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We present a case of reconstruction of the left cheek with a prefabricated musculocutaneous flap. A pedicled serratus anterior muscle flap was transferred to the left chest, deep to skin. The muscle flap and overlying skin were expanded. The expanded, prefabricated musculocutaneous flap was then transferred as a free flap to the left cheek defect.
Superfusion of the cheek pouch with 0.1-10 nM endothelin (E) produced a concentration-related reduction in the clearance of 22Na+ used as an indicator of microvascular plasma flow. The median effective concentration was about 2 nM. The time course of E action was also concentration related. Superfusion with 10 nM E for 10 min caused a greater than 80% reduction in 22Na+ clearance; the rate at which the action of E started was significantly faster than the rate at which its action ended. Recovery did not exceed 70% even though the tissue was superfused with drug-free buffer for 90 min. The E-induced reduction in 22Na+ clearance was associated with vasoconstriction, as determined by intravital microscopy. Arterioles of 4th branching order were more sensitive to E action than arterioles of 1st or 2nd order; however, the constriction lasted considerably longer in the latter vessels. E-induced venular constriction followed a pattern analogous to that of arterioles of the same category, with the exception that the finer venules responded the least. Pretreatment of the cheek pouch with 300 nM nifedipine diminished but did not abolish the 1 nM E-induced reduction in 22Na+ clearance, and the recovery of clearance upon E washout was not accelerated by nifedipine.
A method is described for eliciting a delayed hypersensitive cell mediated immune response in the Syrian hamster cheek pouch. Using a sensitizing dose of 0.1% DNCB and a challenge dose of 0.01% DNCB 14 days later resulted in a histologically positive lymphocyte infiltrate in the challenge area. These results indicate that the hamster cheek pouch may not be an immunologically inert site and may be used for cell mediated immunity studies.
Trypsin-induced acute inflammation was studied in hamster cheek pouch using intravital microscopy, correlative histology, and electron microscopy. Vascular permeability changes were monitored with intravital fluoroscopy, after intravenous injection of FITC-dextran (Mw 150,000), by counting the number of FITC-dextran leakages around the vessels. The number of extravasated polymorphonuclear leukocytes (PMNLs) was calculated by a histological technique. A dose-dependent increase in the number of FITC-dextran leakages, as well as the number of accumulated PMNLs, was found when trypsin was locally deposited in concentrations of 0.25-2.5 microM (15 microliters during 5 min). Local deposition of autologous serum treated with trypsin at final concentrations of 0.25-2.5 microM caused an increase in vascular permeability as equally pronounced as that of pure trypsin, but only a moderate PMNL accumulation which was not dose dependent. Trypsin at a 25 microM concentration resulted in numerous microbleedings and cessation of flow. The electron microscopy demonstrated inflammatory events (PMNL adhesion, diapedesis, and interstitial infiltration) in all treatment groups but they were more pronounced after trypsin exposure. Trypsin did not cause disintegration, cellular lysis, or increased mast cell degranulation. The permeability changes induced by trypsin (2.5 microM) and trypsinated serum (2.5 microM) were significantly suppressed by the addition of the chelating agent potassium-EDTA to the reaction mixture, indicating a calcium- or magnesium-dependent mechanism. Pretreatment of the animals with cobra venom factor (CVF), by which the plasma C3 concentration was reduced to less than 10%, inhibited the vascular leakages almost completely. The trypsin-induced accumulation of PMNLs was significantly reduced by potassium-EDTA as well as by pretreatment with CVF (P less than 0.01). These findings indicate a central role of complement activation in trypsin-induced acute inflammation in the hamster cheek pouch.
We report here a modification of the superfused hamster cheek model for use in vascular permeability studies. Radio-iodine labeled serum albumin (I-125 RISA) is injected prior to the superfusion period. Plasma content is calculated on a microliter/100 mg wet weight basis and compared to the contralateral (non-superfused) cheek pouch. Water content is calculated on a percentage basis and compared in the same manner. Results demonstrate that superfusion causes an increase in permeability of protein and water. Plasma content is reduced by catalase, indomethacin or FPL 55712 pretreatment, suggesting that free-radicals, prostaglandins and leukotrienes are released during superfusion. Water content increase is refractory to pretreatment. The advantages of this system and its application are discussed.
Hamster cheek pouch vascular tissues contain an angiotensin II-forming enzyme which is inhibited by chymostatin but not by any angiotensin-converting enzyme inhibitors. The enzyme was purified to apparent homogeneity by gel filtration and heparin-Sepharose affinity chromatography. The molecular mass estimated by sodium dodecyl sulphate polyacrylamide gel electrophoresis was 28 kDa and the optimum pH was between 7.5 and 9.0. The angiotensin II-forming activity was inhibited by chymostatin, soybean trypsin inhibitor and phenylmethylsulfonyl fluoride, but not by aprotinin. The N-terminal sequence showed high homology with chymases from various species. Thus, the angiotensin II-generating enzyme obtained from hamster cheek pouch vessels is a chymase.
Revascularization of bundles of skeletal muscle fibers transplanted into the cheek pouch of hamsters was examined previously by intravital and light microscopy. Some blood vessels survived the ischemia of transplantation and revascularization resulted from the growth of surviving vessels. We have now examined the cellular events of graft revascularization by electron microscopy (EM). Approximately 20 skeletal muscle fibers were autografted into the hamster cheek pouch. Segments of the graft were prepared for EM from 0.5 to 5 days after transplantation. At 0.5 day, the endothelial cells of surviving blood vessels had short processes extending from them. By 1.0 day, some endothelial cells had separated. At 1.5 days, many endothelial cells were undergoing mitosis. Blood vessels at 2 to 2.5 days were of narrow diameter and most were densely packed with erythrocytes. Circulation was reestablished between 2.5 and 3 days. The fine structure of the blood vessels changed little after 3 days except for a decrease in the number of vesicles in the endothelial cell cytoplasm and the formation of normal endothelial cell injections. After 5 days, blood vessels were larger in diameter, but otherwise similar to control capillaries. We conclude that, despite the initial absence of circulation, surviving blood vessels underwent a rapid, orderly sequence of growth.
The role of calcium in contractile mechanisms has been well documented. Since the formation of intraendothelial gaps may be due to a contractile process, these studies were initiated to describe the effects of altering the external calcium concentration and a calcium blocker, verapamil, on the development of leaky sites and clearance of dextran in the hamster cheek pouch under normal and histamine-stimulated conditions. Adult Syrian hamsters were anesthetized and tracheostomized, and the femoral vein was cannulated for injecting the FITC-Dextran-70K. In all hamsters, a removable plastic chamber was placed in the cheek pouch to observe and collect suffusate from the microvasculature. In one series of experiments, suffusion was begun with either "normal" calcium (1.5 mM) or a calcium-free, Ringer's bicarbonate (pH 7.4, 36 degrees) buffer. After a 30-min period, fluorescein-labeled dextran (FITC-Dextran-70K) was given intravenously and the number of leaky sites and dextran clearance determined for 30-45 min. Two 5-min periods of stimulation with histamine (10(-7) and 10(-6) M) followed by a 30-min equilibration were completed while the above measurements were repeated. Then, the suffusate was switched to the opposite calcium buffer and the same sequence repeated. A similar protocol was followed using either the "normal" buffer or a high (4.5 mM)-calcium buffer. In another series of experiments, similar measurements were completed with and without verapamil (10(-4) M) using a "normal" calcium buffer and histamine-stimulated conditions. In the control, nonstimulated state, there was a significant increase in the leaky sites while suffusing with low-calcium buffer; however, there were no changes in leaky sites while suffusing with the high-calcium buffer. In the histamine-stimulated state, the increase in the number of leaky sites and dextran clearance was attenuated with the low-calcium buffer and potentiated with the high-calcium buffer. While suffusing with the verapamil buffer, there was an increase in the control number of leaky sites and in the histamine-stimulated state there was an attenuation of the histamine-stimulated response. These results indicate that external calcium influences and modulates microvascular leaky sites in normal and stimulated states and that the formation of leaky sites and dextran clearance after histamine stimulation require the transmembrane flux of calcium. Also, the formation of leaky sites was coupled directly to the clearance of dextran.
An intravital microscopic method for quantitative measurement of interstitial concentrations of fluorescent tracers has been applied to the investigation of microvascular permeability in the hamster cheek pouch. Some nanoliters of FITC-dextran mean mol wt (Mw) 20,000, 3000, or sodium fluorescein (Mw 376) were injected into an arteriole of the exposed cheek pouch via micropipet. The extravasation of fluorochromes was measured by a photodensitometric method including two sets of calibration procedures (in vitro and in vivo). Postcapillary and collecting venules exhibited the highest absolute increase of fluorochrome concentration in the tissue for all tracer molecules tested when compared to arterioles or capillaries. The permeability of the vascular wall was quantified, assuming that diffusion processes play the main role for the transport of the investigated molecules under the experimental conditions of a high concentration gradient across the membrane. Permeability coefficients P (cm/sec) and apparent diffusion coefficients D' (cm2/sec) of the microvascular wall were calculated using a mathematical model for one-dimensional diffusion in composite media. The analysis is based on measured data of interstitial diffusion coefficients of the tracers used. For all tracer molecules tested, the wall of the capillaries and postcapillary venules was significantly more permeable than the arteriolar wall. For the largest test molecule (FITC-dextran Mw 20,000), the permeability coefficient of the vessel wall showed a maximum in the postcapillary venules. These findings support the concept of a "gradient of permeability" with a nonuniform distribution of exchange capacity only for the precapillary microvessels. A marked preponderance of venular over capillary permeability could, if at all, only be detected for FITC-dextran Mw 20,000. The present study characterizes the vessel wall by apparent diffusion coefficients which are, for FITC-dextran Mw 3000, and free fluorescein, roughly three orders of magnitude lower than the apparent diffusion coefficients in connective tissue.
Leukotriene B4 (LTB4) is known to induce neutrophil-dependent macromolecular leakage in the hamster cheek pouch. LTB4 was superfused over cheek pouches dissected for intravital microscopy; and leukocyte rolling and firm adhesion in venules, neutrophil emigration, and macromolecular permeability as leakage of fluorescent dextran was quantified. Dextran sulfate (MW 500,000; 17.5 mg/kg iv bolus), but not uncharged dextran, reduced the LTB4-induced venular leakage of macromolecules by 85%. Histamine-induced leakage, which is neutrophil independent, was left unaffected. Dextran sulfate had no effect on leukocyte adhesion in postcapillary venules induced by LTB4, nor on their subsequent emigration to the surrounding tissue. Dextran sulfate significantly inhibited leukocyte rolling during nonstimulated conditions along the walls of collecting venules, but not postcapillary venules. Consequently, neutrophil-induced macromolecular leakage and neutrophil emigration appear to be independent, separable events. As an explanation of the present results it is proposed that the dextran sulfate complexes neutrophil granule cationic proteins, thus preventing neutrophil-mediated permeability increase.
The cheek mucosa reacted to the implantation of cotton and silk with an aseptic inflammatory exudate which was found 24 hours and 4 days postoperatively. The leukocytic infiltrate was followed by a histiocytic reaction. Which was established at 7 days but which later progressively declined. The comparison of these findings with those previously obtained from gingival tissues revealed that the leukocytic infiltration in the gingiva was minimal or nonexistent. Probably, the difference in the leukocytic reacting capacity of the gingiva and cheek mucosa was due to the different histologic architecture present in both tissues and directly related to the active capacity of the suture materials to modify the internal biologic medium.
Tumors were allowed to develop in the cheek pouches in two groups of hamsters following topical application three times per week of a 0.5% solution of 7, 12-dimethylbenz(alpha)anthracene (DMBA) in liquid paraffin administered for 10 weeks. Two control groups received no DMBA treatment. After carcinogen application, the animals in one DMBA-treated group and those in one of the control groups were given indomethacin daily; this was administered through the oral route for an additional 10 weeks. At this time, all of the animals were killed and their cheek pouches, the draining cervical lymph nodes, and other organs were removed for examination. The number and size of tumors in each pouch were recorded, and each pouch was weighed. Indomethacin, in the dosage administered, was not found to cause regression of established tumors. The effects of prostaglandins, indomethacin, and other prostaglandin-synthesis inhibitors in tumor tissue are discussed. It is suggested that more knowledge is needed about the role of prostaglandins, and the related products of AA metabolism, in squamous cell cancer before indomethacin is used therapeutically.
Regional blood flow to the cheek and tongue of anesthetized dogs was measured before and after application of six different doses of snuff (3.12 to 100 mg/kg body weight) to the right cheek. Dose-independent vasodilation was observed at the site of application, whereas dose-dependent vasoconstriction was observed contralaterally. Aortic, central venous, and ventricular pressures were significantly increased (p < 0.05) at the higher doses. Plasma nicotine concentrations increased stepwise with dose.
Human choriocarcinoma (JEG-3) cells were transplanted into the cheek pouch of hamsters and treated with photodynamic therapy. Twenty-four hours after intraperitoneal injection of the photosensitizer dihematoporphyrin ether (DHE), 20 tumors were illuminated with 100 J/cm2 of 630-nm light from an argon pumped dye laser. Contralateral tumors served as controls. Dihematoporphyrin ether alone had no effect on tumor growth, while laser light in the absence of DHE resulted in complete regression in 3 tumors (17%), and partial regression in 4 of 18 tumors (22%), possibly due to hyperthermia, P greater than 0.10. Using the combination of DHE plus light (photodynamic therapy) complete tumor regression was noted after a single treatment in 11 of 20 tumors (55%, mean tumor volume 279 mm3) and in 7 of 7 tumors (100%) after a second treatment. Two of 20 tumors were not retreated. Therefore, 18 of 20 tumors (90%) were grossly destroyed by one or two photodynamic treatments. Contralateral control tumors continued to grow to a median volume of 990 mm3 (chi 2 = 26.30, P less than 0.0001). Choriocarcinoma transplanted into the hamster cheek pouch is highly responsive to photodynamic therapy.
An acute mastoiditis can occasionally present as a swelling in front of the ear. An inflammation of the air cells of the mastoid cavity can spread, via the cells in the root of the zygomatic arch, to the soft tissues of the cheek. Unfamiliarity with this underlying cause of a swollen cheek can lead to delay of proper treatment with potential harm to the patient. This case presents such an uncommon form of mastoiditis in a 3-year-old boy; the failure to recognize the disease initially led to extensive osteomyelitis of the temporal bone. CT scanning was important in establishing the cause of the persistently severe condition of the boy, in spite of bilateral myringotomies and mastoidectomy on the right side. Destruction of bone from the zygomatic arch to the suture between temporal and occipital bone was shown. Extensive removal of diseased bone was achieved neurosurgically, thus leading to uneventful recovery.
Hamster cheek pouch was treated with carcinogen for 5 or 8 weeks. Part of the carcinogen treated area was excised and the lesion allowed to heal by secondary intention. At follow-up the biopsied pouches were compared with control pouches and potentiation of the development of carcinomas was seen. It is suggested that these results have relevance to the previously demonstrated tumour potentiating effect of cryosurgery in hamster cheek pouch, in that the important tumour potentiating influence may be regeneration involving dysplastic epithelium and not a function of cryosurgery per se.
A 14-year-old boy presented with a Grade II left cheek fistula and inability to open the mouth following gangrenous stomatitis in early childhood. The treatment of the patient by multistaged reconstruction of the cheek defect is discussed. A large turnover flap was used for the lining, a technique which obviates the need for a second lining flap, and thus eliminates the disfigurement of a donor site. Also, it uses the healthy skin that would otherwise have been discarded in the creation of mucosal flaps.
Experiments were performed to study the early and late ultrastructural changes during hamster cheek pouch carcinogenesis using a regimen of topical application of 9,10 dimethyl-1-1-2 benzanthracene (DMBA) twice a week in liquid paraffin oil. The DMBA was administered for a period of 2 and 4 1/2 months. Hamsters exposed to DMBA for 2 months developed moderate precancerous changes, whereas the hamsters treated with DMBA for 4 1/2 months developed frank and multiple oral tumors with a cauliflower appearance. The ultrastructural pathological changes seen were considerably increased at 4 1/2 months compared with a 2 month period of DMBA treatment. Untreated and solvent control hamsters cheek pouch treated for 2 and 4 1/2 months with liquid paraffin oil alone did not show any premalignant or malignant changes during this period.