Changes in intestinal vascular diameter during norepinephrine vasoconstrictor escape

1976 ◽  
Vol 230 (6) ◽  
pp. 1466-1468 ◽  
Author(s):  
PH Guth ◽  
G Ross ◽  
E Smith
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Time Course ◽  
Vessel Diameter ◽  
Mesenteric Arteries ◽  
In Vivo Microscopy ◽  
Mesenteric Vessels ◽  
Arterial Constriction ◽  
Electro Magnetic

The hypothesis that escape from norepinephrine-induced vasoconstriction in the intestine is due to relaxation of initially constricted vessels was tested in 18 anesthetized cats. Intestinal blood flow was measured by an electro magnetic probe on the superior mesenteric artery. Intestinal submucosal and muscle arterioles and small mesenteric arteries were studied by in vivo microscopy with an image-splitting technic. Continuous recordings of mesenteric flow and vessel diameter were made during the infusion into the superior mesenteric artery of norepinephrine (NE) at a rate of 1-2 mug/min for 3 min. Mesenteric flow decreased soon after the NE infusion began but then escaped. Microscopically, arterial constriction and escape were noted in submucosal, muscle, and mesenteric vessels with a time course similar to that for flow. Arteriovenous anastomoses were not seen. These findings support the hypothesis that escape from Ne-induced vasoconstriction is due to relaxation of initially constricted vessels.

Intestinal Luminal Microdialysis 

1999 ◽  
Vol 91 (6) ◽  
pp. 1807-1807 ◽  
Author(s):  
Jyrki J. Tenhunen ◽  
Hannu Kosunen ◽  
Esko Alhava ◽  
Leena Tuomisto ◽  
Jukka A. Takala
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Intestinal Ischemia ◽  
Lactate Concentration ◽  
Total Occlusion ◽  
Total N ◽  
Arterial Blood ◽  
Arterial Blood Lactate ◽  
Jejunal Wall

Background The authors developed a microdialysis method for sampling lactate from the gut lumen to evaluate the metabolic state of the intestinal mucosa. The aim of the study was to evaluate the method in vivo during nonischemic systemic hyperlactatemia and gut ischemia. Methods Microdialysis capillaries were inserted in the lumen of jejunum, in the jejunal wall, and in the mesenteric artery and vein in anesthetized, normoventilated pigs. In the first experiment, infusion of lactate was used to clamp the arterial blood lactate at 5 mM and 10 mM (n = 6). In the second experiment, 90 min of intestinal ischemia was induced by total (n = 6) or partial (n = 6) occlusion of the superior mesenteric artery followed by 60 min of reperfusion. Sham-operated animals were used as controls (n = 6). Results Gut luminal lactate increased only slightly during the nonischemic hyperlactatemia: from a median baseline value of 0.10 (range, 0.06-0.28) to 0.50 (range, 0.15-1.18) and 0.86 (range, 0.35-2.05) mM. Total occlusion of superior mesenteric artery increased luminal lactate from a median of 0.09 (range, 0.06-0.17) to 2.37 (range, 1.29-2.98) and further up to 3.80 (range, 2.55-6.75) mM during reperfusion. Partial occlusion of superior mesenteric artery induced an increase from a median of 0.09 (range, 0.06-0.51) to 1.66 (range, 0.07-3.97) mM. Gut wall microdialysate lactate in deep and superficial layers followed the arterial and mesenteric vein microdialysate lactate. Conclusions Luminal lactate concentration, as measured by microdialysis, increases substantially during gut ischemia but does not respond to systemic hyperlactatemia per se. In contrast, gut wall microdialysis cannot distinguish between gut ischemia and systemic hyperlactatemia. Gut luminal microdialysis provides a method for the assessment of intestinal ischemia with a potential for clinical application.

scholarly journals Duplex criteria for native superior mesenteric artery stenosis overestimate stenosis in stented superior mesenteric arteries

2009 ◽  
Vol 50 (2) ◽  
pp. 335-340 ◽  
Author(s):  
Erica L. Mitchell ◽  
Eugene Y. Chang ◽  
Gregory J. Landry ◽  
Timothy K. Liem ◽  
Fredrick S. Keller ◽  
...  
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Artery Stenosis ◽  
Mesenteric Arteries ◽  
Mesenteric Artery Stenosis

scholarly journals Spontaneous dissection of coeliac and superior mesenteric artery: double whammy

2021 ◽  
Vol 14 (3) ◽  
pp. e240047
Author(s):  
Kanhai Lalani ◽  
Tom Devasia ◽  
Ganesh Paramasivam
Keyword(s):  
Abdominal Pain ◽  
Ct Scan ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Thrombus Formation ◽  
Hybrid Approach ◽  
Transluminal Angioplasty ◽  
Mesenteric Arteries ◽  
Visceral Artery ◽  
Bowel Rest

Isolated dissection of one of the mesenteric arteries without concurrent involvement of the aorta is a rare clinical entity and an unusual cause of abdominal pain. It usually involves one artery, most commonly the superior mesenteric artery (SMA) followed by the coeliac artery. We are reporting a rare case where both coeliac and SMA were showing dissection. We are reporting a case of 60-year-old hypertensive male who came with worsening abdominal pain for 5 days; CT scan showed coeliac and SMA dissection without any imaging evidence of intestinal ischaemia. He was successfully managed medically with bowel rest and anticoagulation. Two weeks of follow-up CT scan showed no progression or thrombus formation. For complicated cases, percutaneous transluminal angioplasty of a visceral artery or open surgical exploration or hybrid approach is required. However, for stable uncomplicated cases, medical therapy alone is sufficient.

scholarly journals Common celiacomesenteric trunk: a rare anatomic variation

2009 ◽  
Vol 8 (3) ◽  
pp. 271-273 ◽  
Author(s):  
K. Sridhar Varma ◽  
Narendra Pamidi ◽  
Venkata R. Vollala
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Anatomic Variation ◽  
Celiac Trunk ◽  
Vascular Anomalies ◽  
Common Origin ◽  
Mesenteric Arteries ◽  
Surgical Approaches ◽  
Celiacomesenteric Trunk

Common celiacomesenteric trunk, with the celiac and superior mesenteric arteries having a common origin from the aorta, is the least frequently reported anatomic variation of all abdominal vascular anomalies. Knowledge of variations concerning the celiac trunk and superior mesenteric artery are of great importance for both surgical approaches and angiographic examinations. Clinicians should keep in mind these variations to avoid complications.

Superior Mesenteric Artery and Vein Injuries: Operative Strategies and Outcomes

2021 ◽  
pp. 153857442110424
Author(s):  
Patrick D. Melmer ◽  
Brant Clatterbuck ◽  
Virginia Parker ◽  
Christine A. Castater ◽  
Nathan J. Klingensmith ◽  
...  
Keyword(s):  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Surgical Intervention ◽  
Management Strategies ◽  
Mortality Rates ◽  
Traumatic Injuries ◽  
Improved Outcomes ◽  
Operative Strategies ◽  
Mesenteric Vessels ◽  
Prompt Diagnosis

Traumatic injuries to the mesenteric vessels are rare and often lethal. Visceral vessels, such as the superior mesenteric artery (SMA) and vein (SMV), supply blood to the small and large bowel by a rich system of collaterals. Because fewer than 100 such injuries have been described in the literature, they pose challenges in both diagnosis and management and can unfortunately result in high mortality rates. Prompt diagnosis, surgical intervention, and resuscitation can lead to improved outcomes. Here, we review the literature surrounding traumatic injuries of the SMA/SMV and discuss management strategies.

Vascular escape from vasoconstriction and post-stimulatory hyperemia in the superior mesenteric artery of the cat

1988 ◽  
Vol 66 (9) ◽  
pp. 1174-1180 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare ◽  
Leslie K. Lockhart
Keyword(s):  
Superior Mesenteric Artery ◽  
Adenosine Receptors ◽  
Mesenteric Artery ◽  
Vascular Tone ◽  
Low Dose ◽  
Data Interpretation ◽  
High Dose ◽  
Partial Recovery ◽  
Sympathetic Nerve Stimulation

Vascular escape is seen as a partial recovery from initial vasoconstriction despite continued constrictor stimuli. Escape in the feline intestine (superior mesenteric artery) occurred for i.a. norepinephrine (NE) infusions (56% escape for low dose, 40% for high dose NE) and for sympathetic nerve stimulation (SNS) (65% for 1 Hz, 49% for 3 Hz, 44% for 9 Hz). Adenosine infusion or blockade of adenosine receptors (8-phenyltheophylline) did not alter the escape, showing that endogenous adenosine levels are unlikely to play any role in the mechanism of escape. Other aspects of escape were studied: equiconstrictor doses of NE given i.a. or i.v. lead to similar degrees of escape; propranolol and ouabain did not alter escape; the degree of escape was significantly greater for the low dose NE and the 1-Hz SNS than for higher intensities of stimulation, however, escape did not inversely correlate significantly with the initial degree of vasoconstriction when all data were pooled. Post-stimulatory hyperemia occurs upon cessation of vasoconstrictor stimuli, reaches a peak conductance within 1 min, and returns to baseline within about 3 min. Hyperemia was quantitated from the peak vasodilation and from the area under the flow–hyperemia curve. The hyperemias were not related to NE dose or SNS frequency nor did they correlate with initial vasoconstriction or extent of vascular escape. Contrary to the hypothesis that adenosine may mediate hyperemia, adenosine infusions reduced the response and adenosine receptor antagonism tended to elevate the response. Propranolol and ouabain did not produce significant effects on post-stimulatory hyperemia. A discussion of the merits of using vascular resistance or conductance to assess vascular tone and vascular escape concludes that in the in vivo systems in which changes in vascular tone result mainly in changes in blood flow, the use of resistance is unacceptable and may lead to serious error in data interpretation.

Detection of reticuloendothelial-depressing substance in shock

1965 ◽  
Vol 209 (1) ◽  
pp. 71-74 ◽  
Author(s):  
Benjamin Blattberg ◽  
Matthew N. Levy
Keyword(s):  
Escherichia Coli ◽  
Superior Mesenteric Artery ◽  
Whole Blood ◽  
Mesenteric Artery ◽  
The Other ◽  
In Vitro Method ◽  
Carbon Particles ◽  
Normal Rat

In an effort to find an in vitro method to detect the presence of reticuloendothelial-depressing substance (RDS), two tests were devised which measured phagocytic activity. One used carbon particles to measure phagocytosis and the other P32-labeled Escherichia coli. Neither method demonstrated an in vitro difference in granulopectic activity between dog plasmas from sham-operated and hemorrhagic-shock or superior mesenteric artery-occluded (SMAO) animals. An in vivo method was used in which the reticuloendothelial activity of the rat was measured in terms of the rate of clearance of injected carbon particles. Occlusion of the superior mesenteric artery of the rat led to the production of RDS. The RDS could be transferred to and demonstrated in a normal rat by means of SMAO rat whole blood, plasma, and dialysate of plasma, but not in RBC or plasma which had been dialyzed. Sham-operated animals were used as controls.

Elucidation of the temporal relationship between endothelial-derived NO and EDHF in mesenteric vessels

2007 ◽  
Vol 293 (3) ◽  
pp. H1682-H1688 ◽  
Author(s):  
Louise S. Harrington ◽  
Martin J. Carrier ◽  
Nicola Gallagher ◽  
Derek Gilroy ◽  
Chris J. Garland ◽  
...  
Keyword(s):  
Time Course ◽  
Temporal Relationship ◽  
Mesenteric Arteries ◽  
Third Order ◽  
Physiological Importance ◽  
Relative Contribution ◽  
Mesenteric Vessels ◽  
Lipid Metabolites ◽  
First Time ◽  
Subsequent Addition

Although the endothelium co-generates both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), the relative contribution from each vasodilator is not clear. In studies where the endothelium is stimulated acutely, EDHF responses predominate in small arteries. However, the temporal relationship between endothelial-derived NO and EDHF over more prolonged periods is unclear but of major physiological importance. Here we have used a classical pharmacological approach to show that EDHF is released transiently compared with NO. Acetylcholine (3 × 10−6 mol/l) dilated second- and/or third-order mesenteric arteries for prolonged periods of up to 1 h, an effect that was reversed fully and immediately by the subsequent addition of l-NAME (10−3 mol/l) but not TRAM-34 (10−6 mol/l) plus apamin (5 × 10−7 mol/l). When vessels were pretreated with l-NAME, acetylcholine induced relatively transient dilator responses (declining over ∼5 min), and vessels were sensitive to TRAM-34 plus apamin. When measured in parallel, the dilator effects of acetylcholine outlasted the smooth muscle hyperpolarization. However, in the presence of l-NAME, vasodilatation and hyperpolarization followed an identical time course. In vessels from NOSIII−/− mice, acetylcholine induced small but detectable dilator responses that were transient in duration and blocked by TRAM-34 plus apamin. EDHF responses in these mouse arteries were inhibited by an intracellular calcium blocker, TMB-8, and the phospholipase A2 inhibitor AACOCF3, suggesting a role for lipid metabolites. These data show for the first time that EDHF is released transiently, whereas endothelial-derived NO is released in a sustained manner.

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