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Volume 95 (1990)
- Issue 6 Pages 279-
- Issue 5 Pages 229-
- Issue 4 Pages 139-
- Issue 3 Pages 83-
- Issue 2 Pages 47-
- Issue 1 Pages 7-
Volume 95, Issue 6
Displaying 1-9 of 9 articles from this issue
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Takehiko HUKUHARA Jr.1990 Volume 95 Issue 6 Pages 279-293
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSThe present physiological and neuropharmacological views and the essentials of the experimental results on the anatomical localization, functional and neuronal organization of the central respiratory mechanisms, classically expressed as the respiratory centers, in the brain stem were reviewed and discussed. The brain stem neural mechanism for central regulation of breathing is regarded as a complex neuronal mechanism consisting of several functional subsystems subserving different functions. One of its functions is the generation of respiratory rhythm. The subsystem for respiratory rhythm-generating mechanisms is located in the medullary reticular formation outside the DRG and VRG regions, which are thought to be premotor neuron pools. Rhythmic activity orginating in the medulla is dominant in terms of the spontaneity over other rhythmic activity in the pontine and spinal cord mechanisms. Evidences for heterogeneity of the functional properties of brain stem respiratory neurons have been demonstrated. Neuronal mechanisms involving respiratory neurons identified as members of the primary respiratory neuron population or neuronal networks consisting of different types of respiratory neurons located in the lateral region of the bulbar reticular formation may play important roles in the generation of respiratory rhythms. These aspects contribute to the understanding of the neurophysiological basis, providing important prerequisites for further neuropharmacological studies on neurotransmission within the neuronal network of the central respiratory mechanisms.View full abstractDownload PDF (13966K) -
Noboru TODA, Tomio OKAMURA1990 Volume 95 Issue 6 Pages 295-308
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSThe great discovery by Furchgott of the relaxing factor released from the endothelium (EDRF) awakened us to the necessity to reevaluate the functional importance of endothelial cells that have been chemically or physically stimulated. EDRF was first demonstrated to be released by acetylcholine, substance P, bradykinin and calcium ionophore A23187; thereafter, many substances have been found to release EDRF. This factor is quite unstable, is not produced by cyclooxygenase, and is an activator of soluble guanylate cyclase that synthesizes cyclic GMP; its action is suppressed by antioxidants via the superoxide anions produced, potentiated by superoxide dismutase and abolished by methylene blue and oxyhemoglobin. Recently, the role of lipoxygenase products in the production of EDRF was evaluated with new 5-lipoxygenase inhibitors without antioxidant activity. During the last couple of years, the actions and chemical properties of EDRF were verified to be quite similar to those of nitric oxide (NO); therefore, the hypothesis of “EDRF=NO” is widely being accepted. NO is produced from L-arginine via catalysis by an enzyme that is activated by Ca2+. The enzyme activity is inhibited by L-monomethyl arginine and other L-arginine analogs. Chemical and physical stimulations increase intracellular Ca2+ in endothelial cells that seems to be associated with K+-channel opening and hyperpolarization. Current interests are directed to the possible roles of NO in the regulation of nerve function. There are evidences suggesting that NO modulates adrenergic nerve function in blood vessels and some brain cell functions regulated by cellular cyclic GMP. Particularly, NO may be a transmitter substance in non-adrenergic, non-cholinergic vasodilator nerves innervating the cerebral arteries. Future investigations will determine the physiological roles of EDRF or NO and its relationships to pathophysiology of vascular dysfunctions, such as vasospasm and those related to hypertension, diabetes, aging, etc., and the extended roles of NO in nerve function, inflammation, immune reactions, etc. would be clarified more extensively by accelerated progress in this field of research.View full abstractDownload PDF (11988K) -
Naoyuki HIRONAKA, Hisatsugu MIYATA, Kohji TAKADA, Kiyoshi ANDO1990 Volume 95 Issue 6 Pages 309-318
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSDelayed discrimination experiments were conducted to examine drug effects on memory in rats. Three kinds of experimental situations: a Y-maze, an operant chamber with two retractable levers, and an operant chamber with two fixed levers were used. A discriminative stimulus light either on the left or the right side of a stimulus panel was presented for a brief period in each situation. After a certain delay time following extinguishment of the light, a choice response to the previously lighted side was termed as a correct choice. Scopolamine at 0.015 ?? 0.06 mg/kg, s.c., decreased the correct choice ratio in trials with a delay time of 0 sec in the Y-maze situation and in trials with longer delay times in the operant chamber situations. Nicotine at 0.06 ?? 1 mg/kg, s.c., decreased the correct choice ratio in trials with a delay time of 0 ?? 4 sec in the Y-maze situation, a delay time of 4 sec in the retractable-lever operant chamber situation, and a delay time of 0.1 sec in the fixedlever operant chamber situation. Using this delayed discrimination procedure, drug effects on the relationship between delay time and correct choice ratio were observed. From these results, the present procedure was found to be useful for the evaluation of drug effects on memory in rats.View full abstractDownload PDF (8477K) -
Yuji ABE, Akihiro NARIMATSU, Akihiro TOBE1990 Volume 95 Issue 6 Pages 319-325
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSThe effect of betaxolol, a beta s-adrenoceptor antagonist, on ischemic myocardial metabolism was studied in dog hearts subjected to an occlusion of the left anterior descending coronary artery for 10 or 30 min. Betaxolol (0.1 or 0.3 mg/kg) was injected i.v. 5 min before ischemia. Betaxolol decreased heart rate, (+)dp/dt, coronary flow and blood pressure. Coronary occlusion decreased the levels of creatine phosphate, adenosine triphosphate, total adenine nucleotides and energy charge potential in the ischemic myocardium. Ten minutes after ischemia, betaxolol significantly diminished these impairments of energy metabolism. Even 30 min after ischemia, a higher dose of betaxolol significantly inhibited the depletion of total adenine nucleotides. Myocardial ischemia produced a breakdown of glycogen, an accumulation of lactate and an inhibition of glycolytic flux through the phosphofructokinase reaction. Betaxolol also reduced these alterations of carbohydrate metabolism 10 min after ischemia. These results indicate that betaxolol delays the onset of myocardial metabolic change from aerobic to anaerobic during ischemia and hence reduces the severity of myocardial ischemic injury.View full abstractDownload PDF (5976K) -
Hiroshi AKITA, Miyuki HASHIMOTO, Mitsuhiko YAMADA, Yuji KIUCHI, Katsuj ...1990 Volume 95 Issue 6 Pages 327-333
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSBehavioral characteristics associated with acoustic stimulation and the neurochemical alterations of monoaminergic systems in rat brain at the steady state of repeated methamphetamine administration were investigated. We confirmed that reverse tolerance in stereotyped behavior was constructed up to the 28th day after repeated intermittent pretreatment with increasing doses of MAP (2.5, 5, and 7.5 mg/kg × 3 and 10 mg/kg × 2, every other day). During acoustic stimulation, locomotor activity in the saline group was significantly increased, but the activity after the stimulation was completely suppressed. In contrast to the saline group, locomotor activity was not influenced by the acoustic stimulation in the MAP group, suggesting that behavioral hyporesponsiveness to acoustic stimulation was induced by MAP treatment. Two days after the last injection, the contents of 5-hydroxytryptamine (5-HT) and 5-hydroxyphenylacetic acid (5-HIAA) in the cerebral cortex, midbrain + thalamus, hypothalamus and striatum were significantly decreased. These changes were maintained up to the 28th day after the drug withdrawal in the cerebral cortex and the midbrain + thalamus. From these results, the persistence of behavioral hyporesponsiveness to acoustic stimulation might be associated with long-lasting reduction of 5-HT synthesis.View full abstractDownload PDF (5501K) -
Hisato KAKUSHI, Tsutomu SHIKE, Yoko HAYASAKI, Takashi MATSUBARA, Kiyoh ...1990 Volume 95 Issue 6 Pages 335-346
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSEffects of cefaclor (3-chloro-7-D-(2-phenyl-glycinamido)-3-cephem-4-carboxylic acid) on PAF, ADP, collagen, endotoxin, and thrombin-induced platelet aggregation were examined in vitro with the use of guinea pig platelet-rich plasma and washed platelets. PAF, even at concentrations lower than its minimum effective concentration, enhanced ADP or endotoxin-induced platelet aggregation and prolonged the time to attain the maximum aggregation. PAF also enhanced collagen-induced platelet aggregation and shortened the lag time. Cefaclor (CCL) inhibited the PAF, ADP or thrombin induced platelet aggregation and shortened their maximum aggregation times at higher concentrations such as 300 μg/ml or more. CCL also inhibited the collagen-induced platelet aggregation and prolonged the lag time, but showed no effect on endotoxin-induced platelet aggregation. The effect of CCL was almost the same as that of latamoxef (LMOX). CCL and LMOX, however, showed no effect on cellular Ca2+ increase produced by PAF, ADP, or thrombin, suggesting that the inhibitory effect of CCL and LMOX on platelet aggregation is caused by the inhibition of fibrinogen binding to the glycoprotein IIb/Illa complex.View full abstractDownload PDF (8384K) -
Hideki BESSHO, Junko SUZUKI, Akihiro NARIMATSU, Akihiro TOBE1990 Volume 95 Issue 6 Pages 347-354
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSBetaxolol is a highly selective β1-adrenoceptor antagonist without intrinsic sympathomimetic activity. In this study, the antihypertensive effect of betaxolol was investigated in experimental hypertensive rats; and the antihypertensive mechanism was also studied. Betaxolol (1 and 10 mg/kg, p.o.) produced acute hypotensive effects in conscious spontaneously hypertensive rats (SHR), renal hypertensive rats, deoxycorticosterone/saline hypertensive rats and normotensive rats. The effect was particularly marked in SHR. Furthermore, daily oral administration of betaxolol to SHR for 3 weeks showed sustained antihypertensive effects without producing tolerance. In pithed rats, the pressor response induced by an electrical stimulation of the spinal cord was inhibited by both betaxolol and atenolol. However, only betaxolol reduced the pressor response to norepinephrine. These findings suggest that a certain relaxing effect on peripheral vascular beds in addition to inhibition of presynaptic β-adrenoceptors may contribute to the antihypertensive mechanism of betaxolol.View full abstractDownload PDF (6090K) -
Hideki BESSHO, Junko SUZUKI, Yoshimi KITADA, Akihiro NARIMATSU, Akihir ...1990 Volume 95 Issue 6 Pages 355-360
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSThe antihypertensive effect of betaxolol, a highly selective β1-adrenoceptor antagonist, was investigated in renal hypertensive dogs, and the mechanism was also studied. A single oral administration of betaxolol (1 and 10 mg/kg) lowered blood pressure dose-dependently. The hypotensive effect of betaxolol was enhanced by daily oral administration for 10 days. In anesthetized dogs, intraarterial injection of betaxolol produced a dose-dependent increase in femoral artery flow; and in this test, betaxolol was 3 times less potent than papaverine. The increase in blood flow with betaxolol was not affected by pretreatment with propranolol. These findings indicate that a certain vasodilating activity may contribute to the antihypertensive mechanism of betaxolol.View full abstractDownload PDF (4578K) -
Shinjiro SUZUKI, Sadayoshi SAKUMOTO, Hideto MIYAZAKI, Tetsuro TANEIKE1990 Volume 95 Issue 6 Pages 361-368
Published: 1990
Released on J-STAGE: February 20, 2007
JOURNAL FREE ACCESSThe disposition characteristics of theophylline from two sustained release formulations (Theolong and Theodur) administered orally at the dose of 100 mg/head were compared in two groups of nonanesthetized dogs following a 24-hr period of starvation (fasting) and immediately after feeding (nonfasting). The pharmacokinetics of the two sustained release theophylline preparations could be analyzed by a two-compartment open model. The peak plasma concentration, area under the curve and bioavailability of theophylline in Theolong in the fasting group were significantly higher the respective parameters in the nonfasting group, suggesting a decrease in the absorption process. In contrast, there were no significant differences in these parameters in Theodur between both the groups. The increase in urinary flow rate induced by Theolong was significantly lower in the nonfasting group. In both the groups, two metabolites of theophylline were isolated from the urine and identified as 3-methylxanthine and 1, 3-dimethyluric acid by HPLC. When the animals were administered Theolong after feeding the cumulative urinary excretion of theophylline and its metabolites was about 50% lower than that after fasting medication. These results suggest that effects of food intake on the absorption of theophylline in dogs are different depending on the sustained release formulations.View full abstractDownload PDF (6494K)
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