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Biomedical subjects

K Isozumi

Publications and source records attributed to K Isozumi.

34 records · Page 2Linked to original sources
PubMed1994

Effect of sympathetic stimulation on cerebral circulation.

The role of sympathetic regulation in cerebral circulation was studied in the cat by continuous measurement of cerebral tissue oxygen tension (BrPO2), carbon dioxide tension (BrPCO2), pH(BrpH) and blood pressure. The ipsilateral superior cervical ganglion was electrically stimulated for 3 min. A slight decrease in BrPO2 and a slight but significant increase in BrPCO2 were observed during sympathetic stimulation. These changes suggested that sympathetic stimulation slightly decreased cerebral blood flow. The present results do not rule out a significant role for sympathetic regulation of cerebral circulation. Sympathetic constriction of the extraparenchymal vessels might be compensated for by secondary dilation of the intraparenchymal vessels elicited by a chemical control (escape phenomenon).

Animals↗
PubMed1993

Cerebrovascular NADPH diaphorase-containing nerve fibers in the rat.

Recently, neuronal nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase has been elucidated to be the nitric oxide synthase (NOS) per se. In order to examine the existence and distribution of cerebrovascular nerve fibers containing these substances, NADPH-diaphorase histochemistry was applied to the cerebral blood vessels and the cranial ganglia known to innervate the cerebral vessels in the rat. Numerous nerve fibers with varicosities forming plexuses were observed in the circle of Willis and its branches. In addition, thick nerve bundles were seen to run along the wall of the internal ethmoidal artery. NADPH-diaphorase reaction was prominent in neurons of the sphenopalatine, otic and internal carotid ganglia. This study demonstrated, for the first time, the NADPH-diaphorase-containing nerve fibers in the cerebral vessels and ganglion cells in the parasympathetic and sensory ganglia known to innervate the cerebral vessels.

Animals↗
PubMed1993

Changes of pial vessel diameter and CO2 reactivity during insulin-induced hypoglycemia and in the recovery period following glucose administration.

The present study examined the changes of cerebrovascular CO2 reactivity during insulin-induced hypoglycemia and in the recovery period following glucose administration in cats. The diameters of pial vessels were continuously measured using the vidicon camera system. Hypoglycemia was induced by intraperitoneal injection of Actrapid insulin (100 IU/kg). Cerebrovascular CO2 reactivity was estimated by the changes of pial vessel diameters during 3 min inhalation of 5% CO2 in air at each stage of glucose level. CO2 reactivity was impaired in the hypoglycemic stage and this impairment was further enhanced in the early recovery stage. In the late recovery stage, CO2 reactivity was restored particularly in the small arteries which were less innervated by autonomic nerves. These results suggest that the sympathetic activity plays an important role in the impairment of cerebrovascular CO2 reactivity during hypoglycemia.

Animals↗
PubMed1993

Alpha-adrenergic blockade with phenoxybenzamine enhances cerebrovascular CO2 reactivity.

The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated by an alpha-adrenergic blockade with phenoxybenzamine (PBZ). Cerebral oxygen and carbon dioxide tension (BrPo2, BrPco2) and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 5 mg/kg of PBZ. The effects of 5% CO2 inhalation were measured before and after the infusion of PBZ. Following the intracarotid infusion of PBZ, BrPo2 and BrPco2 did not change significantly. After the alpha-adrenergic blockade the degree of the increase in BrPo2 during 5% CO2 inhalation was significantly enhanced. The increase in the cerebrovascular CO2 reactivity produced by low dose PBZ suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.

Animals↗
PubMed1993

Effect of clonidine on the cerebrovascular system in cats.

The effects of clonidine, a potent alpha 2 adrenergic agonist and an imidazole/imidazoline receptor agonist, were examined in the cat cerebrovascular system, measuring cerebral oxygen and carbon dioxide tension (BrPo2, BrPco2) and arterial blood pressure. Intracarotid injection of clonidine (2 micrograms/kg) produced a gradual decrease in systemic blood pressure without initial hypertension, while BrPo2 decreased slightly but significantly. Before and after intracarotid administration of clonidine, cerebrovascular reactivity to carbon dioxide was estimated by changes in BrPo2 and BrPco2 during and after 3 min inhalation of 5% CO2. Clonidine significantly enhanced cerebrovascular reactivity to carbon dioxide. The data suggest that the alpha 2-adrenoceptor and/or imidazoline receptor play an important role in the regulation of cerebral circulation.

Animals↗
PubMed1993

Effect of sympathetic nervous system stimulation on cerebrovascular CO2 responsiveness.

Cerebrovascular CO2 responsiveness, following noradrenaline (NA) infusion, was studied in the cat by continuous measurement of cerebral tissue oxygen tension (BrPO2), carbon dioxide tension (BrPCO2), pH (BrpH), and blood pressure (BP). Intravenous infusion of NA (1 microgram/kg/min) was done to stimulate the adrenergic nervous system. Inhalation of 5% CO2+air was performed for 3 minutes before, during, and after NA infusion. Cerebrovascular CO2 responsiveness was estimated from changes in BrPO2, BrPCO2, and BrpH. CO2 inhalation increased BrPO2, BrPCO2, and BP, but decreased BrpH, in the respective 3 stages. delta BrPO2 decreased significantly during NA infusion, but recovered after cessation of NA. NA infusion caused a decrease in CO2 responsiveness. This suggests that sympathetic hyperactivity can modify cerebrovascular CO2 responsiveness.

Animals↗
PubMed1992

Effects of locus ceruleus lesions on the pericapillary nerve terminals in the feline brain.

The effects of bilateral locus ceruleus (LC) lesions on the pericapillary nerve terminals were investigated in the feline brain parenchyma using electron microscopy. LC lesions were induced stereotaxically and the animals were sacrificed after intravenous administration of 5-hydroxydopamine (5-OHDA). The diameter and number of dense-cored vesicles (DCVs) and clear vesicles (CVs) in the pericapillary nerve terminals were measured. The number of DCVs in the nerve terminal was significantly decreased by bilateral LC lesions. The diameters of the DCVs and CVs decreased significantly as compared with those in the non-operated control group. These data suggest that the LC is closely related to the pericapillary nerve terminals in the brain parenchyma and that not only nerve terminals with DCVs but also those with CVs are affected by LC lesions.

Animals↗
PubMed1992

Controlled ultraviolet irradiation generates endothelial damage without affecting the nerve terminals of the cerebral artery in cats.

The vesicles of adventitial autonomic nerve terminals were examined quantitatively under an electron microscope in controlled ultraviolet ray (UV)-irradiated cerebral vessels. Five cats whose basilar arteries were irradiated with UV (UV group) and 5 cats whose basilar arteries were irradiated with visible rays (control group) were compared. Endothelial vacuolation was observed only in the UV group. There was no statistically significant difference in the diameters of the dense-cored vesicles, related to noradrenaline, and clear vesicles, related to acetylcholine, between the two groups. It is concluded that controlled UV irradiation which generates endothelial damage does not affect the vascular adventitia ultrastructurally.

Acetylcholine↗
PubMed1992

Role of the sympathetic system in impairment of the cerebrovascular CO2 responsiveness during moderate hypoglycemia.

We examined the mechanism of impairment of the cerebrovascular CO2 responsiveness in moderate hypoglycemia. Twelve fasted cats were used. The brain-PO2, brain-PCO2 and brain-pH were measured continuously with electrodes placed on the brain surface. Hypoglycemia was induced with insulin. Intravenous injection of hexamethonium (a sympathetic ganglion blocker, C6; 0.1 mg/kg) was performed at the following stages: Control, hypoglycemia and recovery. Before and after the C6 administration, 5% CO2 in air was inhaled for 3 min at the respective stages. The CO2 responsiveness (cerebrovascular dilatory response to increased PaCO2) at the control stage was not altered after the ganglionic blockade. At the hypoglycemic stage, the increase in BrPO2 by CO2 inhalation was significantly less than that at the control stage. This reduction of delta BrPO2 was significantly improved after the administration of C6. At the recovery stage, the CO2 responsiveness before and after the administration of C6 was not significantly different. An impaired CO2 responsiveness in the hypoglycemic state was improved by sympathetic ganglion blockade with C6 which did not alter the reactivity during normoglycemia. It is suggested that the sympathetic activity plays an important role in impairment of the cerebrovascular CO2 responsiveness during moderate hypoglycemia.

Animals↗
PubMed1992

Role of cyclooxygenase system in cerebrovascular responsiveness: different effects of indomethacin on CO2 responsiveness and dilatation by Ca(2+)-channel blocker.

To investigate roles of prostaglandins in the regulation of cerebral blood flow, we compared effects of indomethacin, a cyclooxygenase inhibitor, on the cerebrovascular CO2 responsiveness with those on the cerebrovascular dilatory action of diltiazem, a Ca(2+)-channel blocker. Fifteen adult cats were used. The cerebral tissue oxygen tension, carbon dioxide tension, pH and blood pressure were measured continuously. Indomethacin (1 mg/kg) was infused into the carotid artery. In 8 cats, 3 min inhalation of 5% CO2 in air was performed before and after the indomethacin infusion. In 7 cats, diltiazem (100 micrograms/kg) was infused into the carotid artery for 3 min before and after the indomethacin infusion. The cerebrovascular CO2 responsiveness was significantly decreased (p < 0.05) after the administration of indomethacin. On the other hand, the cerebrovascular dilatation induced by the Ca(2+)-channel blocker was significantly increased (p < 0.05) after the administration of indomethacin. It is concluded that the products of cyclooxygenase system are involved in the cerebrovascular responsiveness both to CO2 and to Ca(2+)-channel blocker, but action mechanisms of prostaglandins may be different, that is, prostaglandians may enhanced cerebrovascular responsiveness to CO2 but diminish it to Ca(2+)-channel blocker.

Animals↗
PubMed1992

Effects of mergocriptine on cerebral circulation and metabolism in cats.

Mergocriptine (CBM 36-733, CAS 81968-16-3) is an ergot alkaloid derivative and a dopaminergic agonist. Effects of mergocriptine on cerebral circulation and metabolism were examined by monitoring cerebral tissue oxygen and carbon dioxide tension (BrPO2, BrPCO2), cerebral blood flow (CBF) and blood pressure (BP) in 10 cats. Mergocriptine (10 micrograms/kg) infused into the carotid artery produced a significant increase in CBF during the administration followed by a decrease in BrPO2 in parallel with a significant decrease in BP.

Animals↗
PubMed1991

Moderate hypoglycemia induces ultrastructural changes in perivascular nerve terminals of cat cerebral arteries.

A quantitative morphological analysis of the perivascular nerve terminals of cerebral arteries during moderate hypoglycemia was performed. 5-Hydroxydopamine (5-OHDA) was applied to discriminate dense-cored vesicles, related to noradrenaline, and clear vesicles, related to acetylcholine, under the electron microscope. Five hypoglycemic and 5 normoglycemic cats, all receiving 5-OHDA, were compared. In both the middle cerebral artery and vertebral artery, the dense-cored vesicles were significantly smaller and clear vesicles were significantly larger in hypoglycemia than in normoglycemia. These morphological changes in the vesicles may indicate hyperactivity of the sympathetic system and hypoactivity of the parasympathetic system of the cerebral vessels during hypoglycemia.

Animals↗
PubMed1990

Effects of nilvadipine on cerebral circulation and metabolism in cats.

Effects of nilvadipine (FK 235) on cerebral circulation and metabolism were examined measuring cerebral oxygen and carbon dioxide tension (BrPO2, BrPCO2), pH (BrpH) and mean arterial blood pressure (MABP) in cats. Nilvadipine (10 micrograms/kg) infused into the carotid artery produced a remarkable and long-lasting decrease in systemic blood pressure, whereas BrPO2 and BrPCO2 increased significantly. The present study suggests that in addition to the improvement of the cerebral circulation, nilvadipine may augment cerebral metabolism.

Animals↗
PubMed1990

Effects of 3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine on cerebral circulation and metabolism in cats.

Effects of 3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine (KC-404) on cerebral circulation and metabolism were examined measuring cerebral oxygen and carbon dioxide tension (BrPO2, BrPCO2) and mean arterial blood pressure (MABP) in cats. KC-404 (100 micrograms/kg) infused into the carotid artery produced no significant changes in BrPO2, BrPCO2 and MABP. 300 micrograms/kg of KC-404 infused into the femoral vein produced significant decrease in MABP, whereas BrPO2 remained constant. It is suggested that a large dose of KC-404 causes preferential cerebral vasodilation and maintenance of constant blood flow despite marked reduction in MABP.

Animals↗
PubMed1989

Effects of 2-nitratopropyl 3-nitratopropyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate on cerebral circulation and metabolism in cats.

Effects of CD-349 (2-nitratopropyl 3-nitratopropyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate) on cerebral circulation and metabolism were examined measuring cerebral oxygen and carbon dioxide tension (BrPO2, BrPCO2), pH (BrpH) and mean arterial blood pressure (MABP) in cats. CD-349 of 10 micrograms/kg infused into the carotid artery produced a remarkable and long-lasting decrease in systemic blood pressure, whereas BrPO2, BrPCO2 and BrpH did not change significantly. The previous studies have already demonstrated that CD-349 increases cerebral blood flow (CBF). In addition to the improvement of the cerebral circulation, the present study suggests that C-349 may augment cerebral metabolism.

Animals↗