Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 113, Issue 4
Displaying 1-9 of 9 articles from this issue
  • [in Japanese], [in Japanese]
    1999Volume 113Issue 4 Pages 201-202
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
  • Nobufumi ONO
    1999Volume 113Issue 4 Pages 203-210
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The cerebral blood flow (CBF) is autoregulated to a steady flow within certain ranges. CBF increases and cerebrovascular resistance (CVR) decreases dramatically with breakthrough of autoregulation when systemic arterial blood pressure exceeded the upper limit of the range. Many kinds of components in the brain as well neurogenic factors affect the autoregulation. The breakthrough of autoregulation does not occur in the presence of nitric oxide (NO) synthesis inhibitors, angiotensin converting enzyme inhibitor, prostanoids (PG) administered in the brain, sympathetic denervation, and sinoaortic denervation. The abolishment of breakthrough of autoregulation may be due to an increased tolerance of cerebral vessels to hypertension and the inhibition of the release of a vasodilator substance such as NO or PG. It appears that the tone of brain microvessels is controlled towards dilation by cholinergic innervation originating from the nucleus basalis of Meynert, glutamatergic or GABAergic mediated GABAA receptor, and by a mediator such as NO, bradykinin, PGs. Also, it is likely that candidates for constricting factors in intraparenchymal microvessels are norepinephrinergic from the superior cervical ganglion, serotonergic involved in 5-HT1Dβ- and 5-HT2B-specific receptor subtypes, GABAergic mediated GABAB receptor, thromboxane, PG F and the angiotensin system. The autoregulation of CBF is maintained by these neurogenic factors to prevent brain ischemia and hyperemia.
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  • Hiroshi WATANABE, Hiromichi TSURU
    1999Volume 113Issue 4 Pages 211-218
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The nasal mucosa has important physiological roles, including the removal of foreign bodies and the warming and humidification of inspired air. The microcirculation in the nasal mucosa facilitates the above processes and plays a role in the periodic swelling and shrinking of the nasal mucosa. In the present article, we reviewed the unique vascular architecture of the nasal mucosa, the complicated feature of innervations by the sympathetic, parasympathetic and sensory nerves, the actions of some chemical mediators released under some pathologic conditions, and the state of microcirculation in the nasal mucosa in cases of nasal allergy and cold exposure. Although it is likely that the sympathetic neurotransmitter norepinephrine has a major role in controlling the microcirculation in the nasal mucosa, the physiological or pathophysiological roles of other transmitters such as neuropeptide Y, ATP, acetylcholine, and vasoactive intestinal polypeptide seem to be minor and vary between species. Nevertheless, nitric oxide, which is shown to be released from parasympathetic neurons, is believed to have some physiological and/or pathophysiological role. Unfortunately, we have yet to describe the mechanism of nasal congestion. Further study of the function of nasal congestion in various illnesses could result in the alleviation of unpleasant symptoms.
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  • Eiichiro OKABE, Kazuo TODOKI
    1999Volume 113Issue 4 Pages 219-225
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The primary purpose of the microcirculation is to transport nutrients and oxygen and to remove metabolic waste products from tissues. It is also well known that the fundamental mechanism for vascular control is the local regulation of the basal vascular tone, which is reinforced by blood pressure and counteracted by tissue metabolites. Thus, the well-being of the tissue depends on the circulatory transport process, which is governed by many functional parameters of the microcirculation such as blood flow, blood volume, intravascular and extravascular pressures, and capillary permeability. Inflammatory reactions in oral tissues can be initiated by many different insults to the tissues, and the reaction itself can be expressed in various ways. In addition, the tissues seem to have many “backup” systems, so that any one response can be produced in several ways, which is important for a reaction that has a survival value. A recent concept is that repeated stimulation of sensitive teeth may induce pulpal changes; this could occur through induction of neurogenic inflammation and alteration of pulpal blood flow. One possibility is that production of reactive oxygen species, as well as release of the sensory neuropeptides, at sites of inflammation contributes to alterations in local blood flow. In addition to the part played by the neurogenic mediators, nitric oxide participation and its interaction with oxygen-derived free radicals in oral tissue hemodynamics are also discussed.
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  • Kazuo ICHIHARA, Kumi SATOH
    1999Volume 113Issue 4 Pages 227-234
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The coronary artery supplies the arterial blood that contains oxygen and nutrients for the myocardial tissue to produce high-energy phosphates aerobically. The left anterior descending and circumflex coronary arteries run on the epicardial surface of the left ventricle, turn toward the endocardium at a right angle, and nourish the tissues of the subendocardinal layers with the arterial blood. Cessation of coronary blood flow makes the myocardium ischemic. The endocardium is particularly susceptible to ischemia because the arteries that run to the endocardium are pressed due to extravascular compression during every systole. Coronary vasodilators are still used as anti-anginal drugs. However, a potent coronary vasodilator may cause coronary-steal and thereby worsen the ischemia-induced myocardial injury. We will demonstrate changes in the microcirculation of the ischemic myocardium caused by coronary vasodilators and demonstrate that a coronary vasodilator is not always effective on the ischemic myocardium.
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  • Mikiyasu SHIRAI
    1999Volume 113Issue 4 Pages 235-248
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    It was demonstrated that pulmonary vessels, in contrast to systemic vessels, 1) have a low basal vascular tone, 2) constrict in response to hypoxia and 3) do not display significantly prominent vasomotion during autonomic nerve stimulation. However, details about these characteristics have not been clarified sufficiently by conventional methods; namely, measuring pressure-flow relationships and vascular tension of isolated larger conduit pulmonary vessels. Recent technological advances in studying pulmonary circulation now permit us to reveal that vasomotor responses to respiratory gases and neurohumoral factors differ not only quantitatively but also qualitatively between the central conduit and peripheral resistance vessels ( ?? 100- to 500- μm diam.). They also reveal that an increase in pulmonary sympathetic nerve activity can cause pulmonary vasodilation as well as vasoconstriction. The former has been partly explained by the most recent findings regarding the distribution differences of NO synthases and K+ channels between the resistance and conduit vessels. Concerning the latter, initial vascular tone appears to play an important role. The increased pulmonary sympathetic nerve activity has a β-receptor-mediated pulmonary vasodilator effect under low pulmonary vascular tone conditions but an α-receptor-mediated constrictor effect under enhanced vascular tone conditions. This may serve to maintain homeostasis of the pulmonary circulation and a good balance between the right and left ventricle outputs. Here, I have reviewed new developments related to the mechanisms for controlling pulmonary vascular tone under different states: normal, acute and chronic hypoxia, and hemorrhagic hypotension. I have also described the effects of inhaled NO and PGI2 as selective pulmonary vasodilators used for pulmonary hypertension.
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  • Makoto TAKENAGA, Hiromu KAWASAKI
    1999Volume 113Issue 4 Pages 249-259
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The mesenteric circulation plays an important role in maintenance of systemic blood pressure and regulation of tissue blood flow. The tone of the mesenteric artery and resistance blood vessels are mainly regulated by sympathetic adrenergic nerves through the release of neurotransmitter noradrenaline and also controlled by nonadrenergic noncholinergic (NANC) nerves and possibly by parasympathetic cholinergic nerves. Noradrenaline and adrenergic cotransmitters including neuropeptide Y and adenosine triphosphate act as a vasoconstrictor neurotransmitter for sympathetic nerves. While, dopamine, calcitonin gene-related peptide and acetylcholine act as a vasodilator neurotransmitter for adrenergic, NANC and cholinergic nerves, respectively. In the mesenteric circulation, these nerves containing various neurotransmitters and cotransmitters interact and modulate each other via feedback autoregulatory mechanisms and neuromodulation of various vasoactive substance to regulate vascular resistance.
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  • Toshiaki TAMAKI, Masanori YOSHIZUMI
    1999Volume 113Issue 4 Pages 261-267
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    The blood flow to the kidney averages about 20% of the cardiac output and the renal circulation affects urine formation. The renal microcirculation is unique. Glomerular circulation is mainly regulated by two resistance arterioles, the afferent arteriole and the efferent arteriole. Two capillary beds are arranged in series between the arterial and venous circulation. Many experimental findings show that each arteriole has a different sensitivity to various stimuli. Moreover, several anatomic characteristics of the renal circulation display heterogeneity. Several regional differences in the renal microcirculation may subserve the excretory function of the kidney. Technological advances now permit direct observation of renal arterioles and measurements of microvascular pressure, flows and resistances. In this mini review, we introduce 1) characteristics of renal circulation, 2) techniques for study of renal microcirculation, 3) effects of angiotensin II on the renal microvasculature, and 4) future directions for the study of renal microcirculation.
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  • Satoshi KANNO, Hiroshi YAMAZAKI, Sanae KASHIWABARA, Hiroyuki UCHIYAMA, ...
    1999Volume 113Issue 4 Pages 269-276
    Published: 1999
    Released on J-STAGE: January 30, 2007
    JOURNAL FREE ACCESS
    We studied the adhesive and sealing effects of sheet style fibrin adhesive, TO-193 (TachoComb®), on some tissues and organs, comparing them with those of sheet style collagen agent, collagen sponge, Novacol®, and Avitene® and liquid fibrin adhesive agent, Beriplast® P. TO-193 showed more a potent adhesive effect on liver than the sheet style collagen agents and was more potent on bone and skin than the liquid fibrin adhesive agent. Furthermore, TO-193 had a potent sealing effect at the site of incomplete suture immediately after application on a motile organ such as lung and stomach. These effects may be partly attributable to rapid expression of the effect due to the presence of a high concentration of fibrinogen on coverage. Enhancement of fibrin penetrability to the tissues by compression and inhibition of cleavage of coverage by the collagen sponge also may be participating in the effects of TO-193. These results suggest that TO-193 will be a valuable adhesive and sealing agent.
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