The Use of the Hamster Cheek Pouch for Intravital Microscopy Studies of Microvascular Events*

2015 ◽  
pp. 41-53 ◽  
Author(s):  
J. Bj�rk ◽  
G. Smedeg�rd ◽  
E. Svensj� ◽  
K.-E. Arfors
Keyword(s):  
Intravital Microscopy ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch

Neutral endopeptidase modulates substance P-induced vasodilation in vivo

1995 ◽  
Vol 78 (2) ◽  
pp. 562-568 ◽  
Author(s):  
X. P. Gao ◽  
I. Rubinstein
Keyword(s):  
Substance P ◽  
Oral Mucosa ◽  
Intravital Microscopy ◽  
Neutral Endopeptidase ◽  
Cheek Pouch ◽  
Induced Responses ◽  
Hamster Cheek Pouch ◽  
Arteriolar Diameter ◽  
Significant Concentration

The purpose of this study was to investigate whether neutral endopeptidase (NEP; EC 3.4.24.11) modulates substance P-induced vasodilation in the oral mucosa in vivo. Using intravital microscopy, we measured the diameter of second-order arterioles (44–70 microns) in the hamster cheek pouch during suffusion of capsaicin and substance P. We found that capsaicin (0.1 and 10.0 nM) induced significant concentration-dependent vasodilations (13 +/- 4 and 39 +/- 7% increase from baseline, respectively; P < 0.05) that were significantly potentiated by phosphoramidon (10.0 nM), a selective NEP inhibitor (35 +/- 15 and 61 +/- 12% increase from baseline, respectively; P < 0.05). Substance P (0.1 and 10.0 nM) also induced significant concentration-dependent vasodilations (7 +/- 3 and 25 +/- 8% increase from baseline, respectively; P < 0.05) that were mediated by the COOH-terminal of the molecule. Substance P-induced responses were significantly potentiated by phosphoramidon (34 +/- 9 and 53 +/- 10% increase from baseline, respectively; P < 0.05) and thiorphan (10.0 microM), a selective NEP inhibitor (44 +/- 11 and 53 +/- 10% increase from baseline, respectively; P < 0.05). Substance P-(1–9) had no significant effects on arteriolar diameter. Suffusion of captopril, leupeptin, Bestatin, and DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid together had no significant effects on substance P-induced vasodilation. Phosphoramidon did not potentiate nitroglycerin-induced vasodilation. These data indicate that NEP modulates substance P-induced vasodilation in the hamster cheek pouch in vivo. We suggest that any decrease in tissue NEP activity may amplify neurogenic vasodilation in the oral mucosa.

scholarly journals Inhibition of neutrophil migration by a selective inhibitor of matrix metalloproteinase: analysis by intravital microscopy

1995 ◽  
Vol 4 (2) ◽  
pp. 133-137 ◽  
Author(s):  
T. Oda ◽  
M. Katori ◽  
K. Hatanaka ◽  
Y. Nagai
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Matrix Metalloproteinase ◽  
Intravital Microscopy ◽  
Neutrophil Migration ◽  
Selective Inhibitor ◽  
Perivascular Space ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Vascular Lumen

Observation of the microcirculation of the hamster cheek pouch by intravital microscopy revealed five steps of neutrophil migration from the venules after topical application of leukotriene B4to the microvasculature: rolling along the venular wall (Step 1), adhesion to it (Step 2), disappearance from the vascular lumen (Step 3), presence between the endothelial cells and the subendothelial basement membrane (Step 4) and passage through the basement membrane (Step 5). The present study was performed to examine whether a metalloproteinase inhibitor inhibits neutrophil migration at any of the above five steps. Chymostatin and leupeptin did not inhibit any of these five steps. In contrast, FN-439, a selective inhibitor of matrix metalloproteinase, reduced the number of neutrophils in the perivascular space without affecting Steps 1 to 3. It was concluded that neutrophils may use metalloproteinase (collagenase/gelatinase) to penetrate the subendothelial basement membrane.

Prostaglandins do not mediate arteriolar oxygen reactivity

1986 ◽  
Vol 250 (6) ◽  
pp. H1102-H1108 ◽  
Author(s):  
W. F. Jackson
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Intravital Microscopy ◽  
Cheek Pouch ◽  
Cyclooxygenase Inhibitor ◽  
Cremaster Muscle ◽  
Hamster Cheek Pouch ◽  
Nonspecific Effects ◽  
Oxygen Reactivity ◽  
Phospholipase A2 Inhibitors

The hypothesis that prostaglandins mediate arteriolar O2 reactivity was tested by assessing the effects of cyclooxygenase and phospholipase A2 inhibitors on the O2 responses of arterioles in superfused hamster cheek pouch and hamster and rat cremaster muscle preparations by use of intravital microscopy. Superfusion of these three preparations with the cyclooxygenase inhibitor indomethacin (50 microM) completely inhibited the response of the vessels to exogenous arachidonic acid but had no effect on the arteriolar constriction induced by elevation of superfusion solution PO2 from 15 to 150 mmHg. Similar results were obtained in the hamster cheek pouch with another cyclooxygenase inhibitor, meclofenamate, or when indomethacin (5-50 mg/kg) was administered systemically. Dexamethasone (12.7 microM) and quinacrine (10 microM), two reported inhibitors of phospholipase A2, also had no significant effect on arteriolar O2 reactivity in the cheek pouch. At 50 microM, quinacrine significantly depressed arteriolar reactivity to O2, adenosine, methacholine, and phenylephrine, suggesting nonspecific effects. These data do not support the hypothesis that prostaglandins mediate arteriolar O2 reactivity.

Cigarette smoke extract attenuates endothelium-dependent arteriolar dilatation in vivo

1991 ◽  
Vol 261 (6) ◽  
pp. H1913-H1918 ◽  
Author(s):  
I. Rubenstein ◽  
T. Yong ◽  
S. I. Rennard ◽  
W. G. Mayhan
Keyword(s):  
Cigarette Smoke ◽  
Intravital Microscopy ◽  
Cigarette Smoke Extract ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Before And After ◽  
Baseline Diameter

The purpose of this study was to examine the effects of cigarette smoke extract on endothelium-dependent and endothelium-independent dilatation of arterioles in vivo. Using intravital microscopy, we measured diameter of arterioles contained within the microcirculation of the hamster cheek pouch during suffusion with acetylcholine and nitroglycerin, before and after treatment with cigarette smoke extract. Under control conditions, acetylcholine and nitroglycerin produced dose-related dilatation of cheek pouch arterioles. Superfusion of cigarette smoke extract (1.0%) did not alter baseline diameter of arterioles or vasodilatation in response to nitroglycerin but impaired dilatation of arterioles in response to acetylcholine. Next, we examined the possibility that impaired dilatation of cheek pouch arterioles in response to acetylcholine after exposure to cigarette smoke extract may be related to the release of substances produced via the cyclooxygenase pathway. In indomethacin-pretreated hamsters, acetylcholine produced similar vasodilatation before and after exposure to cigarette smoke extract. Thus these findings suggest that cigarette smoke extract impairs endothelium-dependent responses of cheek pouch arterioles. The mechanism of impaired responses of cheek pouch arterioles after exposure to cigarette smoke extract appears to be related to the release of substances produced via the cyclooxygenase pathway.

Effect of cigarette smoke extract on arteriolar dilatation in vivo

1996 ◽  
Vol 81 (5) ◽  
pp. 1996-2003 ◽  
Author(s):  
William G. Mayhan ◽  
Glenda M. Sharpe
Keyword(s):  
Potassium Channels ◽  
Adenylate Cyclase ◽  
Cigarette Smoke ◽  
Intravital Microscopy ◽  
Cigarette Smoke Extract ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Baseline Diameter

Mayhan, William G., and Glenda M. Sharpe. Effect of cigarette smoke extract on arteriolar dilatation in vivo. J. Appl. Physiol. 81(5): 1996–2003, 1996.—The goal of this study was to determine whether cigarette smoke extract alters dilatation of arterioles in vivo in response to agonists that produce activation of ATP-sensitive potassium channels and activation of adenylate cyclase. By using intravital microscopy, we measured diameter of arterioles contained within the microcirculation of the hamster cheek pouch during suffusion with agonists in the absence and presence of cigarette smoke extract (0.1, 0.5, and 1.0%). Before treatment with cigarette smoke extract, activation of ATP-sensitive potassium channels with aprikalim and cromakalim produced dose-related dilatation of cheek pouch arterioles. Similarly, activation of adenylate cyclase with isoproterenol and forskolin produced dose-related dilatation of cheek pouch arterioles before treatment with cigarette smoke extract. Superfusion of 0.1% cigarette smoke extract did not change baseline diameter of arterioles and did not alter responses of cheek pouch arterioles to activation of ATP-sensitive potassium channels and adenylate cyclase. Superfusion of 0.5 and 1.0% cigarette smoke extract also did not alter baseline diameter of arterioles but did impair dilatation of arterioles in response to activation of ATP-sensitive potassium channels and adenylate cyclase. These findings suggest that cigarette smoke extract impairs dilatation of resistance arterioles in response to activation of important cellular dilator pathways.

scholarly journals Perchloric acid-soluble proteins from goat liver inhibit chemical carcinogenesis of Syrian hamster cheek-pouch carcinoma

1998 ◽  
Vol 79 (1) ◽  
pp. 54-58 ◽  
Author(s):  
F Ghezzo ◽  
G N Berta ◽  
B Bussolati ◽  
A Bosio ◽  
G Corvetti ◽  
...  
Keyword(s):  
Perchloric Acid ◽  
Syrian Hamster ◽  
Chemical Carcinogenesis ◽  
Soluble Proteins ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch
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