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At least 289 records · Page 16Linked to original sources
PubMed1997

Effects of oral administration of different doses of purified micronized flavonoid fraction on microvascular reactivity after ischaemia/reperfusion in the hamster cheek pouch.

1. The effects of a purified micronized flavonoid fraction (S5682) on mean internal diameter and blood flow of arterioles and venules, as well as the functional capillary density (FCD) were evaluated in the hamster cheek pouch microvasculature before and after 90 min of total ischaemia. 2. Male hamsters were treated for ten days, twice a day, with oral doses of S5682 (5, 20, 80 and 160 mg kg-1 day-1) or placebo (10% lactose solution). The cheek pouch preparation was placed under an intravital microscope coupled to a closed circuit TV system. Local ischaemia was obtained by a cuff mounted around the neck of the everted pouch where it leaves the mouth of the hamster. 3. Measurements were performed before ischaemia, at the onset of reperfusion and 10, 20, 30, 45 and 60 min thereafter. Diameters were measured by means of an image shearing device. Red blood cell (RBC) velocity was analysed by use of the dual-slit photometric technique. Blood flow was calculated from diameters and RBC velocities. FCD, defined as the number of capillaries with flowing blood per field of observation, was also assessed. 4. During reperfusion, placebo-treated animals showed a significant vasodilatation, a decrease in blood flow and FCD and S5682-treated animals showed a clear trend, dose-dependent, towards maintaining these parameters closer to the value found before ischaemia. 5. In conclusion, our results indicate that S5682 improves the microvascular reactivity and FCD after ischaemia/reperfusion. These data suggest that S5682 could function as an antioxidant, which may explain its beneficial therapeutic effect in chronic venous insufficiency where oxidative stress is involved in the pathological mechanism.

Administration, Oral↗
PubMed1999

Interaction of amylin with calcitonin gene-related peptide receptors in the microvasculature of the hamster cheek pouch in vivo.

1. This study used intravital microscopy to investigate the receptors stimulated by amylin which shares around 50% sequence homology with the vasodilator calcitonin gene-related peptide (CGRP) in the hamster cheek pouch microvasculature in vivo. 2. Receptor agonists dilated arterioles (diameters 20-40 microm). The -log of the concentrations (+/- s.e.mean; n = 8) causing 50% increase in arteriole diameter were: human betaCGRP (10.8 +/- 0.3), human alphaCGRP (10.8 +/- 0.4), rat alphaCGRP (10.4 +/- 0.3). Rat amylin and the CGRP2 receptor selective agonist [Cys(ACM2,7]-human alphaCGRP were 100 fold less potent (estimates were 8.5 +/- 0.4 and 8.2 +/- 0.3 respectively). 3. The GCRP1 receptor antagonist, CGRP8-37 (300 nmol kg(-1); i.v.) reversibly inhibited the increase in diameter evoked by human alphaCGRP (0.3 nM) from 178 +/- 22% to 59 +/- 12% (n = 8; P < 0.05) and by rat amylin (100 nM) from 138 +/- 23% to 68 +/- 24% (n = 6; P < 0.05). CGRP8-37 did not inhibit vasodilation evoked by substance P (10 nM; n = 4: P > 0.05). 4. The amylin receptor antagonist, amylin8-37 (300 nmol kg(-1); i.v.) did not significantly inhibit the increase in diameter evoked by human alphaCGRP (0.3 nM) which was 112 +/- 26% in the absence, and 90 +/- 29% in the presence of antagonist (n = 4; P < 0.05); nor that evoked by rat amylin (100 nM) which was 146 +/- 23% in the absence and 144 +/- 32% in the presence of antagonist (n = 4; P > 0.05). 5. The agonist profile for vasodilatation and the inhibition of this dilatation by CGRP8-37, although not the amylin8-37 indicates that amylin causes vasodilatation through interaction with CGRP1 receptors in the hamster cheek pouch.

Amyloid↗
PubMed2001

Vascular endothelial growth factor and the in vivo increase in plasma extravasation in the hamster cheek pouch.

1. The purpose of this study in the hamster cheek pouch was to determine whether or not vascular endothelial growth factor (VEGF) induced changes in plasma extravasation and if so, the mechanism(s) involved. 2. The cheek pouch microcirculatory bed of the anaesthetized hamster was directly observed under microscope and the number of vascular leakage sites, as shown by fluorescein isothiocyanate (FITC-dextran, 150 kD) extravasation, was counted. Drugs and VEGF were applied topically. VEGF from 0.05 to 0.5 microg ml(-1) (1.2 to 12 nM) produced a dose-dependent increase in the number of microvascular leakage sites from virtually none in basal conditions to up to 250 in some pouches. The effects of VEGF (0.1 microg ml(-1) or 2.4 nM) were blocked in a concentration-dependent manner by the non-specific heparin growth factor antagonist TBC-1635 (0.1, 1 and 3microM). The placenta growth factor (PlGF-1: 0.1 and 0.5 microg ml(-1) or 3.4 and 17 nM) did not increase plasma extravasation, per se, but abolished the effects of VEGF (2.4 nM). 3. The increases in microvascular leakage produced by VEGF (2.4 nM) were partially but significantly (P<0.05) inhibited by genistein (5 and 10 microM, up to 33% inhibition), LY 294002 (30 microM, 41%), bisindolylmaleimide (1 microM, 65%) and virtually abolished by indomethacin (3 microM, 88%) and L-nitro-arginine (10 microM, 95%), these drugs being inhibitors of tyrosine kinase, phosphatidylinositol-3-kinase, protein kinase C, cyclo-oxygenase and nitric oxide synthase respectively. None of these inhibitors, at the concentration tested, induced alone an increase in plasma extravasation. 4. These results indicate that the VEGF-induced plasma extravasation may involve the stimulation of VEGF-R2 (Flk-1/KDR) and the activation of phosphatidylinositol-3-kinase and protein kinase C. The production of both nitric oxide and prostaglandin is required to observe an increase in vascular leakage.

Animals↗
PubMed2001

Localized adenovirus-mediated gene transfer into vascular smooth muscle in the hamster cheek pouch.

OBJECTIVE: Our purpose was to develop a method for adenovirus delivery to the hamster cheek pouch to experimentally target gene transfer in tissue used for microvascular studies. METHODS: Separate constructs were tested with transgenes for lacZ or green fluorescent protein (GFP) driven by three promoters: RSV, CMV, and SM22. With university approval, adenovirus was delivered in anesthetized (pentobarbital, 70 mg/kg) hamsters (n = 28) by using either a vascular systemic injection or tissue infiltration (interstitial space behind the pouch). During 3 days, animals receiving infiltration gained the expected weight, whereas those receiving vascular injection lost weight; no other behavior changes were noted. RESULTS: On day 3 postadenoviral delivery (infiltration), expression of lacZ (histology, beta-galactosidase) or GFP (fluorescence microscopy) was confirmed across the tissue (CMV and RSV promoters) and exclusively in vascular smooth muscle cells (specific SM22 promoter), without evidence of tissue inflammation. In vitro microvascular experiments verified normal responses in the cheek pouch of day 3 postadenoviral delivery animals. We tested local dilation to methacholine, adenosine, remote dilation to methacholine, adenosine, nitroprusside, and LM609 (alpha(v)beta3 integrin agonist), flow-dependent dilation, and flow recruitment. CONCLUSIONS: Thus, this method enables targeted, cell-specific gene transfer to one tissue important for microvascular studies, without significant systemic exposure and without adverse inflammation.

Adenoviridae↗
PubMed2003

Changes in lip, cheek, and tongue pressures after rapid maxillary expansion using a diaphragm pressure transducer.

The purpose of this study was to investigate the changes in pressures that are exerted to maxilla by the tongue, lip, and cheek before and after expansion and during the retention period. Twelve patients (five males, seven females) with maxillary transverse deficiencies were randomly selected. The first pressure measurements were made before expansion using a diaphragm pressure transducer. The second measurements were made right after the maxillary expansion procedure, which lasted about 20 days. The expansion devices were replaced with retention devices, and measurements were made at the end of the first, second, and third months of retention. Pressure values on the buccal side of upper first molar and incisor increased significantly right after expansion but started decreasing during retention. The values at the end of the third month of retention were similar to the preexpansion values (P < .05). Tongue pressures on the lingual side of the upper first molar and upper incisor decreased significantly with expansion but started increasing after the expansion procedure. Even at the end of the third month of the retention period, the values were not similar to the preexpansion values (P < .05). These values show that the cheeks and lips almost adapt to the new position of dental arches at the end of the third month, whereas tongue adaptation took comparatively longer.

Adaptation, Physiological↗
PubMed2002

Characterization of adenosine receptors mediating the vasodilator effects of adenosine receptor agonists in the microvasculature of the hamster cheek pouch in vivo.

1 The aim of this study was to characterize the adenosine receptor mediating vasodilation in the microvasculature of the hamster cheek pouch in vivo. A range of adenosine agonists was used including N6-cyclopentyladenosine (CPA) (A1 agonist), 5'-N-ethylcarboxamidoadenosine (NECA) (non-selective), 2-chloroadenosine (2CADO) (non-selective), 2-p-(2-carboxyethyl)-phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680) (A2A agonist), N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (IBMECA) (A3 agonist) and adenosine, as well as the adenosine antagonists 8-sulphophenyltheophylline (8-SPT) (A1/A2 antagonist), 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (A1 antagonist) and 4-(2-[7-amino-2-(2-furyl)[1,2,4]-triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM 241385) (A2A antagonist). 2 All the adenosine analogues used induced vasodilation at concentrations between 10 nm and 1 microm, and the potency order was NECA > CGS 21680 > 2CADO > CPA=IBMECA >> adenosine, indicating an action at A2A receptors. 8-SPT (50 microm) antagonized vasodilator responses to NECA with an apparent pKB of 5.4, consistent with an action at A1 or A2 receptors and confirming that A3 receptors are not involved in this response. 3 DPCPX (10 nm) had no effect on vasodilation evoked by NECA, suggesting that this response was not mediated via A1 receptors, while ZM 241385 (10 nm) antagonized dilator responses to NECA with an apparent pKB of 8.9 consistent with an action via A2A receptors. 4 Overall these results suggest that adenosine A2A receptors mediate vasodilation in the hamster cheek pouch in vivo.

Animals↗
PubMed1999

Congenital cheek fistula: a report of three cases.

Three cases of the rare condition of congenital cheek fistulae are presented. These differ from preauricular fistulae in terms of their location and the direction in which the fistula is lying. Each cheek fistula seemed to be situated along the line of the junction between the mandibular and maxillary processes of the first branchial arch.

Cheek↗
PubMed2006

Involvement of the 5-lipoxygenase/leukotriene A4 hydrolase pathway in 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinogenesis in hamster cheek pouch, and inhibition of carcinogenesis by its inhibitors.

Previous studies have shown that aberrant arachidonic acid (AA) metabolism, especially cyclooxygenase-2 (Cox-2) and 5-lipoxygenase (5-Lox) pathways, are activated during oral carcinogenesis, and can be targeted for cancer prevention. This study was designed to investigate the importance of 5-Lox/leukotriene A4 hydrolase (LTA4H) pathway of AA metabolism in 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster cheek pouch carcinogenesis. In a short-term study, topical application of DMBA for 3 weeks induced severe inflammation and aberrant AA metabolism. Subsequent topical treatment with zileuton, celecoxib, or their combination for 1 week significantly suppressed aberrant AA metabolism and cell proliferation in the oral epithelium. Interestingly, zileuton was effective in inhibiting biosynthesis of multiple AA metabolites, including leukotriene B4 (LTB4), 5-, 12-, 15-hydroxyeicosatetraenoic acid and prostaglandin E2 (PGE2), while celecoxib only suppressed PGE2 biosynthesis significantly at a high dose. In a long-term carcinogenesis study topical application of LTB4 or PGE2 enhanced oral carcinogenesis by increasing the incidence and volume of visible tumors, and the incidence of squamous cell carcinoma (SCC). To further examine the role of LTB4 in oral carcinogenesis, two LTA4H inhibitors, bestatin and SA6541, were evaluated in a long-term chemoprevention experiment. Both agents significantly inhibited SCC, and such an inhibition correlated with reduced levels of LTB4 in hamster cheek pouch. In summary, our studies have demonstrated that 5-Lox/LTA4H pathway is one of the major AA-metabolizing pathways involved in DMBA-induced oral carcinogenesis in hamsters, and may be targeted for chemoprevention.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

Changes in cheek pressure following rapid maxillary expansion.

The purpose of the present investigation was to study the effects of rapid maxillary expansion on the pressures exerted by the cheeks on the maxillary arch. The sample consisted of 15 patients (five males, ten females) who received either a Hyrax or Haas type expansion appliance for treatment of a bilateral maxillary constriction of more than 5 mm. The median age of the sample was 12 years. Buccal pressures were measured at the upper first molar on the left and right side, before and after active expansion, and also after an average of 3-4 months of retention with the appliance in place. Buccal pressures on the maxillary first molar averaged approximately 3 g/cm2 before expansion and increased significantly to a value of approximately 9 g/cm2 after expansion. Pressure change was approximately 0.6 g/cm2 for each millimetre of expansion. During the 3-4-month period of stabilization of the appliance, the pressures remained at the post-expansion levels and no adaptation of the soft tissues was observed. These results lead to the conclusion that cheek pressures on the maxillary arch may be implicated in the relapse occurring after rapid expansion, even after the usual 3-month period of stabilization.

Adaptation, Physiological↗
PubMed1999

Cheek and tongue pressures in the molar areas and the atmospheric pressure in the palatal vault in young adults.

The pressures acting on the maxillary and mandibular posterior teeth from the tongue and cheeks were measured in 24 adults aged 22-29 years. In addition, the pressure in the palatal vault was recorded. The pressure at two maxillary (buccal and lingual) and two mandibular (buccal and lingual) measuring points, and in the palatal vault was recorded simultaneously. Repeated recordings of the pressures at rest, and during chewing and swallowing were made. The pressures at rest were of similar magnitude (about 2 g/cm2) at the buccal and lingual sides of the mandibular posterior teeth. The median resting pressure at the maxillary posterior teeth was 2.7 g/cm2 on the buccal side and 1.0 g/cm2 on the lingual side. The difference in the maxilla was significant, but not in the mandible. It was concluded that the equilibrium of tooth position is maintained by the pressure from the cheeks and the tongue. During chewing and swallowing the pressures on the lingual side of the teeth were greater than those on the buccal side. At rest about half of the subjects had a negative pressure at the palatal vault, but no correlations between the resting pressure at the palatal vault and the resting pressures on the teeth were found.

Adult↗
PubMed1990

Effect of nicotine on 7,12-dimethylbenz[a]anthracene carcinogenesis in hamster cheek pouch.

We divided 40 male Syrian golden hamsters into four groups of 10 animals each, and we treated both cheek pouches of each hamster three times a week as follows: group 1, 50 microL of sesame oil; group 2, 50 microL of 6% nicotine in sesame oil; group 3, 50 microL of 1% 7,12-dimethylbenz[a]anthracene (DMBA) in sesame oil; and group 4, 50 microL of 1% DMBA in 6% nicotine in sesame oil. Cheek pouches were examined clinically and histologically after 12 weeks of treatment. Hamsters treated with DMBA and nicotine showed significantly (P less than .001) more tumors and a significantly (P less than .05) greater-than-expected proportion of large tumors (greater than or equal to 3-mm diameter) than hamsters treated with DMBA alone. Histologically, there was a greater degree of dysplasia in lesions from the group receiving DMBA plus nicotine than in the DMBA only group. The results suggest that nicotine acts as a cofactor in DMBA tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Diameter of arterial microvessels trapping 8--10 micron, 15 micron and 25 micron microspheres as determined by vital microscopy of the hamster cheek pouch.

An assumption inherent in the use of microsphere methodology for measuring regional blood flow is that microspheres are removed from the circulation by impacting in arterial vessels of approximately their own diameter. We investigated the in vivo relationship between the diameter of varying size microspheres and the calibre of trapping microvessels within the hamster cheek pouch. Intracardiac injection of 8-10, 15 +/- 5, 25 +/- 5 micron carbonized microspheres with diversion of the cardiac output into the bracheocephalic trunk provided direct, in vivo visualization of the impaction sites of these various size microspheres within the cheek pouch microvasculature. Fifteen micron microspheres usually impacted at the orifice or neck of small arterioles and protruded into the lumen of the parent vessel. Eight to ten micron microspheres lodged in vessels with a mean diameter of 11.5 +/- SD 3.4 micron indicating that they usually impacted primarily in terminal arterioles.

Animals↗
PubMed1987

Microsphere distribution in normal and tumor-bearing (DMBA-induced carcinogenesis) hamster cheek pouch.

This study evaluates, for the first time by direct visualization, the microvascular distribution of microspheres in normal hamster cheek pouch and in hamster cheek pouch bearing tumor induced by 7, 12 Dimethylbenz (A) Anthracene solution (DMBA). In contrast to the results of the previously used open-chest technique, this carotid injection technique does not lead to irregular distribution of 15-mu carbonized microspheres, chain, or impaction phenomena. It is concluded that methodology differences may account for different results.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2000

Prudent management of the mid-cheek mass: revisiting the accessory parotid gland tumor.

OBJECTIVES/HYPOTHESIS: The head and neck surgeon's fascination with parotid surgery arises from the gland's spectrum of histopathological presentations, as well as the diversity of its morphological features. A mass arising in the mid-cheek region may often be overlooked as a rare accessory lobe parotid neoplasm. This report serves to revisit the topic of accessory parotid gland neoplasms to emphasize proper management, particularly the surgical aspects, so that consequences of salivary fistula, facial nerve paralysis, and recurrence are avoided. STUDY DESIGN: This is a retrospective review of our experience with four accessory parotid gland neoplasms and five other masses mimicking this lesion. METHODS: A literature review and retrospective chart review. RESULTS: Over a 6-year period, we have encountered four true accessory lobe tumors, all pleomorphic adenomas. These presented very similarly to four other more commonly encountered masses not of salivary origin and one normal but hyperplastic accessory parotid gland. All were removed through a wide parotidectomy-style approach modified by extending incisions anterosuperiorly and inferoanteriorly. The only complication was a minor salivary fistula in one patient. There were no permanent facial paralyses. CONCLUSIONS: Accessory parotid gland neoplasms are rare and may present as innocuous extraparotid mid-cheek masses. A high index of suspicion, prudent diagnostic skills (including fine-needle aspiration [FNA] biopsy followed by computed tomography [CT] imaging), and meticulous surgical approach (extended parotidectomy-style incision and limited peripheral nerve dissection when possible) are the keys to successful management of these lesions.

Adult↗
PubMed1976

Resurfacing large cheek defects with rotation flaps from the neck.

A neck flap based on the midline many provide excellent cover for large cheek defects. The technical aspects of planning and replacement, with emphasis on positioning to prevent ectropion of the lower lid, are presented. Alone, or in conjunction with the multiple excision technique, this flap can produce a superior cheek surface.

Cheek↗
PubMed1994

Deep-plane cervicofacial rotation-advancement flap for reconstruction of large cheek defects.

The blood supply and reliability of cervicofacial rotation-advancement flaps for cheek reconstruction can be improved significantly by dissecting the flap in the deep plane (i.e., below the superficial musculoaponeurotic system and the platysma). This modification, similar in technique to that used in composite or deep-plane face lift, was used successfully in seven patients, including several heavy cigarette smokers who were unlikely to have achieved a successful outcome with a conventional cervicofacial flap. No facial nerve weaknesses were observed. We now believe that the deep plane is the level of choice for dissection of cervicofacial flaps when used for reconstruction of cheek or other facial defects.

Basal Cell Carcinoma↗
PubMed2001

Reconstruction of the cheek.

LEARNING OBJECTIVES: After studying this article, the participant should be able to: 1. Describe the cheek unit and its specific requirements for quality, outline, and contour. 2. Identify factors involving the patient, wound, and donor materials that determine technique. 3. Understand the application of anteriorly based, posteriorly based, and advancement flaps, and the use of serial excisions for specific defects. 4. Identify, prevent, and treat complications of cheek reconstruction.

Adult↗