Spontaneous vasomotion in hamster cheek pouch arterioles in varying experimental conditions

Grampp, W.

doi:10.1152/ajpheart.1992.262.2.h478

Cited by 53 publications

(78 citation statements)

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“…The study was carried out in the hamster cheek pouch preparation according to procedures described by Duling [10] and Svensjö et al [11] recently modified by Bouskela and Grampp [12] on the 11th day after the onset of the treatment with placebo, S-5682 or ·-tocopherol. Anesthesia was induced with 0.1-0.2 ml of sodium pentobarbital (Sanofi, France, 60 mg/ml) given intraperitoneally.…”

Section: Animal Model and Preparationmentioning

confidence: 99%

Leukocyte Adhesion after Oxidant Challenge in the Hamster Cheek Pouch Microcirculation

Bouskela

Cyrino²,

Lerond³

1999

J Vasc Res

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Oral administration of S-5682 (Daflon 500 mg, 90% diosmin, 10% hesperidin) inhibits oxidant-induced increase in macromolecular permeability in the postcapillary venules of the hamster cheek pouch microcirculation. In this study, the effect of S-5682 on leukocyte-endothelium interaction was evaluated using the same experimental model. Hamsters kept on a standard diet were divided into 5 groups (n = 6) and treated orally, twice a day, with placebo (10% lactose solution), S-5682, 5, 20 or 80 mg/kg/day (suspended in 10% lactose solution) or α-tocopherol, 1 mg/kg/day, for 10 days prior to the oxidant challenge with tert-butylhydroperoxide (TBOOH). Topical application of TBOOH (10^–4 M for 5 min) to hamsters given acridine orange prior to TBOOH resulted in increases in the number of rolling and sticking (no movement for at least 30 s) leukocytes in postcapillary venules. No changes in the number of rolling leukocytes could be observed in the treated groups compared with the placebo group (p > 0.05). On the contrary, leukocyte adhesion was inhibited in groups treated with S-5682 (5, 20 and 80 mg/kg/day) or α-tocopherol: placebo 105 ± 3/6 mm² (mean ± SEM); S-5682, 5 mg/kg/day 68 ± 3/6 mm² (p < 0.01), 20 mg/kg/day 55 ± 3/6 mm² (p < 0.001) and 80 mg/ kg/day 39 ± 2/6 mm² (p < 0.001) and α-tocopherol 36 ± 1/6 mm² (p < 0.001). The inhibition of oxidant-induced leukocyte adhesion by S-5682 was similar to that seen for ischemia-reperfusion and the higher dose of S-5682 was as effective as α-tocopherol in inhibiting it.

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Section: Animal Model and Preparationmentioning

confidence: 99%

Leukocyte Adhesion after Oxidant Challenge in the Hamster Cheek Pouch Microcirculation

Bouskela

Cyrino²,

Lerond³

1999

J Vasc Res

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“…Vasomotion is a physiological process in which blood vessels rhythmically dilate and constrict [1, 2, 3, 4]. It can occur spontaneously [2, 3]or in response to vasoactive stimuli [4, 5]and is thought to have such beneficial effects on vascular beds as the maintenance of perfusion pressure and diminished extravasation of fluid [6, 7, 8].…”

Section: Introductionmentioning

confidence: 99%

“…It can occur spontaneously [2, 3]or in response to vasoactive stimuli [4, 5]and is thought to have such beneficial effects on vascular beds as the maintenance of perfusion pressure and diminished extravasation of fluid [6, 7, 8]. Vasomotion is not neuronal in origin [2, 3, 9, 10]but is inherent to the smooth muscle layer of the vessel wall [1, 11]. In arteriolar networks, this activity may originate from specialized pacemaker cells near bifurcations [12].…”

Section: Introductionmentioning

confidence: 99%

Electrophysiological Basis of Arteriolar Vasomotion in vivo

et al. 2000

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We tested the hypothesis that cyclic changes in membrane potential (E_m) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min^–1) were preceded (∼3 s) by oscillations in E_m of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E_m were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E_m observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s^–1) with no diameter change; (3) a fast (9.1 ± 0.8 mV s^–1) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s^–1) and relaxation. The absolute change in E_m correlated (r = 0.60, p < 0.01) with the most negative E_m. Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO₂ caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E_m of SMC and EC corresponding with cation fluxes across plasma membranes.

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“…In iso lated electrically stimulated guinea-pig heart preparations (papillary muscles and atria), buflomedil has shown a weak calcium antagonistic activity and has also produced a dose-dependent negative inotropic effect [9], The present study was carried out to obtain direct information on the effects of buflomedil on vasomotion. Previous experiments in our laboratory [10] have demon strated that the hamster cheek pouch is a suitable model for this study. In the preparation, spontaneous arteriolar vasomotion occurs both regularly and in such a way that is readily influenced by various changes in the physical and chemical environment of the preparation [10], In this study we have explored how vasomotion and the mean arteriolar diameter were affected by buflomedil in the fol lowing experimental conditions: (1) control; (2) in combi nation with different concentrations of an a-adrenergic receptor blocker (phentolamine), and (3) in combination with different concentrations of norepinephrine.…”

Section: Introductionmentioning

confidence: 99%

Effects of Buflomedil on Spontaneous Vasomotion and Mean Arteriolar Internal Diameter in the Hamster Cheek Pouch

Cyrino¹

1994

J Vasc Res

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Intravital microscopy of the hamster cheek pouch microvasculature was used for in vivo studies on the effects of buflomedil, phentolamine (α-adrenergic receptor antagonist) and norepinephrine on the mean internal arteriolar diameter and spontaneous vasomotion. All drugs were applied topically. The vasomotor activity was studied in 125 arterioles (internal diameter range 18.0–62.0 µm) of 34 preparations. Addition of buflomedil (10^–9 to 10^–5M) did not affect the arteriolar diameter significantly (from 100.7 ± 3.5 to 106.4 ± 1.8%, values expressed in percent of the initial diameter as mean ± SE), but increased the vasomotion frequency and amplitude by approximately 20% (from 7.5 ± 0.3 to 9.2 ± 0.2 cpm) and 30% (from 7.3 ± 0.3 to 10.0 ± 0.5 µm), respectively. Phentolamine (10^–9 to 10^–5M) dose-dependently increased the microvascular diameter (from 102.3 ± 1.2 to 139.1 ± 4.3%) and reduced the vasomotion frequency and amplitude (from 8.0 ± 0.3 to 1.9 ± 0.5 cpm and from 9.0 ± 2.1 to 3.1 ± 0.2 µm, respectively). Addition of buflomedil (10^–7M) reduced the vasodilation evoked by phentolamine (from 103.3 ± 0.7 to 127.0 ± 1.5%) and potentiated its depressive effect on vasomotion frequency and amplitude (from 7.6 ± 0.1 to 1.0 ± 0.3 cpm and from 9.0 ± 0.3 to 1.9 ± 0.6 µm, respectively). Norepinephrine (10^–9 to 10^–5M) dose-dependently decreased to arteriolar diameter (from 102.3 ± 0.7 to 69.6 ± 1.6%) and the vasomotion frequency and amplitude (from 8.4 ± 0.2 to 0.4 ± 0.3 emp and from 8.7 ± 0.2 to 0.5 ± 0.4 µm, respectively). Addition of buflomedil (10^–7 M) reduced the vasoconstriction elicited by norepinephrine (from 103.2 ± 0.9 to 82.9 ± 3.9%) and restored the vasomotion frequency and amplitude (from 8.4 ± 0.3 to 7.8 ± 0.4 cpm and from 8.6 ± 0.2 to 7.8 ± 0.3 µm, respectively). The effects observed with buflomedil on the hamster cheek pouch microcirculation suggest a direct action on the smooth muscle excitability and further support its properties as a competitive inhibitor of α-adrenergic receptors and as a weak calcium antagonist.

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Spontaneous vasomotion in hamster cheek pouch arterioles in varying experimental conditions

Cited by 53 publications

References 0 publications

Leukocyte Adhesion after Oxidant Challenge in the Hamster Cheek Pouch Microcirculation

Leukocyte Adhesion after Oxidant Challenge in the Hamster Cheek Pouch Microcirculation

Electrophysiological Basis of Arteriolar Vasomotion in vivo

Effects of Buflomedil on Spontaneous Vasomotion and Mean Arteriolar Internal Diameter in the Hamster Cheek Pouch

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