Biomedical subjects

M Takayasu

Publications and source records attributed to M Takayasu.

At least 55 records · Page 3Linked to original sources

PubMed1995

The effects of pituitary adenylate cyclase-activating polypeptide on cerebral arteries and vertebral artery blood flow in anesthetized dogs.

We investigated and compared the effects of pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) on cerebral circulation in anesthetized dogs. The intracisternal administration of PACAP-27, PACAP-38, and VIP dilated canine cerebral arteries in a dose-dependent manner. A 10 nmol dose of PACAP-27, PACAP-38, and VIP dilated the basilar artery by 23 +/- 3, 27 +/- 3 and 30 +/- 3%, respectively. Rostrally located arteries tended to be more responsive to PACAP-27. Pretreatment with NG-monomethyl-L-arginine did not affect PACAP-27-induced vasodilation. Vertebral artery blood flow was also affected by intra-arterial injection of these peptides in a dose-dependent manner. A 100 pmol dose of PACAP-27, PACAP-38, and VIP increased the vertebral artery blood flow by 42 +/- 10, 29 +/- 4, and 62 +/- 11%, respectively. The VIP receptor antagonist, [Lys1,Pro2,5,Arg3,4,Tyr6]VIP, inhibited both the VIP- and PACAP-38-induced increase in vertebral artery blood flow. These findings suggest that PACAP plays a role in the regulation of cerebral circulation.

Anesthesia↗

PubMed1995

Microclip haemostasis for surgical treatment of cerebral arteriovenous malformations. Technical note.

The authors describe newly designed microclips and their utility in obtaining haemostasis during the surgical resection of cerebral arteriovenous malformations. The microclips are particularly well-suited for controlling bleeding from small fragile vessels often encountered on the periphery of large arteriovenous malformations during the final stages of a surgical procedure. Histological examination of these vessels revealed very thin dilated walls without elastic layers, causing easy rupture. Hence, haemostasis using conventional means, such as bipolar coagulators, can be extremely difficult. We have used microclips on such vessels in 14 patients with arteriovenous malformations and controlled bleeding successfully.

Cerebral Angiography↗

PubMed1995

Oxyhemoglobin enhancement of vasopressin-induced constriction in rat cerebral arterioles.

This study was undertaken to determine the effects of oxyhemoglobin on vasopressin-induced responses in cerebral arterioles. Rat intracerebral arterioles about 60 microns in diameter were isolated and cannulated using pipettes. Changes in diameter secondary to the extraluminal application of drugs were monitored through a video micro-scaler. Vasopressin produced a triphasic, dose-dependent response consisting of vasodilation (10(-11) M), vasoconstriction (10(-9)-10(-8) M) and a decrease in vasoconstriction (10(-7)-10(-6) M). Pretreatment with oxyhemoglobin (10(-5) M) abolished the vasodilation induced by the lower dose vasopressin and doubled the vasoconstriction induced by the higher dose. The combination of L-arginine (10(-4) M) and superoxide dismutase (600 U) restored low-dose vasopressin vasodilation and suppressed high-dose vasoconstriction in oxyhemoglobin-pretreated arterioles, while they showed little effect when used singly. This study indicates that oxyhemoglobin enhances vasopressin-induced constriction of intracerebral arterioles and these effects can be inhibited by the combination of L-arginine and superoxide dismutase.

Animals↗

PubMed1995

Regional differences in cerebral vasomotor control by nitric oxide.

Regional differences in the role of nitric oxide in cerebral vasomotor control were investigated with a nitric oxide synthesis inhibitor, NG-monomethyl-L-arginine, or a precursor of nitric oxide, L-arginine using both dog cerebral angiography for the larger artery study and rat isolated arterioles for the microcirculation study. NG-monomethyl-L-arginine (10 mumol) constricted the dog cerebral arteries, by 15.6%, 17.5%, and 27.3% in the middle cerebral, anterior cerebral, and basilar arteries, respectively. The greater constriction of the basilar artery did not reach statistical significance. However, L-arginine (100 mumol) produced significantly greater dilation of basilar arteries than the middle cerebral or anterior cerebral (31.3% vs. 16.7% or 13.1%). NG-monomethyl-L-arginine at 10(-3) M constricted rat arterioles originating from basilar arteries significantly more than the middle cerebral arteries (23% vs. 14%). L-arginine at 10(-3) M dilated rat arterioles from basilar arteries significantly more than from the middle cerebral artery (24 vs. 11%). These findings suggest that the roles of nitric oxide in vasomotor control differs by region in the brain, and it may be greater in vessels of the posterior than of the anterior circulation.

Animals↗

PubMed1995

Effects of adrenomedullin, calcitonin gene-related peptide, and amylin on cerebral circulation in dogs.

The effect of human adrenomedullin on cerebral circulation was investigated in dogs in vivo and in vitro. Bolus administration of adrenomedullin or its homologous peptides, calcitonin gene-related peptide (CGRP) and amylin, into the vertebral artery induced a dose-dependent increase in vertebral blood flow. The potencies of adrenomedullin and CGRP were similar and approximately 100 times more than that of amylin. The effects of adrenomedullin and CGRP were inhibited by CGRP8-37, an antagonist of CGRP. In contrast to substance P, adrenomedullin did not induce an increase in blood flow after prior administration of CGRP. Pretreatment with either NG-nitro-L-arginine methyl ester or indomethacin did not affect the adrenomedullin-induced increase in blood flow. Intracisternal administration of adrenomedullin induced dilation of the basilar and other major cerebral arteries in a dose-dependent manner, accompanied by an increase in the concentration of cyclic AMP in the cerebrospinal fluid. Adrenomedullin also induced relaxation of isolated basilar and middle cerebral arterial rings. These data suggest that adrenomedullin induces vasodilation of cerebral arteries and an increase in vertebral blood by acting at CGRP receptors positively coupled to adenylate cyclase, and that these effects are not dependent on nitric oxide or prostaglandin formation.

Adrenomedullin↗

PubMed1995

Central cardiovascular effects induced by intracisternal PACAP in dogs.

The cardiovascular responses to intracisternally administered pituitary adenylate cyclase-activating polypeptide (PACAP) were investigated and compared with those of vasoactive intestinal peptide (VIP) in anesthetized dogs. Intracisternal administration of 10 nmol of PACAP-27 increased mean arterial blood pressure (MABP) significantly with a simultaneous increase of plasma arginine vasopressin and epinephrine concentrations. Intracisternal administration of VIP increased plasma arginine vasopressin concentration significantly but caused no appreciable change in MABP. Systemic infusion of the nonpeptide vasopressin V1 receptor antagonist OPC-21268 did not inhibit the PACAP-27-induced increase in MABP, whereas phentolamine, an alpha-adrenoceptor blocker, reversed the increase. Intracisternal pretreatment with the vasopressin V1 receptor antagonist [Pmp1, Tyr(Me)2]Arg8-vasopressin also inhibited the increase. These findings suggest that PACAP has a central pressor action by increasing sympathetic outflow, which is probably mediated by the vasopressinergic neural network. PACAP seems to play important roles in hormonal and neural control of systemic circulation.

Adrenergic alpha-Antagonists↗

PubMed1995

The use of self-retaining retractors in surgery for spinal cord tumors: technical note.

Self-retaining retractors may be useful in spinal tumor surgery. In this study, the tumors were retracted away from the surrounding tissue by pronged hooks attached to flexible self-retaining retractors; by this process, we could avoid placing pressure on the spinal cord. A clear dissection plane was exposed between the underside of the tumor and the surrounding spinal cord, so that the surgeon had both hands free to perform the operation. Two retractor base systems were used: 1) Sugita's multipurpose headframe for the cervical region, and 2) a newly designed U-shaped, table-fixed retractor base for the thoracic and lumbosacral regions. Most retracting instruments used in cranial surgery can be used with either system.

Humans↗

PubMed1994

Differing effects of vasopressin on regional cerebral blood flow of dogs following intracisternal vs. intra-arterial administration.

We investigated the differential effect of the intracisternal and intraarterial administration of vasopressin on the regional cerebral blood flow (rCBF) in the parietal cortex of dogs. Regional CBF, velocity and blood volume were assayed by laser flowmetry. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF and velocity, without affecting blood volume. However, the intravertebral arterial injection of 1 nmol vasopressin significantly decreased the rCBF and velocity. This discrepancy can be explained by a difference in the affected vasculature; large blood vessels in the subarachnoid space vs. whole cerebral vascular system. The intracisternal and intraarterial injection of the nitric oxide inhibitor NG-monomethyl-L-arginine reduced the rCBF from the base line, and significantly suppressed the rCBF elevation induced by vasopressin. The effect of vasopressin may be considered as the summation of the increased flow from the dilated large vessels via the release of nitric oxide from the endothelium, and of the decreased flow from the contracted small vessels.

Animals↗

PubMed1994

A role of nitric oxide in vasomotor control of cerebral parenchymal arterioles in rats.

The present study was undertaken to determine the role of nitric oxide (NO) in the regulation of vasomotor tone in rat cerebral parenchymal arterioles under physiological and pathological conditions. Cerebral arterioles, about 60 microns in diameter, were isolated from rats and cannulated with glass pipettes. Changes in the arteriolar diameter secondary to extraluminal application of drugs were monitored continuously through a videodimension analysis system. The arterioles were dilated by L-arginine (12.2 +/- 2.2% at 10(-3) M) and were constricted by NG-monomethyl-L-arginine (L-NMMA) (13.8 +/- 1.5% at 10(-4) M) in a dose-dependent manner. Pretreatment with superoxide dismutase (600 U) increased sensitivity to L-arginine. These results suggest that NO plays an important role in regulation of basal vasomotor tone of cerebral parenchymal arterioles under physiological conditions. Next, NO-modification of vasomotor responses to an endogenous vasoactive substance, arginine vasopressin (AVP) was studied in cerebral parenchymal arterioles. Increasing concentrations of AVP produced biphasic responses of vasodilation (10(-11) M) and vasoconstriction (10(-10)-10(-8) M). Inhibition of NO by pretreatment with L-NMMA (10(-4) M) or oxyhemoglobin (10(-5) M) abolished the vasodilation and enhanced the vasoconstriction by AVP. Therefore, under pathological conditions in which NO function was suppressed, such endogenous substances may produce contraction in parenchymal arterioles instead of dilation with aggravation of cerebral ischemia.

Animals↗

PubMed1994

Dysfunction of nitric oxide in the spastic basilar arteries after subarachnoid hemorrhage.

The function of nitric oxide in spastic cerebral arteries after subarachnoid hemorrhage (SAH) was angiographically investigated in dogs. On days 4 and 7, after two intracisternal injections of autologous blood, higher concentrations of L-arginine than those of endogenous L-arginine in the cerebrospinal fluid produced a transient vasodilation of the spastic basilar artery, whereas NG-monomethyl-L-arginine (L-NMMA) produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on day 4 than day 7, but less than that in intact dogs. Vasopressin, which is known to activate the endothelial L-arginine pathway, could induce a vasodilation only after the treatment with L-arginine. Intracisternal injection of superoxide dismutase (SOD), which caused no effect by itself, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on day 4 and both the magnitude and duration of that effect on day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. Enhancement of L-arginine's effect by SOD suggested that the inactivation of nitric oxide by superoxide anion contributed to the development of vasospasm.

Animals↗

PubMed1994

Vasopressin mediated vasodilation of cerebral arteries.

The bolus injection of vasopressin into the vertebral artery produced a dose-dependent vasodilation in the major cerebral arteries, detected angiographically, while it elicited a decrease in vertebral blood flow. One nanomol of vasopressin was the optimal dose for producing maximal vasodilation. The basilar, posterior communicating, and internal carotid arteries showed the most dilatation, followed by the middle cerebral, the intracranial portion of the vertebral artery and the anterior spinal artery. The extracranial portion of the vertebral artery was less sensitive to vasopressin. The vasodilation was inhibited by a V1-antagonist and NG-monomethyl-L-arginine. These results suggest that the arteries of the circle of Willis at the base of the brain are more sensitive to nitric oxide release induced by vasopressin compared with other intracranial and extracranial arteries.

Anesthesia↗

PubMed1994

Effects of vasopressin on regional cerebral blood flow in dogs.

Vasopressin may regulate the regional cerebral blood flow (rCBF) via two balancing effects: increased flow from the vessels dilated by nitric oxide from the endothelium, and decreased flow from the vessels contracted by direct stimulation of smooth muscle. The effect on the rCBF in anesthetized dogs following the intracisternal or intraarterial administration of vasopressin was investigated by laser flowmetry with the device placed on the dura over the parietal cortex. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF to 145.3 +/- 27.3% of base line. In contrast, the intravertebral arterial injection of vasopressin had no significant effect on the rCBF. This can be explained by a difference in the affected vasculature; mainly large vessels in the subarachnoid space vs. whole vascular system supplied by the vertebral artery. The intracisternal injection of 10 mumol of NG-monomethyl-L-arginine (L-NMMA) reduced the rCBF; pretreatment with this agent significantly suppressed the elevation in rCBF induced by vasopressin. The intraarterial injection of L-NMMA reduced the rCBF more than its intracisternal administration. It also suppressed the rCBF induced by vasopressin.

Animals↗

PubMed1994

Combined effect of L-arginine and superoxide dismutase on the spastic basilar artery after subarachnoid hemorrhage in dogs.

To investigate the function of nitric oxide (a major endothelium-derived relaxing factor) in cerebral arteries after subarachnoid hemorrhage (SAH) in vivo, several nitric oxide-related substances were administered to dogs that had undergone double SAH. These included L-arginine (a substrate for the formation of nitric oxide), NG-monomethyl-L-arginine (L-NMMA, an analog of L-arginine that inhibits the formation of nitric oxide from L-arginine), and superoxide dismutase (SOD, which protects nitric oxide from oxidation by superoxide anion), which were given via intracisternal injection. The diameter of the basilar artery was assessed angiographically. In intact dogs, intracisternal bolus injections of L-arginine (1, 10, or 100 mumol) produced a dose-dependent increase in the internal diameter of the basilar artery; conversely, L-NMMA reduced the diameter of the basilar artery from baseline in a dose-dependent manner. On Days 4 and 7, after two intracisternal injections of autologous blood, L-arginine produced transient vasodilation of the spastic basilar artery, whereas L-NMMA produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on Day 4 than on Day 7, but less than in intact dogs. Intracisternal injection of SOD, which caused no effect per se, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on Day 4 and both the magnitude and duration of that effect on Day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. The finding that the simultaneous injection of SOD enhanced and prolonged the vasodilation induced by sufficient exogenous L-arginine suggests that the inactivation of nitric oxide by superoxide anion contributes to the development of vasospasm.

Animals↗

PubMed1993

Vasodilatory effects of okadaic acid on the canine cerebral artery.

We investigated the in vivo and in vitro vasodilatory effects of okadaic acid, an inhibitor of protein phosphatases, in canine basilar arteries. Angiography revealed that the intracisternal injection of okadaic acid produced a long-lasting increase in the internal diameter of the canine basilar artery. The maximal increases in diameter induced by 1 and 10 nmol of okadaic acid were 23.3 +/- 13.5 and 33.8 +/- 11.9%, respectively. Okadaic acid in the concentrations of 10(-7) and 10(-6) M also exerted a dose-dependent, long-lasting relaxation without any contraction in isolated basilar arteries, even in the resting condition. Similar effects (ED50 values and maximal relaxation) were observed in arterial strips precontracted with K+, prostaglandin F2 alpha, and phorbol 12-myristate 13-acetate. These in vito and in vivo results suggest that inhibition of protein phosphatases by okadaic acid produces a vasodilation in the cerebral artery.

Angiography↗

PubMed1993

Role of nitric oxide in the cerebral vasodilatory responses to vasopressin and oxytocin in dogs.

We angiographically assessed the vasodilatory effects of vasopressin and oxytocin on the basilar arteries in dogs. Intracisternal bolus injections of vasopressin (100 pmol and 1 nmol) and oxytocin (1 and 10 nmol) produced dose-dependent increases in the internal diameter of the basilar arteries without affecting mean arterial blood pressure. The maximal dilatations of the basilar arteries induced by 1 nmol vasopressin and 10 nmol oxytocin were 142.3 +/- 19.9 and 136.8 +/- 25.5% of the baseline, respectively. When the same peptides were injected into the vertebral artery, the maximal dilatations were similar, but the duration of response was shorter. Pretreatment with intracisternal injection of 10 mumol NG-monomethyl-L-arginine (L-NMMA), which inhibits the synthesis of nitric oxide from L-arginine, suppressed the vasodilatory responses induced by intracisternal injection of vasopressin and oxytocin and by intraarterial injection of vasopressin. Calcitonin gene-related peptide also caused dilatation of the basilar artery when injected into the cisterna magna, but its effect was not blocked by L-NMMA. L-NMMA reduced the basal diameter of the basilar artery in a dose-dependent manner; L-arginine produced dose-dependent increases in diameter. The vasoconstriction induced by L-NMMA was reversed by high concentrations of L-arginine. These results suggest that vasopressin and oxytocin dilate the basilar arteries via the release of nitric oxide from both the intraluminal and the extraluminal sides and that synthesis and release of nitric oxide in the vascular wall contribute to maintenance of basal vascular tonus.

Animals↗

PubMed1993

Triphasic response of rat intracerebral arterioles to increasing concentrations of vasopressin in vitro.

To determine how vasopressin affects the vascular tone of the smaller cerebral arterioles, we carried out an in vitro study of isolated and cannulated intracerebral arterioles of rats. We found that increasing concentrations of vasopressin induced a triphasic response of vasodilation (10(-12)-10(-11) M), vasoconstriction (10(-10)-10(-8) M), and vasodilation stabilizing to control diameter (10(-7)-10(-6) M) and that the maximum constriction was twice the maximum dilation in these smaller arterioles [21.2 +/- 13.1% (mean +/- SD) decrease in diameter vs. 11.2 +/- 5.7% increased]. Pretreatment of the arterioles with NG-monomethyl-L-arginine (10(-4) M), a specific inhibitor of endothelium-derived relaxing factor, abolished the vasopressin-induced vasodilation and significantly increased the vasoconstriction. These results suggest that these arterioles were maintained in a dilated state by an endothelium-derived relaxing factor activated by vasopressin. Both vasodilation and vasoconstriction were found to be mediated through vasopressin V1 receptors in a study of arterioles pretreated with d(CH2)5Tyr(Me)arginine vasopressin (10(-6) M), a vasopressin V1 receptor antagonist. These results support the hypothesis that vasopressin may constrict smaller cerebral arterioles while simultaneously dilating larger cerebral arteries. Our results also suggest that vasopressin may aggravate cerebral ischemia in pathological conditions, such as subarachnoid hemorrhage, when the arteriolar response to vasopressin shifts from vasodilation to vasoconstriction due to increased vasopressin levels in plasma and CSF and impaired endothelium-derived relaxation.

Animals↗

PubMed1993

Regional differences in the vasodilator response to vasopressin in canine cerebral arteries in vivo.

BACKGROUND AND PURPOSE: The aim of this study was to investigate the regional differences in the in vivo vasodilator responses to vasopressin, which is thought to stimulate the release of nitric oxide from the endothelium, in canine cerebral arteries by angiography. METHODS: Angiograms were performed through a catheter inserted directly into the right vertebral artery and were taken periodically after the infusion of vasopressin. The diameters of various segments of the major arteries were measured using a computerized image analysis system. RESULTS: The bolus administration of vasopressin (10 pmol to 1 nmol) into the vertebral artery produced a long-lasting, dose-dependent vasodilation in the major cerebral arteries centering around the circle of Willis. One nanomole of vasopressin appeared to be the optimal dose for producing maximal vasodilation. The internal diameters of the basilar, posterior communicating, and internal carotid arteries experienced the most dilation (approximately 150% that of control) 2 minutes after the infusion of 1 nmol of vasopressin, followed by those of the middle cerebral, the intracranial portion of the vertebral, and the anterior spinal arteries (approximately 130% that of control). The extracranial portion of the vertebral artery (109.8 +/- 4.8% that of control, n = 4) was less sensitive to 1 nmol of vasopressin. Pretreatment with an intracisternal injection of 10 mumol of NG-monomethyl L-arginine suppressed the vasodilator effect of vasopressin and substance P, whereas it did not affect the response to vasoactive intestinal peptide. CONCLUSIONS: These results suggest that the arteries composing the circle of Willis at the base of the brain are more sensitive to nitric oxide release induced by vasopressin compared with other intracranial and extracranial arteries.

Angiography↗

PubMed1993

Occipital-axis posterior wiring and fusion for atlantoaxial dislocation associated with occipitalization of the atlas. Technical note.

The authors present their technique of occipital-axis posterior wiring and fusion for atlantoaxial dislocation associated with an occipitalized atlas. The technique consists of drilling a 3 x 1-cm horizontal groove in the occipital bone 1 cm posterior to the foramen magnum and building up a bony bridge along the posterior margin of the foramen magnum. This bony bridge is referred to as an "artificial atlas." Conventional wiring and fusion is performed between the artificial atlas and the C-2 lamina, interposing a strut bone graft. Since the compression force on tightening the wire is vertical, a very high degree of stability for the occipital-C-2 complex is achieved, facilitating early mobilization without postoperative redislocation.

Atlanto-Axial Joint↗