Biomedical subjects

K Fujii

Publications and source records attributed to K Fujii.

At least 559 records · Page 31Linked to original sources

PubMed1992

Changes in lipid peroxidation levels and lipid composition in the lungs, livers, kidneys and brains of mice treated with paraquat.

We examined lipid peroxide levels and the lipid composition of homogenates prepared from the lungs, livers, kidneys and brains of 48 male ICR mice treated with 30 mg kg-1 paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride). The mice were divided into eight groups, in which they were killed 0, 1.5, 3, 6, 12, 24, 48 and 120 h after the administration of paraquat. A significant increase in the lipid peroxide level was identified only in the liver. Change in lipid composition was identified in all the examined organs. However, the change was not a characteristic one in which there is a selective decrease of polyunsaturated fatty acids which become degraded in a lipid peroxidation reaction. It is possible that the mechanism of paraquat toxicity may differ in different organs.

Animals↗

PubMed1992

The diagnostic significance of anti-type II collagen antibody assay in rheumatoid arthritis.

An improved enzyme-linked immunosorbent assay (ELISA) for the detection of anticollagen antibodies in human serum has been developed. With the use of this method, antibodies against native human Type II collagen were detected in 22.7% of sera from 480 patients with rheumatoid arthritis (RA). The antibodies were found to be collagen type specific, showing no reaction with human Type I and Type III collagens. The antibodies appeared in high incidence during the early phase of the disease, and RA patients with involvement of a single joint, mono-articular arthritis, were often positive for anti-Type II collagen antibodies. In most of these patients, anti-Type II collagen antibodies preceded the appearance of rheumatoid factors. The antibodies were all negative in sera from patients with gout, osteoarthritis (OA) and non-arthritic diseases. Thus, anti-Type II collagen antibody assay may have diagnostic significance for RA patients, especially those in whom laboratory and clinical findings provide only minimal help in diagnosis.

Adult↗

PubMed1992

Expression of cadherin cell adhesion molecules during human skin development: morphogenesis of epidermis, hair follicles and eccrine sweat ducts.

Expression of E (epithelia) and P (placental) cadherin cell adhesion molecules was examined immunohistochemically using human developing skin. In adult skin, E-cadherin was expressed on cell surfaces of whole epidermal layers including skin appendages, whereas P-cadherin was expressed only on those of basal layers and the outer layers of skin appendages, which was consistent with the compartment of proliferating cells. In fetal skin, while the patterns of E- and P-cadherin expression were generally similar to those in the adult, P-cadherin temporarily showed a unique spatiotemporal expression pattern in developing sweat ducts. During this stage, the expression of P-cadherin accumulated in the epidermal ridges and showed a discrepancy with the compartment of proliferating cells. These results suggest that the expression of P-cadherin is spatiotemporally controlled, and may be closely related to the segregation of basal layers as well as to the arrangement of epidermal cells into eccrine sweat ducts, but is not closely related to cell proliferation.

Adult↗

PubMed1992

MR imaging and angiography of cerebral venous angiomas associated with brain tumors.

MR study of 6 patients with concurrent venous angioma and brain tumor revealed that in 2 of the 6 cases, the draining vein of the venous angioma was located near to the tumor and was displaced by the tumor. Two of the 6 venous angiomas were too small to visualize prior to contrast enhancement, but could be detected following administration of Gd-DTPA. Angiography was required for definitive diagnosis of the venous angiomas. When a venous angioma is suspected or is detected incidentally, especially when very near a brain tumor, angiography should be considered before performing surgery to avoid surgical complications. Otherwise, ligation of the vein draining the venous angioma may lead to venous infarction.

Adolescent↗

PubMed1992

Follow-up MRI in dural arteriovenous malformations involving the cavernous sinus: emphasis on detection of venous thrombosis.

Six patients with a dural arteriovenous malformation (dural AVM) involving the cavernous sinus were followed up with magnetic resonance imaging in order to assess change in the lesions. Spin-echo (SE) imaging of three patients in whom the AVM appeared to have closed at least 1 month earlier (two of them spontaneously, and one after external carotid artery embolization) showed neither apparent flow void in the involved cavernous sinus nor evidence of venous thrombosis. SE images of the other three patients who had not been cured by external carotid artery embolization (two of whom were examined within a week of treatment), detected persisting arteriovenous shunts, including high-flow cortical venous drainage, seen as flow void. Two-dimensional time-of-flight MR angiography (2D TOF MRA) was performed simultaneously in three patients. Whereas shunting blood and the normal cavernous sinus were of high intensity, presumed thrombosed cavernous sinuses were isointense with stationary brain tissue. SE imaging can confirm the resolution of arteriovenous shunts, but poorly delineates very acute and chronic thrombosis of the draining veins. In contrast, 2D TOF MRA directly demonstrates flowing blood, permitting the diagnosis of venous thrombosis; it should be included in follow-up of a dural AVM involving the cavernous sinus when venous thrombosis is suspected.

Adult↗

PubMed1992

Natural history and choice of treatment in forty patients with medullary venous malformation (MVM).

Follow-up studies of forty patients with forty-one medullary venous malformations (MVM's) are described. The patients included nineteen males and twenty-one females in an age range from eight to seventy-two years (mean 43.4 years). All cases were diagnosed angiographically. Of the forty-one lesions, twenty-five were located in supratentorial and sixteen in infratentorial regions. In twenty-five supratentorial MVM's, thirteen had superficial drainage, eight deep drainage and three both superficial and deep drainage. Fifteen patients presented with intracranial hemorrhage and eleven patients with complaints or symptoms not related to hemorrhage. Fourteen hemorrhages were found incidentally. The mean follow-up period was three years and eleven months and the longest was sixteen years. No patient died of recurrent hemorrhage and only two had recurrent hemorrhage after a short interval. One patient died of malignant glioma. Thirty-seven out of thirty-nine patients (95%) were in an excellent or good clinical condition with a score above 80% on the Karnofsky Performance Test. This study indicates the low incidence of rebleeding in ruptured MVM's (2/15, 13.3%) and of bleeding in incidentally found unruptured MVM's (0/25, 0%). However, this evidence may be sufficient to support aggressive radical surgery for MVM's.

Adolescent↗

PubMed1992

Hemifacial spasm due to tumor, aneurysm, or arteriovenous malformation.

The authors report eight cases of so-called symptomatic hemifacial spasm. They had gross pathological lesions such as a tumor (one epidermoid, one neurinoma, and two meningiomas), vascular malformation (one medullary venous malformation and two arteriovenous malformations), and aneurysm. In all four cases with a tumor, no artery compressed the facial nerve at the root exit zone. In three of the four cases, the hemifacial spasm disappeared after removal of the tumor in contact with the facial nerve. Compression or encasement of the facial nerve by the tumor was the pathogenesis of the hemifacial spasm in these three cases. The remaining case with tumor (tentorial meningioma) did not have a mass or vessel that directly compressed the facial nerve at the root exit zone. However, the hemifacial spasm disappeared after the removal of the tumor. In a case with a medullary venous malformation with arterial component, an engorged draining vein compressed the root exit zone of the facial nerve. In the remaining three vascular cases--two cases of arteriovenous malformation and a case of saccular aneurysm--enlarged feeding arteries and an aneurysm directly compressed the root exit zone of the facial nerve. Not only arterial or venous but also mass compression can cause hemifacial spasm in some symptomatic cases. Surgical decompression of the facial nerve from the causative organic lesion is the primary choice of treatment.

Adult↗

PubMed1992

Role of adrenergic neuronal activity in the yawning induced by tacrine and NIK-247 in rats.

The present experiments were performed to investigate the potential role of central adrenergic neurons in regulating occurrence of yawning in rats. Intraperitoneal injection of tacrine (THA) or 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta(b)-quinoline monohydrate HCl (NIK-247), cholinesterase inhibitors, induced yawning, which was markedly increased by pretreatment with the beta-adrenoceptor antagonist, pindolol. The yawning evoked by tacrine or NIK-247 given alone or in combination with pindolol was inhibited by pretreatment with scopolamine but not by mecamylamine or spiperone. Treatment with tacrine or NIK-247 increased acetylcholine content of the striatum, but this effect was not enhanced by pindolol, which per se did not affect basal acetylcholine content. Moreover, pretreatment with the central adrenaline synthesis inhibitors, (+-)-2,3-dichloro-alpha-methylbenzylamine HCl (LY-78335) and 2-cyclooctyl-2-hydroxyethylamine HCl (UK-1187A), increased tacrine-induced yawning. Subcutaneous injection of talipexole (B-HT 920), a dopamine D2 receptor agonist, evoked yawning, which was also increased by pindolol, LY-78335, and UK-1187A. These receptors antagonists and synthesis inhibitors per se did not cause yawning responses. The results suggest that the beta-adrenoceptor blockade and the inhibition of adrenaline synthesis facilitate the occurrence of yawning induced by cholinergic and dopaminergic agonists, and thus the central adrenergic neuronal systems may be implicated in the regulation of yawning responses.

Acetylcholine↗

PubMed1992

FMRFamide-like immunoreactivity in the brain and pituitary of the goldfish, Carassius auratus.

The distribution of FMRFamide-like immunoreactivity was determined in the brain and the pituitary of the goldfish, Carassius auratus. Immunoreactive perikarya were observed in the olfactory nerve, nucleus entopeduncularis, nucleus anterioris periventricularis, nucleus posterioris periventricularis, lateral part of the nucleus lateralis tuberis pars posterioris, midbrain tegmentum, and medulla oblongata. Immunoreactive fibers were widely distributed in the brain, in particular in the ventral telencephalon and the hypothalamus. A few immunoreactive nerve fibers were observed in the pituitary. The findings are discussed in relation to male sexual behavior and the involvement of FMRFamide-like peptide in pituitary functions in the goldfish.

Animals↗

PubMed1992

Determination of thiocyanate in human saliva and urine by ion chromatography.

A simple ion-chromatographic method has been developed for the determination of trace amounts of thiocyanate in human saliva and urine. Thiocyanate separation and detection were carried out on an ODS column coated with cetyldimethylamine and by an ultraviolet detector, respectively. Citrate solution (1 mmol l-1) was used as the mobile phase. Thiocyanate was clearly separated from many organic and inorganic anions found in saliva and urine samples. The analytical results obtained by the proposed method agreed with those of the Fe(3+)-thiocyanate spectrophotometric method. Thiocyanate concentrations in the saliva and urine of smokers were found to be significantly higher than those of non-smokers.

Chromatography, Ion Exchange↗

PubMed1992

Reaction of sevoflurane and its degradation products with soda lime. Toxicity of the byproducts.

Sevoflurane previously has been reported to undergo extensive degradation in the presence of soda lime. To more completely characterize the extent and significnce of this reaction, we studied degradation of sevoflurane with and without soda lime, as well as the toxicity and mutagenicity of the degradation products. Two degradation products detected were CF2 = C(CF3)OCH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B). During circulation of 1%, 2%, and 3% sevoflurance in a closed anesthesia circuit for 8 h, peak concentrations of compound A were 13.3 +/- 0.27, 30.2 +/- 0.10, and 42.1 +/- 1.07 ppm at 2 h, respectively. The concentrations of compound B did not exceed 2 ppm. The temperature of the soda lime was 43.3 +/- 2.8 degrees C at 1 h and increased gradually to 47.9 +/- 1.5 degrees C after 8 h. In closed flasks with soda lime, the magnitude of the decrease in sevoflurance concentrations (3%) and of the increase in compound A concentrations was temperature dependent. The peak concentrations of compound A at 23 degrees C, 37 degrees C, and 54 degrees C were 32.8 +/- 6.8 at 2 h, 46.6 +/- 1.0 at 0.5 h, and 78.5 +/- 2.3 ppm at 0.5 h, respectively. The LC50 (50% lethal concentration) of compound A in Wistar rats was 1,090 ppm in males and 1,050 ppm in females exposed for 1 h. The LC50 was 420 ppm in males and 400 ppm in females exposed for 3 h. The chronic toxicity of compound A in Wistar rats was studied by exposing rats 24 times, for 3 h each, to initial concentrations of 30, 60, or 120 ppm in a ventilated chamber. At all concentrations, there were no apparent effects other than a loss of body weight in females (120 ppm) on the final day (P < 0.01). Compound A did not induce mutation on the reverse (Ames) test at less than 2,500 micrograms/dish (culture medium 2.7 ml) with activation by S-9 mixture, and below 1,250 micrograms/dish (culture medium 2.7 ml) without activation, in four strains of S. typhimurium and in 1 strain of E. coli. Exposure of fibroblasts to 7,500 ppm of compound A for 1 h, compound A did not induce structural change. In a study of acute toxicity of compound B, there was no toxicity in Wistar rats after 3 h of exposure at 2,400 ppm. The reverse (Ames) test for compound B was negative at 625-1,250 micrograms/dish.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗

PubMed1992

Chemotherapeutic efficacy of a newly synthesized benzoxazinorifamycin, KRM-1648, against Mycobacterium avium complex infection induced in mice.

Newly synthesized benzoxazinorifamycin, KRM-1648, was studied for its in vivo anti-Mycobacterium avium complex (MAC) activities. When the MICs were determined by the agar dilution method with Middlebrook 7H11 agar medium, KRM-1648 exhibited similarly potent in vitro antimicrobial activities against the MAC isolated from AIDS and non-AIDS patients, indicating possible usefulness of KRM-1648 against AIDS-associated MAC infections. KRM-1648 exhibited potent therapeutic activity against experimental murine infections induced by M. intracellulare N-260 (virulent strain) and N-478, which has much weaker virulence. Similarly, KRM-1648 exhibited an excellent therapeutic efficacy against M. intracellulare infection induced in NK-cell-deficient beige mice (as a plausible model for AIDS-associated MAC infection), in which a much more progressed state of gross lesions and bacterial loads at the sites of infection were observed. When the infected beige mice were killed at weeks 4 and 8, obvious therapeutic efficacy was seen on the basis of reduction in the incidence and degree of lung lesions and bacterial loads in the lungs and spleen with infections due to M. intracellulare N-241, N-256, and N-260. In this case, the efficacy was the highest in N-260 infection, followed by strain N-241. When mice were observed until infection-induced death, survival time of the infected beige mice was found to be prolonged by KRM treatment. However, KRM-1648 was not efficacious in suppressing the progression of pulmonary lesions and the increase in bacterial loads at the sites of infection, including lungs and spleen, at the late phase of infection. This may imply some difficulty with chemotherapy for AIDS-associated MAC infection, even with KRM-1648 treatment, which has excellent in vitro and in vivo anti-MAC activities, as shown in present study.

Acquired Immunodeficiency Syndrome↗

PubMed1992

Detection of antibodies against streptococcal peptidoglycan and the peptide subunit (synthetic tetra-D-alanyl-bovine serum albumin complex) in rheumatic-diseases.

Serum antibodies reactive with streptococcal cell wall peptidoglycan (PG) and its peptide subunit (synthetic tetra-D-alanine) were measured by enzyme-linked immunosorbent assay (ELISA) in patients with rheumatoid arthritis (RA), juvenile rheumatoid arthritis (JRA), osteoarthritis and acute rheumatic fever (RF) compared with healthy subjects. Using 'checkerboard' titrations, anti-PG antibody in human serum was detected at a concentration of PG antigen at 10 micrograms per well with serum dilutions of 1:1,000. For measurement of anti-tetra-D-alanine antibody, the antigen, (D-Ala4)31 was used at 0.5 micrograms per well and sera were diluted to 1:200. When the IgG antibody levels to the PG and the tetra-D-alanine of the sera of patients with RA, JRA and RF were compared with sera from healthy subjects, the sera of the patients had significantly higher levels than did healthy subjects. Antibody that reacted with the PG in serum was absorbed with purified group-specific C-carbohydrate (A-CHO), but A-CHO was not capable of absorbing anti-(D-Ala4)31 antibodies. Therefore, the peptide subunit should be used as antigen in order to measure the specific antibody to PG. Both anti-PG and anti-tetra-D-alanine antibody in human sera primarily belonged to the IgG2 subclass.

Adolescent↗

PubMed1992

Lack of myocardial perfusion immediately after successful thrombolysis. A predictor of poor recovery of left ventricular function in anterior myocardial infarction.

BACKGROUND: We investigated myocardial perfusion dynamics after thrombolysis and its clinical implications. METHODS AND RESULTS: We studied 39 patients with acute anterior myocardial infarction (AMI). Myocardial contrast echocardiography (MCE) was performed before and immediately after successful reflow with intracoronary injection of sonicated Ioxaglate. The average segmental score by two-dimensional echocardiography (graded 0, normal, to 3, akinetic/dyskinetic) and global ejection fraction (left ventricular ejection fraction, LVEF%) by left ventriculography were measured at 1 day and at 4 weeks after reflow. Hypokinesis in the infarct region was assessed by the centerline method and expressed in terms of standard deviations (regional wall motion [RWM]: SD/chord) of normal. Immediately after reflow, 30 of 39 patients (group A) showed significant contrast enhancement within the risk area. The other nine patients (23%, group B), however, showed the residual contrast defect in the risk area (myocardial no reflow). There were no significant differences in the elapsed time, angiographic collateral grade, and degree of residual stenosis between group A and group B. Before reflow, both groups exhibited similar levels of global and regional left ventricular function. Improvement in global (LVEF, average segmental score) and regional left ventricular function was greater in group A than in group B (average segmental score, 0.44 +/- 0.41 versus 0.97 +/- 0.36, p less than 0.01; LVEF, 56.4 +/- 13.4 versus 42.7 +/- 8.9, p less than 0.05; RWM, -1.87 +/- 0.85 versus -3.18 +/- 0.52, p less than 0.005). CONCLUSIONS: MCE demonstrates that angiographically successful reflow cannot be used as an indicator of successful myocardial reperfusion in AMI patients. The residual contrast defect in the risk area demonstrated immediately after reflow is a predictor of poor functional recovery of the postischemic myocardium.

Coronary Circulation↗

PubMed1992

Age-related changes in P2-purinergic receptors on vascular smooth muscle and endothelium.

The present study examined age-related changes in the vascular relaxation response to adenine nucleotides in hypertensive and normotensive rats. Aortic ring segments from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), age 4-6, 9-10, and 13-14 weeks, were examined for relaxation to adenosine 5'-triphosphate (ATP). The extent of ATP-induced relaxation in aortic ring segments with intact endothelium was unchanged with advancing age. Rubbed (endothelium-denuded) ring preparations at the age of 4-6 weeks showed a dose-dependent relaxation similar to that of the unrubbed rings. With advancing age, the ATP-induced relaxation in the rubbed rings decreased and was abolished. The relaxation response did not differ between the SHR and WKY animals at any age, whether the preparations were rubbed or unrubbed. The stable ATP analogue beta,r-methylene ATP induced a relaxation response similar to ATP in rubbed rings at 4-6 weeks of age. In addition, treatment with 8-phenyltheophylline did not diminish the relaxation induced by ATP. ATP-induced relaxation may be manifested via the direct action on the vascular smooth muscle in young rats and may be altered through the response mediated by endothelium with advancing age. This suggests that the vascular smooth muscle of young rats has a P2-purinergic receptor leading to relaxation and that this receptor activity declines with advancing age. In contrast, a P2-purinergic receptor leading to the generation of endothelium-derived relaxing factor may be activated in endothelial cells with advancing age. The alterations with age of P2-purinergic receptor in the vascular smooth muscle and endothelial cell are not affected by genetic hypertension.

Adenosine Triphosphate↗

PubMed1992

Effect of antihypertensive treatment on focal cerebral infarction.

The goal of the current study was to determine whether treatment of hypertension reduces cerebral infarction after occlusion of the middle cerebral artery in stroke-prone spontaneously hypertensive rats (SHRSPs). Three-month-old SHRSPs received untreated drinking water or drinking water containing cilazapril, an angiotensin converting enzyme inhibitor, or hydralazine and hydrochlorothiazide. After 3 months of treatment, the left middle cerebral artery was occluded and neurological deficit was evaluated. Infarct volume was measured 3 days after occlusion using computer imaging techniques from brain slices. Cilazapril and hydralazine with hydrochlorothiazide were equally effective in reducing systolic blood pressure in SHRSPs. One day after occlusion of the middle cerebral artery, neurological deficit was decreased by both cilazapril and hydralazine with hydrochlorothiazide compared with untreated SHRSPs, and the deficit 3 days after occlusion was decreased significantly only by cilazapril. Infarct volume was 178 +/- 7 mm3 (mean +/- SEM) in untreated SHRSPs, and it was significantly reduced to 117 +/- 15 mm3 by hydralazine with hydrochlorothiazide and to 101 +/- 17 mm3 by cilazapril. Infarct volume in Wistar-Kyoto rats was 27 +/- 16 mm3. Thus, reduction in arterial pressure by hydralazine with hydrochlorothiazide or an angiotensin converting enzyme inhibitor is protective against focal cerebral ischemia in SHRSPs.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1992

Decreased endothelium-dependent hyperpolarization to acetylcholine in smooth muscle of the mesenteric artery of spontaneously hypertensive rats.

The endothelium-dependent vascular relaxation to acetylcholine (ACh) in spontaneously hypertensive rats (SHR) may be impaired because of an imbalance of endothelium-derived relaxing factor and contracting factor. However, the role of the endothelium-dependent hyperpolarization remains undetermined. We examined the ACh-induced hyperpolarization and its contribution to relaxation in arteries of SHR. Membrane potentials were recorded from the mesenteric artery trunk of 6-8-month-old male SHR and also Wistar-Kyoto (WKY) rats. Endothelium-dependent hyperpolarization to ACh was unaffected by NG-nitro-L-arginine, indomethacin, or glibenclamide; was reduced by tetraethylammonium or high K+ solution; and was enhanced by low K+ solution or methylene blue, thereby indicating that hyperpolarization is not mediated by nitric oxide (endothelium-derived relaxing factor) but is presumably mediated by a hyperpolarizing factor and is due to an opening of K+ channels that probably differ from the ATP-sensitive ones. Hyperpolarizations to ACh were markedly reduced in SHR compared with findings in WKY rats (maximum, 8 +/- 1 versus 17 +/- 1 mV). In addition, under conditions of depolarization with norepinephrine (10(-5) M), the ACh-induced hyperpolarization was even less and transient in SHR, while it was large and sustained in WKY rats (6 +/- 1 versus 29 +/- 2 mV). Endothelium-dependent relaxations to ACh in arterial rings precontracted with 10(-5) M norepinephrine were far less in SHR than in WKY rats, even in the presence of indomethacin. Furthermore, high K+ solution showed smaller inhibitory effects on the relaxations in SHR than in WKY rats. Endothelium-independent hyperpolarizations and relaxations to cromakalim, a K+ channel opener, were similar between SHR and WKY rats. It would thus appear that the endothelium-dependent hyperpolarization to ACh is reduced in SHR and this would, in part, account for the impaired relaxation to ACh in SHR mesenteric arteries.

Acetylcholine↗

PubMed1992

Effect of diabetes mellitus on flow-mediated and endothelium-dependent dilatation of the rat basilar artery.

BACKGROUND AND PURPOSE: Diabetes mellitus may impair endothelium-dependent responses in cerebral arterioles. The basilar artery dilates in response to increases in blood flow. The goal of this study was to examine effects of diabetes mellitus on "flow-mediated" and endothelium-dependent dilatation of the basilar artery. METHODS: Diabetes was induced in rats with 50 mg/kg streptozotocin. Six months later, vessel diameter and velocity of blood flow through the basilar artery were measured using a cranial window in anesthetized rats under baseline conditions and during occlusion of the carotid arteries. Changes in vessel diameter were also measured during topical application of acetylcholine and sodium nitroprusside. RESULTS: With aortic pressure maintained at baseline levels, blood flow velocity through the basilar artery increased similarly in control and diabetic rats during unilateral common carotid artery occlusion and during bilateral occlusion. In control and diabetic rats, diameter of the basilar artery increased by 10 +/- 2% and 10 +/- 4% during unilateral occlusion and by 27 +/- 5% and 31 +/- 4% during bilateral occlusion, respectively. Thus, diabetes did not impair flow-mediated dilatation of the basilar artery. In contrast, dilatation in response to 10(-5) M topical acetylcholine was less in diabetic rats (13 +/- 2%) than in control rats (45 +/- 8%) (p less than 0.05). Dilator responses to nitroprusside were not impaired by diabetes. CONCLUSIONS: The findings suggest that diabetes produces impairment of endothelium-dependent responses to acetylcholine, but not flow-mediated dilatation, in the basilar artery.

Acetylcholine↗