Development of an Experimental Apparatus for Investigating Lymphatic Pumping Activity of Murine Mesentery In Vivo.

Ono, Nobuyuki; Mizuno, Risuke; Nojiri, Hiroshi; Ohhashi, Toshio

doi:10.2170/jjphysiol.50.25

Cited by 30 publications

(35 citation statements)

References 32 publications

(26 reference statements)

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“…The images were also recorded on a videocassette recorder (VCR; BR-S800, Victor, Japan) through a video timer (VTG-33, For A, Japan) and then displayed on a TV monitor (Trinitron super pitch, Sony, Japan). A video caliper [20] enabled us to measure changes in the diameter of the gingival arterioles. In our preliminary study, the superfusion of 37°C Krebs-bicarbonate solution onto the surface of rat gingival tissue caused a significant constriction of the arterioles.…”

Section: Methodsmentioning

confidence: 99%

Arachidonic Acid–Induced COX-1 and COX-2–Mediated Vasodilation in Rat Gingival Arterioles In Vivo

Nakatsuka

Mizuno

Ono

et al. 2005

JJP

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Abstract:The roles of cyclooxygenase (COX) and prostaglandins (PGs) in the regulation of vasoreactivity of rat gingival arterioles in vivo were evaluated by using an intravital microscope. The superfusion of indomethacin (a nonselective COX inhibitor) or SC-560 (a selective COX-1 inhibitor) onto the gingiva significantly constricted the arterioles, though NS-398 (a selective COX-2 inhibitor) did not affect the diameter of the arterioles. The SC-560-mediated constriction of the arterioles was completely reversed by an additional treatment with arachidonic acid (AA). The superfusion of AA, beraprost-Na (an analogue of PGI 2 ) or PGE 2 onto the gingiva significantly dilated the arterioles dose-dependently. The AALocal gingival blood flow plays a crucial role in maintaining dental health care in physiological conditions [1][2][3]. For evaluating local blood flow in the gingival tissues in vivo, laser-doppler and ultrasonic flowmetry have been used on animals and humans [4][5][6][7], but they are both disadvantageous for evaluating continuous changes in the diameter of gingival microvessels in vivo. On the other hand, an intravital microscope system enables us to continuously measure changes in the diameter of resistant microvessels, including small arteries and arterioles in vivo.PGs are produced via the arachidonic acid-COX pathway. COX is a limiting enzyme in this cascade and has been classified into two isoforms, COX-1 (constitutive type) and COX-2 (inducible type) [8][9][10][11]. induced dilation of the arterioles was significantly reduced by the treatment with SC-560 or NS-398. The expression of COX-1 and COX-2 were positive in the endothelium, but not the smooth muscles, of the arterioles. The expression of PGE synthase (PGES) was found only in the smooth muscles, but not the endothelium, of the arterioles. Neither the endothelium nor the smooth muscles of the arterioles expressed PGI synthase (PGIS). These findings suggest that the COX-2-mediated PG cascade may collaborate with the COX-1 pathway in the regulation of arteriolar myogenic activity in rat gingiva in the case of the supply of a large amount of AA. [The Japanese Journal of Physiology 55: [293][294][295][296][297][298][299][300][301][302] 2005]

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Section: Methodsmentioning

confidence: 99%

Arachidonic Acid–Induced COX-1 and COX-2–Mediated Vasodilation in Rat Gingival Arterioles In Vivo

Nakatsuka

Mizuno

Ono

et al. 2005

JJP

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“…The Krebs-bicarbonate solution, in which PO 2 was maintained at 56.7 Ϯ 1.6 mmHg (n ϭ 10) and pH at 7.4 Ϯ 0.01 by bubbling with 5% CO 2-95% N2 (15,(25)(26)(27), was perfused extraluminally over the lymph vessels within the organ chamber. Physiological salt solution with 5% CO 2-95% N2 is also useful for studying lymphatic circulation (2,36,40,49), because PO 2 in the lymphatic circulation is known to be ϳ25-40 mmHg, which is lower than that obtained with blood circulation in physiological conditions (9,16).…”

Section: Methodsmentioning

confidence: 99%

“…An objective lens (ϫ4), a photo-eyepiece lens (ϫ3.3), and a monochrome charge-coupled device camera (KOKOM KCB-270A) were used to obtain images of the lymph microvessels, which were displayed on a monochrome television monitor (Hamamatsu Photonics). Changes in the diameter of the lymph vessels were manually and automatically measured with a diameter-detection device with an edge-detection method (36). They were recorded on a videocassette recorder (Toshiba) and a directwriting oscillograph (Sanei-Sokki, Recti 8K).…”

Section: Methodsmentioning

confidence: 99%

ATP inhibits pump activity of lymph vessels via adenosine A₁ receptor-mediated involvement of NO- and ATP-sensitive K⁺ channels

Kousai¹,

Mizuno²,

Ikomi³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Kousai, Akira, Risuke Mizuno, Fumitaka Ikomi, and Toshio Ohhashi. ATP inhibits pump activity of lymph vessels via adenosine A 1 receptor-mediated involvement of NO-and ATP-sensitive K ϩ channels. Am J Physiol Heart Circ Physiol 287: H2585-H2597, 2004. First published August 12, 2004 doi:10.1152/ajpheart.01080. 2003.-We examined the effects of ATP on intrinsic pump activity in lymph vessels isolated from the rat. ATP caused significant dilation with a cessation of lymphatic pump activity. Removal of the endothelium or pretreatment with N -nitro-L-arginine methyl ester (L-NAME) significantly reduced ATP-induced inhibitory responses of lymphatic pump activity, whereas reduction was not suppressed completely by 10 Ϫ6 M ATP. L-Arginine significantly restored ATPinduced inhibitory responses in the presence of L-NAME. ATPinduced inhibitory responses in lymph vessels with endothelium were also significantly, but not completely, suppressed by pretreatment with glibenclamide. 8-Cyclopentyl-1,3-dipropylxanthine (a selective adenosine A 1 receptor antagonist), but not suramine (a P2X and P2Y receptor antagonist) or 3,7-dimethyl-1-proparglyxanthine (a selective adenosine A 2 receptor antagonist), significantly decreased ATP-induced inhibitory responses. ␣,␤-Methylene ATP (a selective P2X and P2Y receptor agonist) had no significant effect on lymphatic pump activity. In some lymph vessels with endothelium (24 of 30 preparations), adenosine also caused dose-dependent dilation with a cessation of lymphatic pump activity. L-NAME significantly reduced the inhibitory responses induced by the lower (3 ϫ 10 Ϫ8 -3 ϫ 10 Ϫ7 M) concentrations of adenosine. Glibenclamide or 8-cyclopentyl-1,3-dipropylxanthine also significantly suppressed adenosine-induced inhibitory responses. These findings suggest that ATP-induced dilation and inhibition of pump activity of isolated rat lymph vessels are endothelium-dependent and -independent responses. ATP-mediated inhibitory responses may be, in part, related to production of endogenous nitric oxide, involvement of ATP-sensitive K ϩ channels, or activation of adenosine A 1 receptors in lymphatic smooth muscle and endothelium.rat; endothelium; smooth muscle; nitric oxide THE TRANSPORT OF LYMPH depends on passive and active driving forces as well as the rate of lymph production in organs and tissues. The active driving forces, resulting from intrinsic pump activity of lymph vessels, play a pivotal role in the centripetal propulsion of lymph (1,31,39). Neural (21), humoral (30), and mechanical factors (8,22,23) modify the rhythm and amplitude of lymphatic intrinsic pump activity. Recently, it has become clear that lymphatic endothelium-derived nitric oxide (NO) strongly contributes to regulation of lymphatic intrinsic pump activity. Thus NO causes relaxation of lymphatic smooth muscles and reduces lymphatic intrinsic pump activity (24,26,27,35,40,45,48). ATP-sensitive K ϩ (K ATP ) channels have been found in the plasma membrane of cells, including vascular and nonvascular smooth muscles, and then beca...

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“…A calibration curve was obtained to record the relationship between the output voltage of the device and scale of the micrometer. According to this relationship, the theoretical resolution power of the diameter measurement is 0.38 m [22,23].…”

Section: Methodsmentioning

confidence: 96%

Effects of VEGF on Ca2+-Translent in Cultured Lymphatic Endothelial Cells and Mechanical Activity of Isolated Lymph Vessels.

Arai

Mizuno²,

Ohhashi³

2000

JJP

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Development of an Experimental Apparatus for Investigating Lymphatic Pumping Activity of Murine Mesentery In Vivo.

Cited by 30 publications

References 32 publications

Arachidonic Acid–Induced COX-1 and COX-2–Mediated Vasodilation in Rat Gingival Arterioles In Vivo

Arachidonic Acid–Induced COX-1 and COX-2–Mediated Vasodilation in Rat Gingival Arterioles In Vivo

ATP inhibits pump activity of lymph vessels via adenosine A₁ receptor-mediated involvement of NO- and ATP-sensitive K⁺ channels

Effects of VEGF on Ca2+-Translent in Cultured Lymphatic Endothelial Cells and Mechanical Activity of Isolated Lymph Vessels.

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Development of an Experimental Apparatus for Investigating Lymphatic Pumping Activity of Murine Mesentery In Vivo.

Cited by 30 publications

References 32 publications

Arachidonic Acid–Induced COX-1 and COX-2–Mediated Vasodilation in Rat Gingival Arterioles In Vivo

Arachidonic Acid–Induced COX-1 and COX-2–Mediated Vasodilation in Rat Gingival Arterioles In Vivo

ATP inhibits pump activity of lymph vessels via adenosine A1 receptor-mediated involvement of NO- and ATP-sensitive K+ channels

Effects of VEGF on Ca2+-Translent in Cultured Lymphatic Endothelial Cells and Mechanical Activity of Isolated Lymph Vessels.

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ATP inhibits pump activity of lymph vessels via adenosine A₁ receptor-mediated involvement of NO- and ATP-sensitive K⁺ channels