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PubMed1998

Typology of abdominal arteries, with special reference to inferior phrenic arteries and their esophageal branches.

Origins and distribution of the human inferior phrenic arteries were studied by dissecting 68 Japanese adult cadavers. The inferior phrenic arteries were usually observed as paired (left and right) vessels. Their origins were summarized as follows: a) the aorta itself (85/138 cases, 61.6%), b) the ventro-visceral arteries (celiaco-mesenteric system of the aorta) including the celiac trunk (39/138 cases, 28.2%) and the left gastric artery (4/138 cases, 2.9%), and c) the latero-visceral arteries (adreno-renal system of the aorta) including the middle adrenal artery (4/138 cases, 2.9%) and the renal artery (6/138 cases, 4.3%). The left and right arteries occasionally originated in common trunk from the aorta, celiaco-mesenteric system or adreno-renal system (22/138 cases, 15.9%). A typological diagram explaining these variations is given. The inferior phrenic arteries, especially the left ones, sometimes issued visceral or esophageal branches. This fact indicates that the inferior phrenic arteries are homologous with the celiac trunk and mesenteric arteries. It is further discussed that the celiac trunk and mesenteric arteries are originally paired vessels, through introduction of our previous typological diagram of the abdominal arteries.

Abdomen↗
PubMed1996

Pharmacological characterization of the ETA receptor in the vascular smooth muscle comparing its analogous distribution in the rat mesenteric artery and in the arterial mesenteric bed.

The potency of ET-1, ET-2, and ET-3 to contract the isolated perfused rat arterial mesenteric bed was 2.73 +/- 0.57, 1.63 +/- 0.32, and 144 +/- 30 nM, respectively. The vasomotor effect of the ETs was slow in onset, persistent but reversible. Sarafotoxin S6b mimicked the ETs with a potency twofold lower than ET-1; sarafotoxin S6c and the C-terminal hexapeptide of ET-1 was inactive. ETH agonists such as IRL-1620 and AGETB-89 were inactive as vasoconstrictors within the range of concentrations examined. Minor chemical modifications of ET-1 amino acids residues in position 7 or 21 decreased significantly the peptide potency; ET-1 analogues with one or none of the disulfide bonds resulted inactive. The vasomotor effect of ETs was blocked in a competitive, reversible, and selective manner by FR 139317 and BQ-123, the latter being about threefold less potent than the former antagonist. The potency of FR 139317 was 20-fold higher to antagonize ET-3 than ET-1, and threefold higher to block ET-2 than ET-1. In strict analogy to FR 139317, BQ-123 was 12-fold more potent to antagonize ET-3 than ET-1, and fourfold more potent to antagonize ET-2 than ET-1. Upon removal of the endothelial cell layer, the vasomotor potency of ET-1 or the antagonist potency of FR 139317 remained unaltered, suggesting that the vasomotor receptors are localized in the arterial smooth muscles. The ET-1-induced vasomotor responses desensitized, an effect not crossed to noradrenaline (NA); perfusion with 10 microM indomethacin did not alter the vasomotor potency of ET-1, excluding the participation of eicosanoids in the arteriolar effects of ET-1. In isolated rings of the rat mesenteric artery, set to record isometric contractions of the circular muscular layer, the potency of the ETs and their structural analogues was as follows; ET-2 = ET-1 = sarafotoxin S6b > ET-3 > sarafotoxin S6c. The C-terminal hexapeptide of ET-1 and [Ala 1,3,11,15]ET-1 were inactive. The ET-1-induced vasoconstriction was antagonized in a concentration-dependent fashion by FR 139317. These results allow to conclude that the ETA receptors present in the arterial mesenteric circulation are localized in the vascular smooth muscle of the large-sized arteries as well as the smaller arterioles and precapillary vessels of the rat arterial mesenteric bed.

Animals↗
PubMed1996

Ultrasonography of hepatic arteries in the portacaval space: celiac versus superior mesenteric artery origin.

A hepatic artery coursing within the portacaval space was seen in 30 (18.3%) of 164 consecutive patients in whom this region was seen with ultrasonography. In 12 subjects (40%) this vessel represented the right hepatic artery arising from the proximal celiac artery. In the other 18 subjects (60%) this vessel arose from the superior mesenteric artery. It should not be assumed that a hepatic artery traversing the portacaval space arises from the superior mesenteric artery until its origin is clearly documented.

Adult↗
PubMed2000

Relaxant effects of carbon monoxide compared with nitric oxide in pulmonary and systemic vessels of newborn piglets.

Nitric oxide (NO) has been implicated in a number of diverse physiologic processes, including regulation of vascular tone. Carbon monoxide (CO) is another endogenously generated diatomic gas that may play an important physiologic role in vascular smooth muscle homeostasis. The purpose of this study was to compare the responses to exogenous NO and CO in isolated vessels (pulmonary arteries, pulmonary veins, and mesenteric arteries) from 12- to 24-h-old and 2-wk-old piglets. Vessels precontracted with the thromboxane A(2) mimetic U46619 (10(-7) M) relaxed in response to CO (2 x 10(-6) to 2 x 10(-4) M) and NO (2 x 10(-9) to 2 x 10(-7) M); these effects were not affected by endothelium removal but were completely abolished by the soluble guanylate cyclase inhibitor ODQ (10(-5) M). In pulmonary arteries, the maximal relaxation to NO increased with postnatal age from 33 +/- 4% of the precontraction value to 56 +/- 5%, in 12- to 24-h-old and 2-week-old piglets, respectively (p < 0.01), but the response to CO decreased from 25 +/- 3% to 12 +/- 1%, respectively (p < 0.01). The maximal response to CO was greater in pulmonary veins than in pulmonary or mesenteric arteries for both age groups (p < 0.01). Vasorelaxation induced by endogenous NO (stimulated by acetylcholine) was also greater in pulmonary veins when compared with pulmonary arteries and increased with postnatal age in both vessels. In contrast, no age-related differences were observed in the vasorelaxation induced by the cGMP analog 8-bromo cGMP in pulmonary arteries. When the response to NO was analyzed under three different extracellular O(2) concentrations (PO(2) 4.51 +/- 0.03, 19. 32 +/- 0.17, and 86 +/- 0.62, kPa), no significant differences were found. However, in the presence of superoxide dismutase (100 U/mL). the response to CO remained unchanged, and the response to NO improved in pulmonary arteries from 2-week-old but not from newborn piglets. In conclusion, both NO and CO relaxed neonatal vessels through soluble guanylate cyclase activation. However, when compared with NO, CO exhibited a poor vasorelaxant activity. Pulmonary vasorelaxation induced by NO increased with postnatal age, whereas that induced by CO decreased. Changes in extracellular oxygen concentration did not alter the pulmonary vascular response to NO. However, the presence of superoxide dismutase improved the response to NO, indicating that oxidant activity limits the vasorelaxant response to NO but not to CO.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

Effects of enalapril and amlodipine on small-artery structure and composition, and on endothelial dysfunction in spontaneously hypertensive rats.

OBJECTIVES: To determine whether an angiotensin converting enzyme inhibitor, enalapril, and a dihydropyridine calcium channel antagonist, amlodipine, regress the altered structure, media composition, and vascular relaxation of small arteries of spontaneously hypertensive rats. METHODS: Spontaneously hypertensive rats aged 10 weeks were treated for 12 weeks with 10 mg/kg per day enalapril or 10-20 mg/kg per day amlodipine and compared with age-matched untreated spontaneously hypertensive rats. Small coronary, renal, mesenteric, and femoral arteries (lumen diameter 200-250 microm) were studied isometrically on a wire myograph, and mesenteric arteries isobarically as pressurized vessels. The composition of the vascular media of the latter was studied by electron microscopy. RESULTS: Blood pressure, and cardiac and aortic hypertrophy were reduced in treated spontaneously hypertensive rats. Treatment significantly decreased media thickness and media: lumen ratio of coronary, renal, mesenteric, and femoral small arteries studied isometrically and of pressurized mesenteric small arteries. Media cross-sectional area was smaller for coronary arteries studied isometrically and mesenteric arteries studied isobarically. Electron microscopic analysis revealed an increase in collagen: elastin ratio in the media of spontaneously hypertensive rat vessels, and a decrease under treatment to levels found in Wistar-Kyoto rats, with no significant changes detected in smooth muscle cells. The amplitude of contractions induced by acetylcholine on wire-myograph-mounted mesenteric arteries from spontaneously hypertensive rats were decreased by treatment, and relaxation of pressurized arteries induced by acetylcholine was normalized. CONCLUSION: Treatment of spontaneously hypertensive rats with enalapril or with amlodipine resulted in regression of cardiovascular hypertrophy and amelioration of endothelial dysfunction. Morphometric results obtained using an isometric myograph and a pressurized preparation to study rat small arteries were closely correlated. Regression of structural remodeling in small arteries was outward hypotrophic, with a reduction in the collagen: elastin ratio, and without net change in the absolute and relative volumes of smooth muscle and number of smooth muscle layers.

Amlodipine↗
PubMed1997

Role of nitric oxide and nitric oxide-independent relaxing factor in contraction and relaxation of rabbit blood vessels.

It has been shown that spontaneous release of nitric oxide (NO) from the vascular endothelium attenuates contractile responses of vascular smooth muscles to norepinephrine, and that acetylcholine-induced relaxation is mediated by the evoked release of NO and endothelium-derived hyperpolarizing factor. Since the involvement of these substances (or factors) in mechanical responses is heterogeneous among blood vessels, we have investigated the role of these substances in agonist-induced contraction and relaxation in 6 rabbit blood vessels. Vascular reactivity for the contractile response to norepinephrine was potentiated after removal of endothelium and by 100 microM N(G)-nitro-L-arginine (L-NA) but not by 80 nM-0.4 microM clotrimazole. This potentiation was most marked in the mesenteric artery among the blood vessels tested, suggesting that the basal release of NO reduced the contractile response of the vascular smooth muscle to norepinephrine in this artery. Acetylcholine-induced relaxation was abolished by removal of the endothelium and was attenuated by L-NA (1-100 microM) in all blood vessels. The attenuation by 100 microM L-NA was most obvious in aorta and vein and least in mesenteric resistance artery in which the acetylcholine-induced, L-NA-resistant relaxation was inhibited by 80 nM-0.4 microM clotrimazole. These results suggested that there is a regional difference in the degree of involvement of NO in acetylcholine-induced relaxation. In mesenteric resistance artery, the NO-independent, clotrimazole-sensitive factor, possibly hyperpolarizing factor may also contribute to the response to acetylcholine at high concentrations.

Acetylcholine↗
PubMed2001

[Differences of nitric oxide synthase expression and activity between splanchnic arterial and venous vessels of cirrhotic rats].

OBJECTIVE: To understand the implication of differences of nitric oxide synthase (NOS) expression and activity between splanchnic arterial and venous vessels in the pathogenesis of portal hypertension. METHODS: Cirrhosis was induced in 100 Wistar rats by subcutaneously administration of carbon tetrachloride. NOS localization, activity and gene expression in the mesenteric artery and the portal vein vessels of both cirrhotic and normal rats were investigated by immunohistochemistry, chemoluminescence and reverse transcription-polymerase chain reaction, respectively. RESULTS: There was inducible NOS enzyme isoform in al1 layers of splanchnic vessels of cirrhotic rats, whereas endothelial NOS isoform largely in vascular endothelia. NOS activity and its mRNA expression all were significantly increased in cirrhotic rats when compared with normal rats (P<0.05 or 0.01).Moreover, the activities of general and constitutive NOS and the expression of endothelial NOS mRNA in cirrhotic rats were significantly higher in the mesenteric artery than in the portal vein (P<0.01). CONCLUSIONS: Enhanced expression and activity of endothelial NOS enzyme isoform may be mainly responsible for increased NO production of splanchnic vessels in cirrhotic rats, and the differences of NOS expression and activity between the mesenteric artery and the portal vein vessels may be one of the pathogeneses of portal hypertension in which NO might be involved.

Animals↗
PubMed1992

Calcifications in the portal venous system: comparison of plain films, sonography, and CT.

We describe 10 patients with long-standing portal hypertension and calcifications in the splenoportal and mesenteric venous systems or collateral vessels. The patients were examined with abdominal plain films (n = 10), sonography (n = 10), and CT (n = 9). Calcium was seen on CT scans in nine cases, on sonograms in seven, and on abdominal plain films in five. Calcifications appeared to be located in the wall of the vein in all cases. Sites of detection included the main portal, splenic, superior mesenteric, coronary, and peripancreatic veins. CT was more sensitive than sonography, and both were more sensitive than plain films, in showing portal venous calcification. Detection of such calcifications may influence surgical or percutaneous therapy of portal hypertension.

Aged↗
PubMed2002

Superior mesenteric artery-to-renal artery bypass: a rare but useful alternative for renal artery revascularization.

The aorta, celiac axis, and iliac arteries are the most common inflow arteries used for renal revascularization. When these inflow vessels are diseased, the superior mesenteric artery (SMA) can be an alternative source of renal artery graft inflow. Previous reports have suggested that only an enlarged SMA should be used for this purpose, for fear of developing mesenteric ischemia. We report a patient who required renal artery revascularization with a saphenous vein graft from a normal-caliber SMA who did not develop subsequent mesenteric ischemia. The procedure was unique in demonstrating that the SMA can be used as a viable source of graft inflow even when it is anatomically normal.

Aged↗
PubMed1988

Mesenteric arteriovenous shunt associated with thrombosis of the portal venous system: case report.

We report a rare case of mesenteric arteriovenous shunt associated with thrombosis of the portal venous system. The angiographic features consisted of new vessel formation, thrombosis of the main portal vein, superior mesenteric vein and branches, and early filling of distal mesenteric veins with hepatopetal collateral flow. This phenomenon may be due to new vessel formation within the portal vein thrombosis and active lysis of the thrombus exposing the organizing vessels to the distal superior mesenteric veins.

Arteriovenous Fistula↗
PubMed2003

The effects of nifedipine and thapsigargin on the responses of pressurized rat mesenteric artery to 5-hydroxytryptamine and norepinephrine.

The responses of isolated pressurized second order mesenteric resistance arteries of Wistar rats, superfused with physiological salt solution (PSS) were determined to 5-hydroxytryptamine (5-HT) and norepinephrine (NE). The contractility of the vessel was enhanced in response to 5-HT compared to NE (P<.001, ANOVA). The L-type calcium ion channel blocker, nifedipine (10(-6) M) abolished the response to either 5-HT or NE. In vessels with intact endothelium, thapsigargin (TG, 10(-6) M), which inhibits uptake of calcium ions into intracellular stores, significantly reduced the contractile response to 5-HT (P<.02) but had little or no effect on the response to NE (P=.2). However, in vessels denuded of the endothelium, there was no significant difference in the response of the mesenteric artery, after TG, to either 5-HT or NE. The results indicate that, in the rat mesenteric resistance vessel, both 5-HT and NE use calcium ions from extracellular sources for contraction, while NE relies mainly on extracellular ion influx with little or no contribution from intracellular sources. The reduced response of the de-endothelized vessel to 5-HT after TG suggests that the utilization of intracellular stores by this agonist is endothelium-dependent. These observations may explain the enhanced responsiveness of the mesenteric artery to 5-HT when compared with NE.

Animals↗
PubMed1993

CT of the mesocolon. Part 1. Anatomic considerations.

To define the anatomy of the mesocolic attachment of the colon as seen on computed tomographic (CT) scans, the authors reviewed CT scans of patients with diseases of the colon and the pancreas and found that disease processes in these areas usually spread along the mesocolon. The plane of the mesocolon can be distinguished from the mesentery of the small bowel by identifying the vessels in the mesocolon that serve as its landmarks. These vessels include the ileocolic vessels and right colic vessels for the ascending mesocolon, the middle colic vessels for the transverse mesocolon, and the inferior mesenteric vein for the sigmoid and descending mesocolon. These vessels can be seen routinely on CT scans of the abdomen and pelvis, and knowledge of the anatomy of the mesocolon can help the radiologist understand and identify the pathways for spread of diseases of the colon and pancreas. Recognition of the anatomy of the mesocolon is also helpful in the identification of the pattern of recurrent disease after treatment.

Cecum↗
PubMed1993

[An autopsy case of severe portal hypertensive gastropathy associated with a large shunt from superior mesenteric to left renal vein in a patient with alcoholic liver cirrhosis].

We report an autopsy case of severe portal hypertensive gastropathy with a large shunt from the superior mesenteric to left renal vein in a patient with alcoholic liver cirrhosis. A 60-year-old man with alcoholic cirrhosis was admitted for tarry stool and ascites. Endoscopic finding revealed multiple red spots and hemorrhagic gastritis at prepylorus of the stomach. Angiography showed a large shunt vessel originating from the superior mesenteric to left renal vein. He died of hepatic failure and DIC following frequent gastrointestinal bleeding. At autopsy, the stomach showed marked congestion of the capillary vessels in the tunica propria mucosa. This finding showed that the gastropathy resulted in the congestion of the gastric veins connecting with the large shunt vessel.

Disseminated Intravascular Coagulation↗
PubMed1987

Vascular compromise in chronic volvulus with midgut malrotation.

Three cases of chronic volvulus of the small bowel in midgut malrotation are presented, all of whom manifested similar angiographic findings: proximal occlusion of the superior mesenteric artery and vein and development of collateral vessels. These findings may indicate the pathophysiology of chronic volvulus in midgut malrotation; the volvulus is progressive and eventually results in the twisting of the mesenteric root itself, but because of its chronic nature collateral circulation develops, eliminating bowel necrosis. Computed tomography (CT), performed in two cases, revealed dilated, tortuous vessels in the mesentery in addition to the known CT finding of a whirl-like pattern of the volvulated small bowel loops. Sonography, performed in one case, showed an unique feature of whirling sonolucent layers probably representing the volvulated small bowel loops intermixed with dilated mesenteric collateral vessels. We would like to emphasize the usefulness of CT and sonography in the early diagnosis of those cases with vague and nonspecific clinical manifestations.

Adolescent↗
PubMed1998

Doppler waveforms of the normal and collateralized inferior mesenteric artery.

OBJECTIVE: Our purpose was to analyze Doppler waveform changes and the caliber of the inferior mesenteric artery as a collateral vessel in occlusive disease of the abdominal aorta or its main branches. SUBJECTS AND METHODS: Thirty-three patients were examined in three groups according to the location of their occlusive disease (group 1 [n = 5], occlusion of the celiac and superior mesenteric arteries; group 2 [n = 9], occlusion of the iliac artery; and group 3 [n = 19], occlusion of the abdominal aorta distal to the renal arteries). The main truncus of the inferior mesenteric artery was evaluated along its longitudinal axis using color duplex Doppler sonography. Peak systolic velocity, end-diastolic velocity, mean velocity, resistive index, and pulsatility index were determined from the Doppler spectrum. The inner diameter and cross-sectional area of the inferior mesenteric artery were measured, and blood flow volume was calculated. The data obtained from the three groups were compared with data from a control group (n = 24). RESULTS: In all three patient groups, the mean blood flow volume and the mean flow velocities were significantly higher, the mean pulsatility index was significantly lower, and the mean diameter of the vessel was significantly larger than in the control group. The blood flow volume in patients with aortic occlusion was significantly lower than that in patients with superior mesenteric artery occlusion. In the patients with iliac artery occlusion, the mean resistive index was not significantly different from that in the control group. CONCLUSION: An increase in blood flow volume and the presence of a monophasic waveform indicate increased collateral function of the inferior mesenteric artery. However, blood flow volume in patients with aortic occlusion does not increase as high as in patients with superior mesenteric artery occlusion, and a monophasic waveform is not a distinctive finding in iliac artery occlusion.

Aortic Diseases↗
PubMed1983

[Diagnosis of dissecting aortic aneurysm by digital subtraction angiography].

The aim of the study was to determine whether digital subtraction angiography (DSA) can be used in the diagnosis of aortic dissection. The study group consisted of six patients with aortic dissection including one of type 2 and five of type 3 by the DeBakey classification. DSA findings were compared to cineangiographic findings. The results were as follows; In all the patients, the diagnosis of aortic dissection was possible using DSA. Especially as to the entry, which was not detected by other non-invasive methods, there was an excellent correlation between cineangiograms and DSA (sensitivity 100%). Of the 20 vessels in the abdomen, which included the celiac, superior mesenteric, and right and left renal arteries, three vessels (15%) were not identified by DSA. Causes of the failure were the low spatial resolution and the artifact due to the motion of the patients and intestinal gas movement. The accuracy rate of the abdominal branch involvement was 70%. While using a prototype equipment, the preliminary study showed that DSA is a safe and very useful method not only for diagnosing aortic dissection, but for evaluation of the entry, extension of the dissection, and involvement of major branches of the abdominal aorta and for a follow-up study.

Adult↗
PubMed1995

Antihypertensive effect of an endothelin receptor antagonist in DOCA-salt spontaneously hypertensive rats.

1. Endothelin-1 gene expression is enhanced in aorta and mesenteric arteries, and possibly other vessels, of deoxycorticosterone acetate (DOCA)-salt hypertensive rats but is normal or reduced in spontaneously hypertensive rats (SHR). Bosentan, a mixed ETA/ETB endothelin receptor antagonist, blunts the development of elevated blood pressure of DOCA-salt hypertensive rats but not in SHR. In this study we investigated whether treatment of DOCA-salt SHR with bosentan would result in blunted rise in blood pressure. 2. SHR, aged 13 weeks, were implanted with silastic containing DOCA and offered 1% saline to drink. Systolic blood pressure was measured by the tail-cuff method. Endothelin-1 mRNA abundance in aorta and mesenteric arteries was measured by Northern blot analysis. Content of immunoreactive endothelin in blood vessels was measured by radioimmunoassay. 3. Systolic blood pressure rose less in bosentan-treated DOCA-salt SHR (to 223 +/- 2 mmHg) in comparison to the untreated rats (241 +/- 1), a small but significant difference (P < 0.001). However, blood pressure of bosentan-treated DOCA-salt SHR was still higher than in age-matched SHR. Endothelin-1 mRNA abundance and content of immunoreactive endothelin were increased in the aorta and the mesenteric arterial bed of DOCA-salt SHR, and were unaffected by treatment with bosentan. 4. These data support the hypothesis of a role of endothelin-1 in blood pressure elevation in this hypertensive model with malignant hypertension. They also support the hypothesis that an antihypertensive effect of the mixed ETA/ETB endothelin receptor antagonist, bosentan, is found when experimental hypertensive animals exhibit enhanced endothelin-1 gene expression in blood vessels.

Animals↗
PubMed1993

Persistent hypertension following inhibition of nitric oxide formation in the young Wistar rat: role of renin and vascular hypertrophy.

OBJECTIVE: To determine whether induction of arterial hypertension in young normotensive Wistar rats by chronic inhibition of nitric oxide production with NG-nitro-L-arginine methyl ester (L-NAME) produced a form of self-sustained hypertension, and to investigate the role of the renin-angiotensin system and vascular hypertrophy in the hypertensive process. METHODS: Three-week-old Wistar rats were given 100 or 40 mg/kg per day L-NAME or 40 mg/kg per day L-NAME plus 100 mg/kg per day captopril in their drinking water for between 4 and 7 weeks. Systolic blood pressure was measured by tail-cuff plethysmography both during treatment and after the treatment had been stopped. The effect of treatment on plasma renin was measured and the effect of treatment on mesenteric resistance artery structure was determined using a small-vessel myograph. RESULTS: L-NAME produced a progressive and marked increase in blood pressure during the period of treatment. Hypertension was sustained for 14 weeks after stopping treatment. L-NAME resulted in a fourfold increase in plasma renin which remained elevated after treatment was stopped. Blood pressure was correlated with plasma renin levels. Treatment with L-NAME plus captopril markedly attenuated the rise in blood pressure and captopril also produced a marked fall in blood pressure in rats that developed persistent hypertension. Rats with self-sustained hypertension exhibited both cardiac and mesenteric resistance vessel hypertrophy. The induction of vascular hypertrophy with low-dose L-NAME did not result in the development of self-sustained hypertension. CONCLUSIONS: Chronic L-NAME treatment in young rats can produce a form of persistent hypertension which is renin-dependent and which does not seem to involve a vascular amplifier mechanism.

Animals↗