plate. RESULTS: In 1 6 cancer cell lines, only LNCaP cells expressed especially high PSA mRNA values, with an optical density (OD) greater than 3. In other cell lines, two testicular cells had relatively high ODs, 1.909 and 0.987, respectively. A high PSA mRNA value was obtained by fine needle aspiration from pelvic lymph node specimens of cytologically positive lymph nodes from patients with prostate cancer but not from patients with cytologically proved bladder or penile cancer. Sensitivity and specificity of fine needle aspiration samples were 70% and 100%, respectively. Blood tests obtained from patients with prostate cancer demonstrated high PSA mRNA values. CONCLUSIONS: The PSA mRNA RT-PCR ELISA method provides a sensitive photometric enzyme immunoassay for the detection of PSA mRNA, using nonradioactive techniques.

Enzyme-Linked Immunosorbent Assay↗

Itch-associated response induced by intradermal serotonin through 5-HT2 receptors in mice.

Serotonin (5-HT) is pruritogenic in humans and suggested to be involved in some pruritic diseases. Our experiments were carried out to determine whether an intradermal injection of 5-HT would elicit itch-associated response in mice and to elucidate the 5-HT receptor subtypes involved in this 5-HT action. 5-HT (14.1-235 nmol site(-1)) injected intradermally into the rostral back elicited scratching of the injected site, with bell-shaped dose-response relationship. The scratching induced by 5-HT (100 nmol site(-1), peak effective dose) was suppressed by capsaicin (repeated administration) and the opioid antagonist naloxone, features being similar to human itching. Scratching was also elicited by the 5-HT2 receptor agonist alpha-methylserotonin, but not by the 5-HT1A receptor agonist R(+)-8-hydroxy-N,N-dipropyl-2-aminotetralin nor the 5-HT3 receptor agonists 2-methylserotonin and 1-phenylbiganide. Scratching induced by 5-HT and alpha-methylserotonin was inhibited by peroral pretreatment with 5-HT1/2 receptor antagonists methysergide and cyproheptadine. 5-HT-induced scratching was also inhibited by intradermal injection of methysergide. Peroral pretreatment with 5-HT3 receptor antagonists ondansetron and 3-tropanyl-3, 5-dichrobenzoate did not significantly suppress 5-HT-induced scratching. The results suggest that scratching induced by intradermal injection of 5-HT is itch-associated response. The 5-HT action may be mediated at least partly by cutaneous 5-HT2 receptors.

Analysis of Variance↗

A case of anaplastic thyroid carcinoma surviving disease free for over 2 years.

A 52-year female presented with an enlarged thyroid mass and lump sensation in the throat. The cytologic examination showed class five and she was admitted to the hospital to undergo operation. Total thyroidectomy was done and the tumoral invasion of the trachea was removed. We performed tracheoplasty using a sternocleidomastoid muscle-clavicle myoosseous flap in a single stage operation. Histologic diagnosis revealed anaplastic thyroid carcinoma After upper mediastinal dissection had been performed, systemic chemotherapy using pirarubicin, cisplatin and etoposide was administered. In addition, she was treated with radiochemotherapy using pirarubicin, cisplatin and a total of 58 Gy was administered. No recurrence of the tumor has been noted since the above operation 2 years ago. Immunohistochemical studies of primary and metastatic tissues in this case revealed a positive expression of p53 protein in both.

Biopsy, Needle↗

Disparate T cell requirements of two subsets of lupus-specific autoantibodies in pristane-treated mice.

Intraperitoneal injection of pristane induces a lupus-like disease in BALB/c and other non-autoimmune mice characterized by autoantibody production and the development of immune complex disease closely resembling lupus nephritis. Two subsets of autoantibodies are induced by pristane: IgG anti-DNA DNA and -chromatin autoantibodies are strongly IL-6-dependent, whereas IgG anti-nRNP/Sm and -Su antibodies are not. The present studies were carried out to examine the role of T cells in establishing this dichotomy between the production of anti-nRNP/Sm/Su versus anti-DNA/chromatin autoantibodies. Autoantibody production and renal disease were evaluated in athymic (nude) mice treated with pristane. BALB/c nu/nu mice spontaneously developed IgM and IgG anti-single-stranded (ss)DNA and -chromatin, but not anti-nRNP/Sm or -Su, autoantibodies. Pristane treatment increased the levels of IgG anti-chromatin antibodies in nu/nu mice, but did not induce production of anti-nRNP/Sm or -Su antibodies. In contrast, BALB/c nu/+ and +/+ control mice did not spontaneously produce autoantibodies, whereas anti-nRNP/Sm and -Su autoantibodies were induced by pristane in approx. 50% of nu/+ and +/+ mice and anti-DNA/chromatin antibodies at lower frequencies. Nude mice spontaneously developed mild renal lesions that were marginally affected by pristane, but were generally milder than the lesions developing in pristane-treated nu/+ and +/+ mice. The data provide further evidence that two distinct pathways with different cytokine and T cell requirements are involved in autoantibody formation in pristane-induced lupus. This dichotomy may be relevant to understanding differences in the regulation of anti-DNA versus anti-nRNP/Sm autoantibodies in systemic lupus erythematosus, as well as the association of anti-DNA, but not anti-nRNP/Sm, with lupus nephritis.

Animals↗

Defective immune response and severe skin damage following UVB irradiation in interleukin-6-deficient mice.

Interleukin-6 (IL-6), a multifunctional cytokine, is induced in the acute-phase reaction following ultraviolet (UV) irradiation of humans and mice. Using IL-6-deficient (IL-6-/-) mice, we investigated the role of IL-6 in immunosuppression and inflammatory responses caused by UVB (280-320 nm) radiation. The IL-6-/- mice had a defective contact hypersensitivity (CHS) in response to the sensitizers 2,4-dinitrofluorobenzene and oxazolone. The injection of recombinant IL-6 (rIL-6) into these mice resulted in a marked recovery of the CHS. Serum IL-6 was significantly elevated by UV irradiation of wild-type B6 J/129Sv (IL-6+/+) mice but was not detectable in IL-6-/- mice. Interestingly, there was no induction of serum interleukin-10 (IL-10) by UV irradiation of IL-6-/- mice, whereas UV exposure caused a significant increase in serum IL-10 levels in IL-6+/+ mice. Injection of rIL-6 into IL-6-/- mice increased IL-10 to levels similar to those of IL-6+/+ mice. Being different from IL-6+/+ mice, no epidermal proliferation was found at 48 hr in the IL-6-/- mice, but delayed cell proliferation was observed at 72 hr after UV exposure. Immunohistochemical analysis demonstrated that the epidermis was capable of synthesizing IL-6 at 72 hr after UV irradiation of IL-6+/+ mice. In addition, the IL-6-positive cells appeared to be Langerhans' cells, which were detected with dendritic cell-reactive S-100 antibody. The present study strongly suggests that IL-6 may play a crucial role in the alteration of cutaneous immune responses following UV exposure, and provides evidence that IL-6 is a potent inducer of IL-10. Furthermore, IL-6 production induced by UV radiation appears to be an important early signal for repair of UV-caused skin damage.

Animals↗

Alpha1-antitrypsin deficiency and toxic shock: a Japanese autopsy case.

A 74-year-old Japanese female presented with the sudden appearance of hemorrhagic purpuric ecchymoses on her lower extremities and with fever and chills, and died on the fifth day of hospitalization. A diagnosis of alpha1-antitrypsin (AT) deficiency was made postmortem. The liver weighed 1260 g. Histological sections from the liver revealed rather severe fatty changes of the hepatocytic parenchyma and partial loss of the normal hepatic architecture with fibrosis. The hepatocytes contained periodic acid-Schiff (PAS)-positive, diastase-resistant and alpha1-AT-positive intracytoplasmic globules. There was markedly increased inflammatory infiltration with severe edema and congestion, accompanied by fibrous, thickened pulmonary alveolar walls with fibrin deposition in the lungs (right, 410 g; left, 280 g), which suggest findings similar to those seen in multiple organ failure. Mild pulmonary emphysema was also present in the upper lobes of the lungs. Histological sections from the hemorrhagic necrotic ecchymoses of the skin showed marked neutrophil infiltration over the subcutaneous tissue with bleeding and blistering. A finding of thrombophlebitis was also found in the subcutaneous tissue. No bacteria were detected in the ecchymoses, the urine or the blood. Plasma protein analysis revealed a lower level (9.5 micromol/L) of alpha1-AT and a higher level (330 U) of anti-streptolysin O (ASO). These findings suggest that the patient died of toxic shock-like syndrome and that alpha1-AT deficiency might have facilitated the development of the toxic shock. To our knowledge, this is the first case of toxic shock associated with alpha1-AT deficiency.

Adult↗

Regulation of ventilation before and after sleep in patients with obstructive sleep apnoea.

The objective was to examine whether abnormal breathing during sleep may affect regulation of ventilation after awakening in patients with obstructive sleep apnoea (OSAS). In 19 patients with OSA and 12 normal subjects we examined ventilatory responses to hypoxia (HVR) and to hypercapnia (HCVR) before and after sleep (BS and AS), and compared the changes in ventilatory responses with respiratory events during sleep. In the OSA group, the values of resting ventilation were significantly smaller in AS than those in BS and end-tidal partial pressure of CO2 in arterial blood (Pco2) (PETCO2) rose significantly from BS to AS. The slopes of the HVR or HCVR did not differ between BS and AS. However, both the response lines shifted downward and minute ventilation (VE)80 (VE at arterial oxygen saturation (Sao2) of 80%) in HVR and VE60 (VE at PETCO2 of 60 mmHg) in HCVR decreased significantly from BS to AS. The percentage changes of VE80 and VE60 were significantly correlated with mean Sao2, total sleep time below Sao2 of 90% and lowest Sao2 during sleep. However, in normal subjects we observed no circadian variation in their ventilatory responses. These data support the hypothesis that repeated episodes of nocturnal hypoxia and hypercapnia may modify the regulation of ventilation after awakening in patients with OSA.

Adult↗

The study of PSA gene expression on urogenital cell lines.

PURPOSE: Reverse transcriptase-polymerase chain reaction (RT-PCR) offers a potentially more sensitive assay for detecting cells expressing prostate-specific antigen (PSA) mRNA in peripheral circulation. But the sensitivity and specificity are variable depending on the position of the PSA amplification. To increase sensitivity and specificity, the whole PSA cDNA (1466 bp) was separated into eight different parts. METHODS: We examined RT-PCR on 12 urogenital cell lines, including three prostate cancer (LNCaP, PC3, DU145), five human renal cell carcinoma (SMKT-R3, TOS-1, TOS-2, R4, ACHN), two urinary bladder cancer (YTS-1, KK-47) and two testicular cancer (NEC8, NEC14) cell lines. The sizes of the eight fragmented PSA used in the experiment were PSA-1 (1-257bp), PSA-2 (1-322bp), PSA-3 ( 172-507bp), PSA-4 (172-851 bp), PSA-5 (595-1347 bp), PSA-6 (682 967 bp), PSA-7 (682-1347 bp) and PSA-8 (863-1466 bp). RESULTS: All cell lines had positive signals from PSA-6, PSA-7 and PSA-8. The positive signals from PSA-1, PSA-2 and PSA-3 were detected in some other cell lines in addition to the three prostate cancer cell lines. Only LNCaP which produces the PSA protein had a positive signal from PSA-5. PC3 and DU145 (which do not produce PSA) and LNCaP had a positive signal from PSA-4. Therefore, the inner primer PSA-4' (578-782 bp) used to increase sensitivity and specificity. Nested RT-PCR on the 12 cell lines, using the PSA-4 and 4' primers, detected more clear bands in the three prostate cancer cells. CONCLUSION: Nested RT-PCR using PSA-4 (outer primer) and PSA-4' (inner primer) may be useful for detecting prostate cancer cells in the peripheral blood.

DNA Primers↗

Neoadjuvant therapy and bladder substitute for invasive bladder cancer: 20 years experience at Tohoku University.

BACKGROUND: Neobladder, using the intestine, was performed after neoadjuvant therapy and total cystectomy as a treatment for invasive bladder cancer. METHODS: Between January 1977 and April 1997, an ileocecal neobladder was used for 23 patients and a sigmoid neobladder was chosen for use in 32 patients. For the diagnosis of invasive bladder cancer and the evaluation of neoadjuvant therapy, we used whole-layer core biopsy (WLCB) of the bladder tumor and fine needle aspiration biopsy (FNAB) of pelvic lymph nodes after bipedal lymphography. For neoadjuvant therapy, two to four courses of internal iliac arterial infusion chemotherapy (IIA) were undertaken in 32 patients. Five patients were treated with IIA combined with 40 Gy irradiation to the pelvic space. RESULTS: Pretreatment WLCB revealed a tumor of stage T2b or greater in 10 patients. After neoadjuvant therapy, three patients were down-staged to pT0. In five patients, pretreatment FNAB revealed pelvic lymph node metastases that were not detected by computed tomography or magnetic resonance imaging. Fine needle aspiration biopsy post-neoadjuvant therapy revealed tumor stage N0 in all patients and lymph node dissection revealed pN0 in four patients. Of the five patients who received 40 Gy irradiation, none had any postoperative complications, such as intestinal fistula or urinary leakage. Four male patients (10%) had urethral recurrence, but all were successfully treated by transurethral resection. Two patients treated prior to 1985 experienced local recurrence. Neither was treated by neoadjuvant therapy. Eight patients who died after 1985 had metastatic cancer, but none had local recurrence. None of the patients who received a sigmoid neobladder required clean intermittent catheterization or had bilateral vesico-ureteral reflux. CONCLUSIONS: Neoadjuvant therapy seems to reduce local recurrence in invasive bladder cancer. The sigmoid colon may be suitable for neobladder.

Adult↗

Ultrastructural localization of glucose transporter 1 (GLUT1) in guinea pig stria vascularis and vestibular dark cell areas: an immunogold study.

Glucose transporter 1 (GLUT1) is one of the facilitated-diffusion glucose transporters, which plays a major role in the glucose transport across blood-tissue barriers. We demonstrated localization of GLUT1 in guinea pig stria vascularis (SV) and vestibular dark cell areas, using electron microscopy. GLUT1 immunoreactivity was seen mainly in the SV. Electron microscopically, immunogold particles were localized along the plasma membranes of the basal cells and the basolateral infoldings of the marginal cells. Erythrocyte membranes and the capillary walls in both the SV and the dark cell areas were also positive for GLUT1. These results indicate that GLUT1 is involved in glucose regulation for energy metabolism in the marginal cells and vestibular dark cells, and in glucose transport between blood and perilymph.

Animals↗

Cloning of cDNA for canine interleukin-18 and canine interleukin-1beta converting enzyme and expression of canine interleukin-18.

Cloning of canine interleukin-18 (IL-18) and canine interleukin-1beta converting enzyme (ICE) cDNA was carried out by using murine IL-18 cDNA and human ICE cDNA, respectively, as probes. Sequence homology to known sequences of human, mouse, or rat genes was noted at nucleotide and amino acid levels. Canine IL-18 mRNA was expressed in various canine organs, whereas canine ICE mRNA was expressed in only a few, particularly in the brain and testis. Cloned canine IL-18 cDNA was expressed in Escherichia coli. The resulting protein promoted induction of canine interferon-y (IFN-y) from stimulated canine lymphocytes. Canine IL-18 and canine IL-12 produced canine IFN-gamma synergistically. Canine IL-18 suppressed the growth of tumor cells transplanted in SCID mice. Cloned canine IL-18 should prove useful as an anticancer agent.

Amino Acid Sequence↗

Schwannoma of the oculomotor nerve: a case report with consideration of the surgical treatment.

OBJECTIVE AND IMPORTANCE: Oculomotor schwannoma is extremely rare. We report a case of oculomotor schwannoma with consideration of its surgical management. CLINICAL PRESENTATION: A 64-year-old woman with a history of chronic headache underwent a computed tomographic scan, which revealed a mass lesion in the right prepontine cistern. She had no neurological deficits at admission. INTERVENTION: The tumor originated from the right oculomotor nerve. It was subtotally removed, leaving a tiny part attached to the nerve. The nerve trunk was preserved. A pathological examination revealed a schwannoma. Transient right oculomotor nerve palsy occurred postoperatively, but it improved almost completely. CONCLUSION: The tumor in the present case was resected, preserving serviceable oculomotor function. However, among 16 patients reported in the literature, all but one developed or maintained severe postsurgical oculomotor nerve palsy. We conclude that surgical resection generally is not indicated for oculomotor schwannomas, excluding large tumors that cause intractable symptoms.

Cranial Nerve Neoplasms↗

High-dose growth hormone (GH) treatment in prepubertal GH-deficient children.

Two clinical studies were conducted to determine the effect of different doses of growth hormone (GH) on prepubertal growth in GH-deficient boys. In one study, GH doses of 1.0 and 1.5 IU/kg/week (0.33 and 0.5 mg/kg/week) were given to groups of five children and compared with a conventional Japanese dose of 0.5 IU/kg/week (0.17 mg/kg/week) in 15 children. A significant dose-dependent increase in height velocity occurred in the first year of treatment, but differences between doses were not significant thereafter. In a second study, GH was administered to ten boys at a dose of 0.5 IU/kg/week for the first year, 0.75 IU/kg/week for the second year, 1.0 IU/kg/week for the third year and 0.5 IU/kg/week for the fourth and subsequent years (0.17, 0.25, 0.33 and 0.17 mg/kg/week, respectively). During the second and third years of GH treatment, these boys had significantly higher growth rates than controls, who were given GH at 0.5 IU/kg/week (0.17 mg/kg/week) throughout, indicating successful reduction in 'waning' of the treatment effect. At the end of the fourth year, the different protocols from the two studies had both resulted in a greater height SDS than the controls, and did not advance bone maturation. In conclusion, these protocols may be effective in increasing prepubertal height gain in children with GH deficiency.

Analysis of Variance↗

When and how to combine growth hormone with a luteinizing hormone-releasing hormone analogue.

The effect of combined treatment with growth hormone (GH) and a luteinizing hormone-releasing hormone (LHRH) analogue, or GH alone, on pubertal height gain was assessed in an uncontrolled study in 15 boys and 10 girls with GH deficiency (GHD). Seven boys and six girls were treated with GH alone (group 1), and eight boys and four girls were treated with a combination of GH and an LHRH analogue during puberty (group 2). Mean ages (+/- SD) at the start of GH treatment and at the onset of puberty were significantly lower in group 2 (8.0 +/- 3.3 years and 11.2 +/- 0.8 years, respectively, in boys, and 6.3 +/- 1.6 years and 10.8 +/- 0.7 years in girls) than in group 1 (12.8 +/- 1.9 years and 13.7 +/- 1.4 years in boys, and 11.2 +/- 1.0 years and 12.5 +/- 1.2 years in girls). Height at the onset of puberty was less in group 2 than in group 1, but the difference was significant only for the boys. Combination treatment was started at a mean age of 11.7 +/- 1.2 years in boys and 11.5 +/- 1.0 years in girls. The duration of the combination treatment was 5.1 +/- 1.5 years in boys and 2.3 +/- 0.7 years in girls. The duration of the period between the onset of puberty and the end of GH treatment was significantly longer in group 2 (6.8 +/- 1.2 years in boys and 5.5 +/- 1.0 years in girls) than in group 1 (4.3 +/- 1.6 years in boys and 3.6 +/- 1.4 years in girls). The pubertal height gain was also significantly greater in group 2 (36.7 +/- 6.5 cm in boys and 29.0 +/- 8.3 cm in girls) than in group 1 (21.9 +/- 4.1 cm in boys and 18.6 +/- 4.1 cm in girls). Final height was significantly greater in group 2 than in group 1 in boys. Although there was no significant difference in final height between groups in the girls, the change in height SDS from the start of GH treatment until final height was significantly greater in group 2 (2.7 +/- 1.6 in boys and 4.5 +/- 0.5 SD in girls) than in group 1 (1.0 +/- 0.8 in boys and 1.8 +/- 0.9 SD in girls), in both boys and girls. In conclusion, it appears that combination of an LHRH analogue and GH may increase the pubertal height gain and the final height of children with GHD. The improvement is attributed to the prolongation of the treatment period, permitting slow bone maturation, and to the maintenance of height velocity. This combination treatment appears to be more effective in boys than girls. To fully assess this therapeutic approach, prospective controlled studies are needed.

Adolescent↗

Effect of positive end-expiratory pressure on left and right ventricular diastolic filling assessed by transoesophageal Doppler echocardiography.

The effect of positive end-expiratory pressure (PEEP) on left and right ventricular diastolic filling dynamics was assessed by transmitral and transtricuspid flow patterns. Using transoesophageal Doppler echocardiography in fourteen ASA physical status 1 female patients, the following measurements were performed at baseline (0 cm H2O PEEP) and at 5, 10, 15, and 20 cm H2O PEEP: 1. peak velocity of early filling (peak E velocity), 2. peak velocity of atrial contraction (peak A velocity), 3. the ratio of the peak E to A velocity (peak E/A velocity ratio), 4. isovolumic relaxation time (IRT), 5. acceleration half-time (AHT), 6. deceleration half-time (DHT) of early filling, and 7. end-diastolic and end-systolic areas of both ventricles. Increasing PEEP progressively deceased peak E velocity of both ventricles. In contrast, peak A velocity did not change and the peak E/A velocity ratio decreased significantly with PEEP. IRT and AHTs remained unchanged, but DHTs of both ventricles increased following PEEP. End-diastolic and end-systolic areas of both ventricles decreased gradually and significantly with PEEP. It is concluded that PEEP was associated with decreased preload as well as reduced compliance of both ventricles, which was considered to contribute to the changes in diastolic ventricular filling.

Adult↗

A milk clotting assay for antibody using a fusion protein between protein A and pepsinogen C.

The proteolytic activity of a fusion protein between protein A and human pepsinogen C (PA-PGC) was measured by a modified milk clotting assay on 96-well microtiter plate. The assay ranges for 30 and 120 min-incubation were approximately 0.08-1.25 ng and 0.02-0.16 ng, respectively. Although the absorbance of milk solution decreased by the precipitation of clotted casein, the white precipitate was, if anything, convenient for an easy detection of reaction-positive wells. The borderline between the wells with or without precipitate was very clear and easily detected without the plate reader. This feature was thought to be suitable for the positive-negative judgment of a dilution test in enzyme immunoassay (EIA). Rabbit IgG adsorbed on a microtiter plate was then measured using PA-PGC and this milk assay (designated as PA-PGC assay). Although PA-PGC assay needed slightly longer incubation than the conventional color assay, the sensitivity of both systems was almost identical, and the reaction-positive wells containing white precipitate were easily detected at a very low range by the over night incubation without using the plate reader. PA-PGC assay possesses the unique and useful properties, and it can be used as a convenient and easy EIA technique.

Animals↗

Possible involvement of descending serotonergic systems in antinociception by centrally administered elcatonin in mice.

To elucidate the mechanisms of analgesic action of elcatonin, a synthetic analog of eel calcitonin, the effect of centrally injected elcatonin on acetic acid-induced writhing behavior was examined in mice. Intracisternal or intracerebroventricular injection of elcatonin significantly inhibited acetic acid-induced writhing behavior, while the intrathecal injection of elcatonin did not inhibit it. The inhibitory effect of intracisternal elcatonin was significantly attenuated by subcutaneous pretreatment with methysergide and (+/-)-propranolol or by intrathecal pretreatment with methysergide, (+/-)-propranolol, 1-(2-methoxyphenyl)-4-[4-(2-phthalimido) butyl]-piperazine hydrobromide (NAN-190) and granisetron, but not with (+/-)-atenolol or butoxamine. Further, the depletion of spinal 5-hydroxytryptamine (5-HT, serotonin) by pretreatment with 5,7-dihydroxytryptamine (5,7-DHT) significantly attenuated the inhibitory effect of intracisternally injected elcatonin on acetic acid-induced writhing behavior. These results suggest that the inhibitory descending serotonergic systems may be involved, through 5-HT1A and 5-HT3 receptors, in the production of an antinociceptive effect by centrally injected elcatonin.

5,7-Dihydroxytryptamine↗

Development of ventricular fibrillations with different characteristics in the local electrocardiogram: large and small amplitude of activation, and its implication for implantable cardioverter defibrillator treatment.

An implantable cardioverter defibrillator (ICD) was implanted in 2 patients with ventricular tachyarrhythmia related to old myocardial infarction, and defibrillation tests were attempted at the time of ICD implantation and at 2 or 4 weeks after the operation. Ventricular fibrillation (VF) was induced by T-wave shocks, but the amplitude of the ventricular electrogram was different in each VF. In most of the VFs with large ventricular electrograms, the local activity was appropriately detected. However, many undersensed beats were observed in other VFs that had fine ventricular electrograms and a longer time was needed before delivering the shock. The amplitude of the ventricular electrogram might be small in some cases of VF and this might result in undersensing and/or unsuccessful defibrillation. Close attention must be paid to the amplitude of ventricular activation in each VF to avoid possible difficulty in ICD therapy.

Aged↗