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Featured researches published by Masayoshi Uchida.


Anesthesia & Analgesia | 2001

The differential effects of stereoisomers of ropivacaine and bupivacaine on cerebral pial arterioles in dogs

Hiroki Iida; Hiroto Ohata; Mami Iida; Kiyoshi Nagase; Masayoshi Uchida; Shuji Dohi

We investigated whether the stereoisomers of ropivacaine and bupivacaine exert differential effects on the cerebral microcirculation. Pentobarbital-anesthetized dogs (n = 16) were prepared for measurement of cerebral pial vessel diameters by using a closed cranial window preparation. We administered three different concentrations (10−7, 10−5, and 10−3 M) of each of three drug solutions [R(+), racemic, and S(−) forms of ropivacaine (n = 8) or bupivacaine (n = 8)] under the window in a randomized manner and measured cerebral pial arteriolar diameters. Various physiologic data were obtained before and after topical application of each test solution. All three forms of ropivacaine constricted cerebral pial arterioles, each in a concentration-dependent manner. The rank order for degree of vasocon- striction was S(−) ropivacaine > racemic ropivacaine > R(+) ropivacaine. In contrast, R(+) and racemic bupivacaine dilated, but S(−) bupivacaine constricted, cerebral pial arterioles, each in a concentration-dependent manner. We could find no difference in vascular reactivity to these drugs between large (≥100 &mgr;m) and small (<100 &mgr;m) arterioles. Topical application of these drugs induced no changes in mean blood pressure or heart rate. The observed differences in the microvascular alterations induced by the stereoisomers of ropivacaine and bupivacaine suggest that the vasoactive effects of these drugs on cerebral arterioles could, at least in part, depend on their chirality.


Anesthesia & Analgesia | 2001

The effects of alpha-human atrial natriuretic peptide and milrinone on pial vessels during blood-brain barrier disruption in rabbits

Hiroki Iida; Mami Iida; Motoyasu Takenaka; Akiyoshi Oda; Masayoshi Uchida; Hisayoshi Fujiwara; Shuji Dohi

The effects of &agr;-human atrial natriuretic peptide (HANP) and milrinone on cerebral pial vessels, especially during blood-brain barrier (BBB) disruption, are not clear. We studied topical HANP (10−14, 10−12, and 10−10 M) or milrinone (10−7, 10−5, and 10−3 M), and IV HANP (0.1, 0.2, and 1.0 &mgr;g · kg−1 · min−1) or milrinone (0.5, 5.0, and 20.0 &mgr;g · kg−1 · min−1) with or without hyperosmolar BBB disruption, using a rabbit cranial window preparation. At 10−12 and 10−10 M topical HANP produced significant arteriolar (16%, 20%, respectively), but no venular dilation. Topical milrinone (10−3 M) produced significant arteriolar and venular dilation (21%, 8%, respectively). IV HANP produced no arteriolar or venular changes at any dose except during BBB disruption, when it caused a significant arteriolar (16%, 16%, and 17%, respectively), but no venular dilation. In contrast, IV milrinone caused small but significant arteriolar and venular dilation without BBB disruption (arterioles, 6%, 7% and 8%, respectively; venules, 6% at 20.0 &mgr;g · kg−1 · min−1). During BBB disruption, these responses to milrinone were similar. Although HANP and milrinone each have a direct vasodilator effect on arterioles, their systemic administration at clinical doses could induce different effects. BBB disruptive conditions could increase the response of pial vessels to systemically administered HANP.


Anesthesia & Analgesia | 2005

Both milrinone and colforsin daropate attenuate the sustained pial arteriolar constriction seen after unclamping of an abdominal aortic cross-clamp in rabbits.

Masayoshi Uchida; Hiroki Iida; Mami Iida; Masahiko Kumazawa; Kazuyuki Sumi; Motoyasu Takenaka; Shuji Dohi

We previously reported that unclamping of an abdominal aortic cross-clamp causes initial dilation of pial arteries followed by sustained constriction. Both milrinone and colforsin daropate have a vasodilator action, and both have been used in such critical conditions as abdominal aortic aneurysmectomy. We measured cerebral pial arteriolar diameters using a rabbit closed cranial window preparation before (baseline) and 15 min after the start of an IV infusion of 0.9% saline (control group), milrinone, or colforsin daropate (0.05 and 0.5 &mgr;g · /kg−1 · min−1) (pre-clamp), just after aortic clamping, 20 min after clamping, and at 0 to 60 min after unclamping. In the control group, a significant decrease in diameter persisted for at least 60 min after unclamping (maximum, −15% for large and −26% for small arterioles versus baseline). These values were significantly smaller after both doses of milrinone and the larger dose of colforsin daropate (−5% and −8%, 10% and 12%, and −2% and −5%, respectively vs baseline, at 60 min). In a second experiment, changes in regional cerebral blood flow and tissue oxygen tension reflected changes in vascular variables. Thus, sustained cerebral pial arteriolar constriction induced by aortic unclamping can be attenuated by IV milrinone or colforsin daropate.


European Journal of Anaesthesiology | 2007

Effects of ifenprodil on voltage-gated tetrodotoxin-resistant Na + channels in rat sensory neurons

Shigeaki Tanahashi; Hiroki Iida; Akiyoshi Oda; Yoko Osawa; Masayoshi Uchida; Shuji Dohi

Background and objective: To examine a possible mechanism for the antinociceptive action of the N‐methyl‐d‐aspartate receptor antagonist ifenprodil, we compared its effects with those of ketamine on tetrodotoxin‐resistant Na+ channels in rat dorsal root ganglion neurons, which play an important role in the nociceptive pain pathway. Methods: Experiments were performed on dorsal root ganglion neurons from Sprague‐Dawley rats, recordings of whole‐cell membrane currents being made using patch‐clamp technique. Results: Both drugs blocked tetrodotoxin‐resistant Na+ currents dose dependently, their half‐maximal inhibitory concentrations being 145 ± 12.1 &mgr;mol (ketamine) and 2.6 ± 0.95 &mgr;mol (ifenprodil). Ifenprodil shifted the inactivation curve for tetrodotoxin‐resistant Na+ channels in the hyperpolarizing direction and shifted the activation curve in the depolarizing direction. Use‐dependent blockade of tetrodotoxin‐resistant Na+ channels was more marked with ifenprodil than with ketamine. When paired with lidocaine, these drugs produced similar additive inhibitions of tetrodotoxin‐resistant Na+ channel activity. Conclusions: The observed suppressive effects on tetrodotoxin‐resistant Na+ channel activity may, at least in part, underlie the antinociceptive effects of these N‐methyl‐d‐aspartate receptor antagonists.


Journal of Neurosurgical Anesthesiology | 2013

Nicorandil protects pial arterioles from endothelial dysfunction induced by smoking in rats.

Kenji Iwata; Hiroki Iida; Mami Iida; Motoyasu Takenaka; Kumiko Tanabe; Naokazu Fukuoka; Masayoshi Uchida

Background: Our aims are to investigate the effect of nicorandil, which is used for angina prevention and treatment, on the endothelial dysfunction induced by acute smoking and to clarify the underlying mechanism. Materials and Methods: A closed cranial window preparation was used to measure changes in pial vessel diameters in Sprague-Dawley rats. The responses of arterioles were examined to an endothelium-dependent vasodilator acetylcholine (ACh) before smoking. After intravenous nicorandil (200 &mgr;g/kg bolus infusion and then 60 &mgr;g/kg/min continuous infusion; n=6) or saline (control; n=6) pretreatment, the pial vasodilator response to topical 10−5 M ACh infusion was reexamined both before and 1 hour after 1-minute cigarette smoking. Thereafter, either glibenclamide or N-&ohgr;-nitro-L-arginine methyl ester (L-NAME) was infused 20 minutes before nicorandil infusion. In the glibenclamide (n=6) or L-NAME; n=6 pretreatment group, the pial vasodilator response to topical ACh was examined before and after smoking. Percentage changes in pial vessel diameters were used for the statistical analysis. Results: Cerebral arterioles were dilated during topical ACh infusion. After smoking, 10−5 M ACh constricted cerebral arterioles (−7.7±1.8%). After smoking, in the nicorandil-pretreatment group, 10−5 M ACh dilated cerebral pial arterioles by 10.5±3.0%. When given before nicorandil infusion, glibenclamide, but not L-NAME, abolished the preventive effects of nicorandil against smoking-induced endothelial dysfunction in pial vessels. Conclusions: Acute cigarette smoking causes dysfunction of endothelium-dependent pial vasodilatation, and nicorandil prevents this effect of smoking. The mechanism underlying this protective effect may depend mainly on adenosine triphosphate–sensitive potassium-channel activation.


Anesthesia & Analgesia | 2008

The Effects of Transient Cerebral Ischemia on Vasopressin-induced Vasoconstriction in Rabbit Cerebral Vessels

Masahiko Kumazawa; Hiroki Iida; Masayoshi Uchida; Mami Iida; Motoyasu Takenaka; Naokazu Fukuoka; Tomohiro Michino; Shuji Dohi

BACKGROUND: Vasopressin is a drug of choice for use during cardiopulmonary resuscitation because several experimental studies have shown that it is better than epinephrine at increasing systemic perfusion pressure and improving cerebral perfusion pressure without increasing myocardial oxygen consumption. We used a pial window preparation to determine the effects of vasopressin when applied topically to pial vessels and whether any effects were altered after cerebral ischemia in rabbits (n = 27). METHODS: We first examined the effects of topical application of arginine-vasopressin (AVP) (10−11 M, 10−9 M, 10−7 M, and 10−5 M, sequentially). We then examined the effects of topical application of AVP (10−9 M and 10−7 M, sequentially) before and after a 5-min intervention consisting of cerebral ischemia produced by inflation of a neck tourniquet plus systemic hypotension or systemic hypotension alone. RESULTS: Pial arteriolar diameters were (a) dilated by 10−11 M AVP [7% ± 11% (P = 0.014 versus baseline)], but constricted by 10−9 M, 10−7 M, and 10−5 M AVP [7% ± 14%, 20% ± 14%, and 16% ± 16% (each P < 0.05), respectively], and (b) constricted before hypotension (7% ± 10% at 10−9 M, 20% ± 15% at 10−7 M) or ischemia (7% ± 11% at 10−9 M, 21% ± 15% at 10−7 M). However, after the 5-min of ischemia, the decrease in diameter induced by 10−7 M AVP was significantly reduced but not by hypotension alone [hypotension control group: 7% ± 10% at 10−9 M, 19% ± 14% at 10−7 M; ischemia group: 5% ± 11% at 10−9 M, 10% ± 13% at 10−7 M (P = 0.35 versus hypotension control)]. CONCLUSIONS: Topical application of AVP (except at the lowest concentration used here) induced concentration-dependent vasoconstriction of pial arterioles in anesthetized rabbits. The vasoconstrictor effect of 10−7 M AVP was reduced after transient (5-min) cerebral ischemia.


Anesthesia & Analgesia | 2007

The comparative effects of intravenous nicardipine and prostaglandin E1 on the cerebral pial arteriolar constriction seen after unclamping of an aortic cross-clamp in rabbits.

Masahiko Kumazawa; Hiroki Iida; Masayoshi Uchida; Mami Iida; Motoyasu Takenaka; Shuji Dohi

BACKGROUND:The potent vasodilators nicardipine and prostaglandin E1 (PGE1) are useful for the treatment of systemic hypertension or pulmonary hypertension during aortic surgery. METHODS:We measured cerebral pial arteriolar diameters, using a rabbit closed cranial window preparation: before (baseline) and 15 min after the start of an IV infusion (preclamp) (0.9% saline [control group], nicardipine [at 0.1, 1.0, or 10 &mgr;g·kg−1·min−1], or PGE1 [at 0.1 or 1.0 &mgr;g·kg−1·min−1]), just after aortic clamping, 20 min after clamping, and at 0–60 min after unclamping. RESULTS:In the control group, a significant decrease in diameter persisted for at least 60 min after unclamping (maximum [at 60 min], −16% for large [≥75 &mgr;m], and −27% for small [<75 &mgr;m] arterioles versus baseline). Although the aortic unclamping-induced vasoconstriction was unaffected under the smallest dose of nicardipine, it was significantly attenuated under larger doses in both large and small arterioles (residual vasoconstriction, −10% and −6% for large and −18% and −10% for small arterioles; at 60 min). The pial arteriolar constriction observed at 5 min or more after unclamping in the control group was not altered by PGE1 in either large or small arterioles. CONCLUSIONS:The larger doses of nicardipine, but neither dose of PGE1, attenuated aortic unclamping-induced sustained cerebral pial arteriolar constriction.


Anesthesia & Analgesia | 2003

The comparative effects of prostaglandin E1 and nicardipine on cerebral microcirculation in rabbits.

Motoyasu Takenaka; Hiroki Iida; Mami Iida; Masayoshi Uchida; Shuji Dohi


Anesthesia & Analgesia | 2003

Changes in cerebral microcirculation during and after abdominal aortic cross-clamping in rabbits: the role of thromboxane A2 receptor.

Masayoshi Uchida; Hiroki Iida; Mami Iida; Shuji Dohi


Canadian Journal of Anaesthesia-journal Canadien D Anesthesie | 2004

Clonidine attenuates the hemodynamic responses to hypercapnia during propofol anesthesia.

Masayoshi Uchida; Hiroki Iida; Yoko Osawa; Sigeaki Tanahashi; Masahiko Kumazawa; Kazuyuki Sumi; Shuji Dohi

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