[Changes in arterial blood gas tensions during the recovery period of constant-load exercise].
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Biomedical subjects
Publications and source records attributed to Y Hirose.
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Intraperitoneal injection of ketamine (100 mg/kg body weight) significantly reduces the levels of cholecystokinin (CCK), somatostatin (SRIF), and substance P (SP)-like immunoreactivity in various regions of rat brain. No significant change in thyrotropin releasing hormone (TRH)-like immunoreactivity was observed. Neuropeptide systems may be involved in the neuropharmacologic effects of ketamine.
In the first series of experiments, we studied whether or not strychnine (STR)-resistant inhibition of masseter motoneurons (MASS . MNS) was involved in their rhythmical inhibition that occurs during masticatory activity, induced by repetitive stimulation of the cortical masticatory area (CMA) in the cat. After systemic STR injection, repetitive CMA stimulation induced rhythmically alternating activity in the masseteric and anterior digastric nerves with a shorter cycle time than before STR-administration. The short-latency IPSPS in the MASS . MNS evoked by single shocks applied to the CMA were abolished. In contrast, repetitive CMA stimulation still induced a rhythmical alternation of EPSPS and IPSPS in the MASS . MNS, although the IPSPS were significantly reduced in amplitude. In the second series, we attempted to abolish the STR-resistant component of the rhythmical IPSP with tetanus toxin (TT). This was injected into one superficial masseter muscle of the guinea pig. In the majority of animals, repetitive CMA stimulation induced a tonic EMG superimposed by rhythmical bursts in the TT-intoxicated masseter muscle. Repetitive CMA stimulation induced a rhythmical sequence of EPSPS and superimposed spikes in the MASS . MNS innervating the TT-intoxicated masseter muscle in paralyzed guinea pigs. It was concluded that: (1) the cortically-evoked short-latency inhibition of MASS . MNS is STR-sensitive, as is part of the rhythmical inhibition during CMA-induced mastication; and (2) rhythmical inhibition is not essential for the central generation of the rhythmical activity in the MASS . MNS.
The effects of MPTP administered to mice were examined biochemically and pharmacologically. The dopamine level in the striatum of the mice injected with MPTP decreased markedly, but recovered to 50% of the control level 6 weeks later. Amine fluorescence showed a decrease in the amount of amine especially in the lateral part of the striatum. Of the four neuropeptides, only the concentration of somatostatin changed with time. These findings indicate that the time elapsed after MPTP treatment should be taken into consideration when MPTP-treated mice are used as a parkinsonism model. Six weeks after MPTP treatment, the concentration of the striatal muscarinic cholinergic receptor decreased significantly but recovered to the normal level after the administration of L-dopa. Such a change was not detected with the dopamine D2-receptor. The therapeutic efficacy of medication in MPTP-treated mice as examined by the pole test showed that L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), which is considered to be the precursor of norepinephrine, enhances the effect of L-dopa.
Six patients with malignant lymphomas in autoimmune diseases are described. Four patients who had Sjögren's syndrome (SS) alone or with progressive systemic sclerosis (PSS) or rheumatoid arthritis (RA) developed non-Hodgkin's lymphomas of the B cell type. One patient who had systemic lupus erythematosus (SLE) developed a B cell lymphoma. Another patient with chronic thyroiditis (ChTD) and idiopathic thrombocytopenic purpura (ITP) had a T cell (OKT3/T4) lymphoma. In 5 patients, the autoimmune diseases (2SS, SS/PSS, SS/RA and SLE) preceded B cell lymphomas by one to 11 years. In the patient with ChTD/ITP, ChTD and a malignant lymphoma were found simultaneously. A review of Japanese reports on lymphoproliferative disorders associated with these autoimmune diseases is given. This report offers the suggestion that disorders in the immunoregulatory system caused by autoimmune diseases may predispose lymphoproliferative disorders.
A 53-year-old male with Bence Jones lambda myeloma developed hypercalcemia and acute renal failure (calcium 14.4 mg/dl, BUN 40 mg/dl, creatinine 3.0 mg/dl) after initial response to chemotherapy. A 99mTc-MDP bone scan revealed unusual isotope accumulation in the left hypochondrium. Extensive calcium deposition was confirmed in the gastric mucosa in the postmortem examination. Detection of gastric calcification by a bone scan is very rare. Only two cases of gastric calcification visualized on bone scans can be found in the literature, one with multiple myeloma) and one in Hodgkin's disease).
Biopsy specimens of the major bronchus of sixty-nine patients with sarcoidosis were investigated electronmicroscopically. 22 patients (12 males, 10 females), 32% of the cases, showed concentric lamellar or similar kinds of dense bodies in the bronchial wall. Typically, the concentric lamellar bodies were observed in various numbers, scattered in the collagen-increased tunica propria or superficial submucosal layer, where adjacent or deeply located blood capillary vessels were mostly obliterated. They were generally of 0.2 to 1.8 micron in size, but occasionally smaller ones were observed. We also found large swollen and irregular lamellated bodies greater than 2 microns in the cell cytoplasm. Six cases with particularly large numbers of these bodies in the bronchial wall showed "capped" figures, in which the concentric lamellar bodies were partly attached to other demilunar dense bodies. These figures were assumed to be the very early stage of formation of conchoidal bodies at the LM level, so-called Schaumann bodies. Two cases (5%) (chronic bronchitis, lung cancer) among 40 control patients with other diseases disclosed the same small lamellated bodies in the bronchial wall. We were unable to resolve the problem of the origin of these deposited in them, but assume that they will initially occur in the cell cytoplasm in some patients with sarcoidosis and eventually develop into typical concentric lamellar bodies.
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Administration of p-chlorophenoxyisobutyric acid (clofibric acid) markedly increased the activity of microsomal 1-acylglycerophosphorylcholine (1-acyl-GPC) acyltransferase in kidney, intestinal mucosa and liver, but not in brain, heart, lung, spleen, testis or skeletal muscle. In both kidney and liver, a marked dose-dependent increase in the activities of both microsomal 1-acyl-GPC acyltransferase and peroxisomal beta-oxidation was observed. In the rats treated with clofibric acid at a relatively low dose, the increase in the activity of 1-acyl-GPC acyltransferase in kidney was more marked than that in liver. The extent of the relative increase in the activity of 1-acyl-GPC acyltransferase to the activity of peroxisomal beta-oxidation in kidney was more marked than that in liver. The increased activity of 1-acyl-GPC acyltransferase in both kidney and liver lasted throughout the 8-week treatment period of rat with clofibric acid.
Coenzyme Q10 (CoQ10) and the opiate antagonist naloxone were compared as to their effect on the survival of mongolian gerbils with unilateral carotid ligation-induced stroke. Without medication all of the stroke gerbils died within 28 hours, but with a subcutaneous implantation of a 10 mg pellet of naloxone, 20% of the gerbils lived for 4 weeks. When a 250 mg pellet of CoQ10 was implanted subcutaneously, a definite effect on survival was observed, with 45% of the stroke gerbils living for 4 weeks. Considering that the action mechanisms of CoQ10 and naloxone are different, the combined use of these drugs in the treatment of stroke needs to be investigated.