Gastrointestinal circulation and motor function

Chou, C. C.

doi:10.1002/cphy.cp060140

Cited by 4 publications

(4 citation statements)

References 126 publications

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“…The basal lumen pressure was used as an index of intestinal tonic contractions. A motility index was calculated by dividing all the pressure wave peaks by the number of pressure waves during a 1 min period, and reflects the average strength of intestinal rhythmic contractions (Chou, 1989). The basal lumen pressure and the motility index were expressed in mmHg.…”

Section: Methodsmentioning

confidence: 99%

“…The rhythmic contractions can be accompanied by a decrease, an increase, or no change in blood flow, depending on the strength and pattern of contractions (Kvietys et al, 1986;Chou, 1989). The increase in blood flow during muscle contractions is usually accompanied by an increase in oxygen uptake.…”

Section: Effects Of Nitroglycerin On Action Of L-namementioning

confidence: 99%

“…None of these studies, however, reported the influence of the increased motility on blood flow. It is known that spontaneous, as well as chemically-induced intestinal motility, can influence intestinal blood flow (Kvietys et al, 1986;Chou, 1989). The increase in motility induced by an NO synthesis inhibitor, therefore, might influence and complicate the induced decrease in blood flow.…”

Section: Introductionmentioning

confidence: 99%

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l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

Alemayehu

Lock

Coatney

et al. 1994

British J Pharmacology

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1The effects of the inhibitor of nitric oxide (NO) synthesis, N0-nitro-L-arginine methyl ester (L-NAME), on systemic arteriil blood pressure and jejunal motility, blood flow, and oxygen uptake have been investigated in anaesthetized dogs. 2 L-NAME (cumulative doses of 0.1-20 mg kg-', i.v.) dose-dependently increased blood pressure and jejunal motility and decreased heart rate. The maximal response of these three variables occurred at doses, 3, 10 and 10mgkg-l, respectively. L-NAME (cumulative doses of 0.5-5mgkg-') also dosedependently induced jejunal vasoconstriction. The jejunal vascular resistance returned to control values as the cumulative doses reached 10 and 20 mg kg-', which corresponded to the maximal increase in jejunal motility. 3 A single intravenous injection of L-NAME (10mgkg-') produced a prompt increase in blood pressure, which lasted for at least 50min. 4 L-NAME (10 mg kg-') produced a progressive rise in jejunal motility reaching its maximum (47 ± 6 mmHg) 15 min after the administration, and lasting for 40-50 min. Both the basal lumen pressure and the amplitude of rhythmic contractions increased during this period. 5 L-NAME (10 mg kg-') produced a triphasic change in jejunal vascular resistance and blood flow measured by timed collection of venous outflow. The blood flow decreased initially (-43% at 5 min), increased (+ 35%) and returned to control value between 15 and 35 min, then decreased (-35%) 40-50 min post-infusion. Jejunal vascular resistance reflected the blood flow response (+ 88% at both 5 and 50 min). The time during which the reversal of the vasoconstriction occurred (15-35 min) corresponded to the time of marked increase in motility, and was accompanied by a significant increase in jejunal oxygen uptake (+ 18%). 6 The L-NAME-induced increase in motility was prevented by L-arginine (1 g kg-', i.v.) but not by D-arginine pretreatment. The interim (15-35 min) changes in jejunal blood flow, vascular resistance and oxygen uptake were also prevented by L-arginine pretreatment. 7 L-Arginine pretreatment attenuated L-NAME-induced hypertension for 5 min. 8 The L-NAME-induced increases in jejunal vascular resistance and motility were inhibited by either local intra-arterial infusion of L-arginine (32 mM local arterial blood concentration) or topical application of 2 gM nitroglycerin. Infusion of D-arginine (32 mM local arterial blood concentration) had no such effect. 9 The L-NAME-induced increase in blood pressure was not the mechanism by which jejunal motility was increased, because similar increases in blood pressure by mefenamate (10 mg kg-', i.v.) had no such effect. 10 Thus, inhibition of nitric oxide synthesis by L-NAME increased jejunal motility and vascular resistance and the marked increase in motility can abolish or reverse the vasoconstriction. Endogenous nitric oxide may play a role in regulating motility and blood flow in the resting canine jejunum.

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Section: Methodsmentioning

confidence: 99%

Section: Effects Of Nitroglycerin On Action Of L-namementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

Alemayehu

Lock

Coatney

et al. 1994

British J Pharmacology

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“…Ischemic lesions of the small bowel may be the result of a variety of clinical conditions associated with a decrease or redistribution of blood flow, such as shock, congestive heart failure, mesenteric embolus, small bowel obstruction, cardiopulmonary by pass and hypothermia. It was shown that brief periods of acute intestinal ischemia cause immediate hyperexcitability [2][3][4], longer periods of ischemia cause prolonged inhibition of bowel motility [5,6].…”

Section: Introductionmentioning

confidence: 99%

Ischemia-Reperfusion-Induced Delay in Intestinal Transit

Ali̇can

Yeğen²,

Olcay³

et al. 1998

Digestion

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Background/Aims: To evaluate the involvement of ET-1 in ischemia-reperfusion (I/R) injury. Methods: Superior artery occlusion was performed in Wistar albino rats for 30 min followed by 2-hour (early reperfusion; ER) or 24-hour (late reperfusion; LR) reperfusion periods. Results: Intestinal transit was found to be reduced in the ER and LR groups (19.0 ± 2.5%; p < 0.001 and 72.7 ± 6.0%; p < 0.05, respectively) compared to the control group (85.8 ± 2.5%), while treatment with the ET receptor antagonist bosentan (BOS; 10 mg/kg i.v.) abolished this delay in LR. Myeloperoxidase activity showed a significant increase in ER (7.07 ± 85.70 U/g; p < 0.001) compared to control (281.16 ± 43.23 U/g), but BOS had no effect on this increase. The protein oxidation level was found to be higher in LR (5.92 ± 0.77 nmol/mg protein; p < 0.05) compared to the control (3.77 ± 0.45 nmol/mg protein), and was reversed by BOS treatment. Conclusion: The results of the present study imply that I/R delays intestinal transit involving an endothelin-dependent mechanism.

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The role of muscarinic and nicotinic receptors in the control of the ovine pyloric antral myoelectric response to nutrients during individual phases of the migrating myoelectric complex

Romanski¹

2005

Small Ruminant Research

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Gastrointestinal circulation and motor function

Cited by 4 publications

References 126 publications

l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

Ischemia-Reperfusion-Induced Delay in Intestinal Transit

The role of muscarinic and nicotinic receptors in the control of the ovine pyloric antral myoelectric response to nutrients during individual phases of the migrating myoelectric complex

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