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Evaluation of medial hypertrophy in resistance vessels of spontaneously hypertensive rats.

The role of smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in medial hypertrophy of mesenteric resistance vessels of 107- to 111-day-old spontaneously hypertensive rats (SHR) was examined using a combination of morphometric, biochemical, and immunological techniques. Mesenteric arteries were classified on the basis of branching order for comparative purposes. Branch level I vessels were those that directly enter the jejunal wall, while Branches II to IV represented more proximal vessels; Branch IV vessels were those that branch from the superior mesenteric artery. Medial hypertrophy was assessed in perfusion-fixed vessels by morphometric evaluation of medial cross-sectional area and smooth muscle content. Medial cross-sectional area and smooth muscle content were significantly increased in larger (Branches III and IV) but not smaller (Branches I and II) mesenteric resistance vessels of SHR compared with control normotensive Wistar-Kyoto rats (WKY). Smooth muscle cell hypertrophy and hyperploidy were evaluated in isolated cells obtained by enzymatic dissociation of mesenteric resistance vessels. Approximately 80% of the cells in these preparations were identified as smooth muscle cells using a smooth muscle-specific isoactin antibody. Feulgen-DNA microdensitometric evaluation of isolated cells showed that polyploid cells were present in mesenteric resistance vessels but at very low frequencies, and no differences were apparent between SHR and WKY. Likewise, no differences in cellular protein content or relative smooth muscle cell size (i.e., area profile) were observed between cells obtained from SHR and WKY vessels. These results demonstrate that the increase in medial smooth muscle content observed in larger mesenteric resistance vessels of SHR cannot be accounted for by smooth muscle hypertrophy and hyperploidy, inferring that hyperplasia must be present. Results indicate that studies of the initiating mechanisms for medial smooth muscle hypertrophy in SHR resistance vessels, at least relatively early in hypertension, should focus on examination of factors that induce true cellular proliferation rather than hypertrophy and hyperploidy.

Animals↗

Lack of effect of anti-hypertensive treatment with felodipine on cardiovascular structure of young spontaneously hypertensive rats.

Felodipine (4(2,3-dichlorophenyl)-1,4-dihydro-2, 6-dimethyl-3-ethoxycarbonyl-5-methoxycarbonyl pyridine)), a selective vasodilating anti-hypertensive drug, was used in the treatment of spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto rats (WKYs) from age 6 to 14 weeks, ie during the time of high blood pressure development in SHRs. The effect of treatment on heart weight and on mesenteric resistance vessels (i.d. ca 170 microns) characteristics was investigated. In a first study, two oral doses of felodipine were added to the diet of SHRs, in concentrations of either 0.5 or 1.5 mg X g-1 rat food. Both treatments lowered mean arterial pressure by about 19% (p less than 0.001). In a second study, the lower dose of felodipine (0.5 mg . g-1 rat food) was therefore used to treat both SHRs and WKYs. Treatment did not interfere with weight or food intake of either SHRs or WKYs but increased average weekly water intake significantly. In neither strain was the pulse rate or, surprisingly, heart/body weight ratio affected by treatment. Furthermore, mesenteric resistance vessel morphology and mechanics were not affected by the blood pressure reduction. The noradrenaline and calcium sensitivity of mesenteric resistance vessels from treated rats was greater (p less than 0.001) than those from control rats. These findings indicate that blood pressure reduction with felodipine does not affect cardiovascular structure in young SHRs.

Animals↗

Alteration of histamine, serotonin and primary prostaglandin in case of diarrhea induced by endotoxin and gastrointestinal absorption of drug.

Effects of endotoxin on the motility, the permeability of mesenteric blood vessel and endogenous substances (electrolyte (Na, K), histamine, serotonin and primary prostaglandin) in the small intestine of mice were investigated. Diarrhea was induced by intraperitoneal injection of Salmonella typhosa endotoxin in mice. It is suggested that the diarrheal action of endotoxin is due to the acceleration of intestinal motility and/or the facilitation of mesenteric blood vessel permeability. On the other hand, from the observation of blood concentration of acetaminophen and sulfisoxazole, inhibition of drug absorption was suggested in cases of diarrhea induced by endotoxin. This inhibition of gastrointestinal absorption is due to the delay of the gastric emptying rate, the increase of intestinal transit time of drug in the absorption site and the acceleration of mesenteric blood vessel permeability. Then it is conceivable that these actions may be mediated by biogenic amines (serotonin and histamine) and primary prostaglandins.

Animals↗

Further observations on mesenteric vasoconstriction, survival and the clotting defect after endotoxin administration.

1. The initial response after endotoxin administration (3 mg/kg) in cats involved pulmonary vasoconstriction. This was not seen when endotoxin was given by slow infusion and it could be prevented after a bolus injection of endotoxin by pretreatment of the cats with aspirin (10 mg/kg). Intense mesenteric vasoconstriction occurred in all the cats.2. The mesenteric vasoconstriction was a specific response of the mesenteric blood vessels. At the time the mesenteric bed constricted, the renal bed dilated, the hepatic arterial bed remained unchanged and the smooth muscle of the intestinal wall relaxed.3. Arterial blood from cats with a fully developed mesenteric vasoconstriction after endotoxin administration was perfused through a normal intestine. No immediate vasoconstriction developed but the perfused intestine constricted slowly over 60 minutes. This suggests that mesenteric constriction was not due to circulating vasoconstrictor factors or the intestinal innervation, but involved a slow local mechanism within the intestine. It could not be prevented or reversed by a variety of pharmacological agents.4. These observations suggest that endotoxin caused a unique type of mesenteric vasoconstriction in cats by a local mechanism which took up to 60 min to develop, was sufficiently potent to reduce mesenteric flow to <30% control, and was maintained until death of the cats. Blood from these animals did not clot when placed in a glass tube.5. The mesenteric constriction and the clotting defect could be prevented by repeated administration of aminophylline and dextran solution before and after a bolus intravenous injection of endotoxin. Arterial pressure and mesenteric flow were maintained for at least 10 h in these experiments. Inadequate treatment intensified rather than reduced the intestinal mucosal damage.6. Cats were treated with aspirin, endotoxin and the optimal regimen for prevention of the mesenteric constriction and allowed to recover from the anaesthetic agent. In this series, 63% survived indefinitely compared to 25% after aspirin and endotoxin treatment and 0% after endotoxin alone.7. The possible mechanisms of action of aspirin and aminophylline-dextran solution are discussed. Our failure to obtain 100% survival is probably due to pulmonary damage which develops 10-24 h after endotoxin administration. This delayed pulmonary action of endotoxin is not prevented by aspirin treatment and it seems unlikely that aspirin will be of any value in the treatment of the pulmonary lesion in man.

Aminophylline↗

Hypoxia, metabolic inhibition, and isolated rat mesenteric tone: influence of arterial diameter.

The present study examined and compared the effects of severe hypoxia (induced by either substitution of O(2) in the gassing medium with N(2) or by addition of the O(2) scavenger sodium dithionite) and metabolic inhibition (induced by addition of sodium cyanide) on the tone of isolated rat mesenteric resistance vessels. The influence of vessel diameter and the endothelium on responses to these maneuvers was investigated. Hypoxia (due to both substitution of O(2) with N(2) and by addition of 2 mM sodium dithionite) caused near maximal relaxation of all tissues studied. Addition of 10 mM dithionite, however, produced a significantly smaller response. Two mM cyanide also relaxed mesenteric arteries. In small vessels a near maximal relaxation to cyanide was observed, however, in larger vessels the relaxation to metabolic inhibition was significantly less than that observed to hypoxia. Increasing the concentration of cyanide had no further effect on responses. All responses were found to be endothelium-independent. Thus, as the effects of hypoxia and cyanide are not always similar, care must be taken when extrapolating the effects of metabolic inhibition to those of hypoxia. The results of this study suggest that, in large mesenteric vessels at least, an "O(2) sensing step," in addition to effects of metabolism, may be involved in the hypoxic response.

Animals↗

Blood pressure and vascular reactivity changes in spontaneously hypertensive rats fed fish oil.

1. To examine possible mechanisms of antihypertensive effects of feeding fish oil rich in n-3 fatty acids, we have studied vascular reactivity of aortic rings and perfused mesenteric resistance vessels of spontaneously hypertensive rats (SHR) given such a diet. 2. In two experiments, rats were fed a semi-synthetic diet containing either 'fish oil' (10 and 20% by weight) or hydrogenated coconut oil (control) (10 and 20%) for 4 weeks. 3. Blood pressure rose significantly less in the fish oil group than in controls in both experiments. 4. Aortic rings from control rats showed endothelium-dependent relaxations to low concentrations of acetylcholine (ACh) but relaxed less at higher concentrations. In contrast, rings from the fish oil group had relaxations which increased through the range of concentrations used. Indomethacin (10 microM) also increased the relaxation responses seen in rings from control rats, suggesting that fish oil inhibits a contractile cyclo-oxygenase product. This contractile substance may be thromboxane A2 (TxA2) or its endoperoxide precursor, prostaglandin H2 (PGH2) as aortic incubates and serum levels of TxB2 (the stable product of TxA2) were greatly reduced in fish oil-fed rats, and the decrease of relaxant responses to high concentrations of ACh were also blocked by a TxA2/PGH2 receptor blocker (SQ 29548). 5. In contrast to aortic rings, perfused preconstricted mesenteric resistance vessels of control rats relaxed to ACh in a similar fashion to tissues from fish oil-fed rats. However, in this preparation, fish oil feeding enhanced relaxations to sodium nitroprusside (SNP) and contractile responses to noradrenaline were less than controls. After removal of endothelium with 0.05% saponin, contractile responses to noradrenaline increased in both groups but responses from fish oil-treated rats were still attenuated. This suggests that fish oil feeding alters reactivity of mesenteric resistance vessels at the level of the smooth muscle. 6. The results indicate that fish oil feeding may reduce blood pressure by decreasing vascular smooth muscle reactivity to noradrenaline in resistance vessels. The effect may be enhanced by inhibition of an endothelium-derived cyclo-oxygenase product, such as TxA2 or PGH2 in conduit vessels.

6-Ketoprostaglandin F1 alpha↗

Detection of cancer cells in mesenteric vein and peripheral vessels by measuring telomerase activity in patients with colorectal cancer.

BACKGROUND: Liver metastasis is an important factor determining prognosis in colorectal cancer. The objective of this study was to assess whether colorectal cancer cells in the drainage veins can be detected by measuring telomerase activity and its detection is correlated with liver metastasis. METHODS: Telomeric repeat amplification protocol assay in combination with an immunomagnetic sorting was used for measuring telomerase activity of epithelial cells in blood samples collected from mesenteric (tumor-drainage) vein and peripheral vessels of 41 colorectal cancer patients. Telomerase activity was calculated as relative telomerase activity (RTA) against a control template and analyzed in terms of liver metastasis. RESULTS: RTA of mesenteric blood samples was significantly higher in patients with liver metastasis (60.8%; n=7) than in those without metastasis (19.7%; n=34; P=.019). The RTA of peripheral blood sample was also higher in patients with liver metastasis (26.8%) than in those without metastasis (11.1%; p=.17). Moreover, 57% of cases with liver metastasis exhibited a positive telomerase activity in mesenteric blood sample, whereas it was 18% in cases without metastasis. CONCLUSIONS: Our assay was proven to be a feasible method for detecting cancer cells in tumor-drainage veins. High telomerase activity of mesenteric blood samples reflected the existence of liver metastasis of colorectal cancer.

Adult↗

Relationships of mesenteric thromboembolism, oral feeding, and necrotizing enterocolitis.

Mesenteric blood vessels were examined in postmortem specimens of 30 selected infants. The infants had had necrotizing enterocolitis (16 cases) or other lesions (14 cases). Mesenteric thromboemboli were observed in 12 of the infants with necrotizing enterocolitis (P less than 0.001). Umbilical vessel catheters were apparently responsible for the emboli. Multiple instances of thrombosis and thromboembolism were detected in other organs. Ninety-four percent of infants with necrotizing enterocolitis were orally fed (P less than 0.001). Mesenteric thromboemboli were more frequent in infants who were fed via the digestive route while an umbilical arterial catheter was in place. Mesenteric thromboembolism in these infants was postulated to have been attributable to increased postprandial blood flow in the mesenteric vessels.

Catheterization↗

Does smooth muscle cell polyploidy occur in resistance vessels of spontaneously hypertensive rats?

The ploidy of smooth muscle cells (SMCs) enzymatically isolated from the aorta and superior mesenteric artery (elastic arteries), caudal artery (small muscular artery) and the small mesenteric arteries and arterioles (mesenteric resistance vessels) of the spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats at ages 12, 26, 32 and 40 weeks was determined by flow cytometric DNA analysis and Feulgen-DNA photometric measurements. Frequency of polyploid cells in the aorta and superior mesenteric artery of the SHR increased from 4.43 +/- 1.35 and 7.58 +/- 1.69%, respectively, at 12 weeks to 31.26 +/- 3.00 and 14.13 +/- 1.30% at 40 weeks. There was a smaller increase in the percentage of polyploid cells in these two vessels of the WKY from 4.73 +/- 0.74 and 5.82 +/- 0.33%, respectively, at 12 weeks to 10.64 +/- 0.17 and 7.68 +/- 0.64% at 40 weeks. The caudal artery and mesenteric resistance vessels showed no significant increase in the percentage of 4N (tetraploid) cells in the SHR from 12 weeks (6.80 +/- 0.92 and 6.10 +/- 0.75%) to 40 weeks (7.83 +/- 0.67 and 7.57 +/- 0.07%). Similarly, there was no significant change in ploidy in these arteries of the WKY. Hence, while polyploidy of SMCs increases in the aorta and superior mesenteric artery of the rat with increasing age and with duration of hypertension, there is no significant change in the number of polyploid cells in smaller vessels such as the caudal artery or mesenteric resistance vessels. Since it is the resistance vessels that are involved in the development and maintenance of hypertension, polyploidy of SMCs in the blood vessel wall appears to hold little relevance to the etiology of this disease. As well, increased incidence of polyploidy is not directly attributable to increases in blood pressure as the caudal artery has a high systolic pressure in the SHR yet the incidence of polyploid cells in this artery does not differ from that of the WKY.

Aging↗

Cardiac mass and peripheral vascular structure in hydralazine-treated spontaneously hypertensive rats.

We have examined the effect of antihypertensive treatment on heart weight and on structural and functional characteristics of isolated mesenteric resistance vessels (internal diameter 170-220 micron) in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto rats (WKY). The SHR and WKY were treated with hydralazine from the age of 4 weeks and were examined at ages 12 to 14 weeks and 23 to 27 weeks. Treated SHR had a mean blood pressure as much as 29% below that of control WKY, which in turn was 25 to 40% less than that of control SHR. In 12- to 14-week-old rats the heart to body weight ratio (which in control SHR was 13% greater than of WKY) was unaffected by treatment. Thereafter, the heart to body weight ratio of treated SHR did not increase as much as usual. At both ages, the media thickness and contractile response of the resistance vessels of the SHR (which were, respectively, 37% and 30% greater than those of vessels of WKY) were unaffected by treatment. However, because treatment caused a small (8%) increase in the lumen diameter of the vessels of the SHR, treatment did cause small, but possibly physiologically important, decreases both in the media to lumen ratio (11%) and in the pressure against which these vessels would have been able to contract (10%). Treatment had little effect on the pharmacological characteristics of vessels of either SHR or WKY. The results suggest that the increased heart weight, media thickness, and contractile response in mesenteric resistance vessels of SHR up to ages 23 to 27 weeks are due primarily to factors other than increased pressure.

Aging↗

Inflammatory changes in permeability and ultrastructure of single vessels in the frog mesenteric microcirculation.

1. In fifteen experiments, single microvessels in the exposed mesenteries of pithed frogs were perfused with Ringer solutions containing bovine serum albumin (40 mg ml-1). For each vessel, the hydraulic permeability of its walls (Lp) and effective osmotic pressure exerted across them (sigma delta pi) were determined from measurements of fluid filtration rates at two capillary pressures (Michel, Mason, Curry, Tooke & Hunter, 1974) before and at predetermined times after the tissue temperature had been raised abruptly from approximately 15 degrees C to 30-35 degrees C. Temperatures greater than 30 degrees C appear to damage the tissues of frogs acclimatized to temperatures of 5-10 degrees C. 2. In fourteen out of fifteen experiments Lp rose when the temperature was raised to 30-35 degrees C. In twelve of these experiments the increase in Lp was greater than expected from the fall in water viscosity with temperature, and was progressive. In five vessels where measurements were made 1-2 min after tissue temperature was raised, Lp increased from an initial mean value (+/- S.E.M.) of 3.76 (+/- 0.54) x 10(-3) micron s-1 cmH2O-1 to one of 8.72 (+/- 1.68) x 10(-3) micron s-1 cmH2O-1. In nine vessels where measurements were made at 10 min after tissue temperature was raised, Lp increased from an initial mean value of 4.03 (+/- 0.72) x 10(-3) micron s-1 cmH2O-1 to one of 16.9 (+/- 3.5) x 10(-3) micron s-1 cmH2O-1. Further increases in Lp were seen at 15 and 20 min. 3. The changes in the effective osmotic pressure opposing filtration, sigma delta pi, were very variable. Out of the twelve vessels which showed large changes in Lp with tissue heating, four showed no reduction in sigma delta pi after 10 min, though sigma delta pi fell in three of these vessels at 15 min. In the other eight vessels, sigma delta pi fell as Lp rose. A quantitative theory developed in this paper allowed the changes in sigma delta pi to be analysed in terms of a component across the regions of vessel wall of increased permeability (sigma H delta pi H) and a component across regions where Lp was unchanged. In six vessels sigma H delta pi H approximated to zero; in two vessels sigma H delta pi H was 6.2 and 4.5 cmH2O.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Increased concentration of leukotriene B4 but not thromboxane B2 in intestinal lymph of cats during brief ischemia.

Mesenteric ischemia stimulates both A delta- and C-fiber afferents to reflexly activate the cardiovascular system. Leukotriene B4 (LTB4) concentration is increased in intestinal mucosa following prolonged ischemia (3 h) followed by reperfusion. Because LTB4 sensitizes afferent nerve endings in the skin, we determined whether LTB4 is produced during brief mesenteric ischemia and thus would be present to sensitize afferent nerve endings in the abdominal visceral region. Cannulas were placed in the portal vein and in a mesenteric lymphatic vessel distal to the lymph node. Mesenteric lymph and portal venous immunoreactive LTB4 (iLTB4) and immunoreactive thromboxane B2 (iTxB2) concentrations were measured before, during, and after 5-7 min of ischemia induced by occlusion of the descending thoracic aorta in cats. Simultaneously, lymph and plasma lactate concentrations were measured. During arterial occlusion, femoral arterial pressure dropped to less than 30 mmHg, and portal venous and mesenteric lymph lactate concentrations were increased significantly (3.3 +/- 0.6 to 6.3 +/- 1.0 mM and 5.2 +/- 0.9 to 7.2 +/- 1.1 mM, respectively, P less than 0.05). During ischemia, iLTB4 concentration increased in lymph from 261 +/- 70 to 424 +/- 102 pg/0.1 ml (P less than 0.05) but did not increase in portal venous blood (135 +/- 26 vs. 168 +/- 44 pg/0.1 ml, control vs. ischemia). iTxB2 concentration was not increased during ischemia in either portal venous blood or lymph (12 +/- 4 to 24 +/- 9 pg/0.1 ml and 19 +/- 7 to 24 +/- 11 pg/0.1 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Changes in intestinal vascular diameter during norepinephrine vasoconstrictor escape.

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.

Animals↗

Nerve evoked P2X receptor contractions of rat mesenteric arteries; dependence on vessel size and lack of role of L-type calcium channels and calcium induced calcium release.

1. Contractile responses to short trains of nerve stimulation have been characterized in small, medium and large arteries from the rat mesenteric circulation (5th - 6th, 2nd - 3rd and 1st order, respectively). In addition, sources of calcium for smooth muscle contraction have been investigated. 2. Nerve stimulation (10 pulses at 10 Hz) evoked reproducible contractions. The P2 receptor antagonist suramin (100 microM) reduced constrictions by 65.3+/-7.4, 82.7+/-3.3 and 3.1+/-6.1% in small, medium and large arteries respectively. The alpha-adrenoceptor antagonist prazosin (0.1 microM) reduced responses by 32.6+/-2.6, 27.0+/-1.5 and 97.0+/-1.9% respectively. 3. The L-type calcium channel antagonist nifedipine (1 microM) reduced nerve-evoked contractions by 2.8+/-3.3, 10.0+/-3.7 and 13.5+/-2.7% in small, medium and large arteries respectively. When the adrenergic component of contraction was blocked by prazosin (0.1 microM) nifedipine reduced responses by 4.6+/-7.9, 14.3+/-2.0 and 3.0+/-1.9% respectively. Contractile responses to exogenous alpha,beta-meATP were unaffected by the depletion of calcium stores with cyclopiazonic acid (30 microM). This indicates that mobilization of calcium from internal stores is not required for P2X receptor mediated smooth muscle contraction. We conclude that for neurogenic responses, the P2X receptor mediated component of constriction dominates in small mesenteric arteries (3rd -- 6th order) while in large arteries (1st order) noradrenaline mediates contraction. For P2X receptor mediated responses all the calcium required for smooth muscle contraction enters the cell directly through P2X receptor channels.

Animals↗

Effect of pentobarbital anesthesia and surgery on the control of arterial pressure and mesenteric resistance in cats: role of vasopressin and angiotensin.

We compared the effects of pentobarbital-induced anesthesia and major surgery (laparotomy) on the mesenteric resistance vessels and arterial pressure of cats. Intravenous infusion of sodium pentobarbital (30 mg/kg over 30--60 min) into conscious and unrestrained cats caused only a small increase in superior mesenteric arterial conductance and a small fall in femoral arterial pressure. In contrast to the effects of pentobarbital, major surgery caused marked mesenteric vasoconstrictor and pressor responses. Under these conditions, acute hypophysectomy and infusion of [Sar1, Ala8]angiotension II (saralasin) caused mesenteric conductance and arterial pressure to return towards presurgery control values. The results suggest that the high arterial pressure and constricted state of the mesenteric bed seen in acute experiments appears to be related to surgical stress rather than pentobarbital-induced anesthesia and that both the vasopressin system and the renin-angiotensin system appear to play important roles in the control of arterial pressure and the mesenteric resistance vessels under these conditions.

Anesthesia↗

[Clinical study of the imaging validity in detecting infiltration of the mesenteric-portal axis in pancreatic carcinoma].

The authors examine the value of different imaging techniques (CT, MRI) in the diagnosis of the involvement of the mesenteric-portal vessels in the pancreatic cancer. In 20 jaundiced patients they obtained in all cases a correct diagnosis about the etiology of the jaundice. The correspondence of the preoperative imaging study with the involvement of the mesenteric-portal vessels was respectively 73% for the CT and 78% for the MRI. In all cases the intra-operative echography allowed a correct diagnosis of the vascular involvement.

Humans↗

Influence of patient positioning on sensitivity of mesenteric portography for detecting an anomalous portosystemic blood vessel in dogs: 34 cases (1997-2000).

OBJECTIVE: To determine whether sensitivity of detecting an anomalous portosystemic blood vessel during operative mesenteric portography varied with patient positioning. DESIGN: Retrospective study. ANIMALS: 34 dogs with a portosystemic shunt diagnosed via scintigraphy or surgery. PROCEDURE: Portograms were evaluated for a portosystemic blood vessel. Sensitivity was calculated from results obtained with dogs in left lateral, right lateral, and dorsal recumbency and from results obtained with dogs in 2 or 3 positions. Differences in sensitivity among positions and between 2 examiners were evaluated. RESULTS: Sensitivity was 85, 91, and 100% in dorsal, right lateral, and left lateral recumbency, respectively. Sensitivity was lower in dorsal recumbency than in left lateral recumbency, although differences were not significant. There was no significant difference between sensitivity of results obtained in dorsal and right lateral recumbency or right lateral and left lateral recumbency. Sensitivity for combined right lateral and dorsal positions was 97%, which was better than that in dorsal recumbency alone, although the difference was not significant. Because sensitivity in left lateral recumbency was 100%, there was no need to evaluate the improvement obtained by combining the result of this position with the results of other positions. CONCLUSION AND CLINICAL RELEVANCE: Results of mesenteric portography varied with patient positioning. The optimal position varied among patients but left lateral recumbency may be better and dorsal recumbency worse. Sensitivity may be improved by performing the test with the patient in orthogonal recumbent positions.

Animals↗