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PubMed1994

Comparison of acetylcholine-dependent relaxation in large and small arteries of rat mesenteric vascular bed.

The relative contributions of nitric oxide (NO) to in vitro relaxation responses elicited by acetylcholine (ACh) were compared in vessels of different sizes from the rat mesenteric vascular bed. ACh elicited an endothelium-dependent relaxation in phenylephrine-contracted superior mesenteric arteries (SMA, unstretched luminal diam 650 microns), which was blocked by compounds that inhibited NO, such as hemoglobin (10 microM), methylene blue (10 microM), and NG-monomethyl-L-arginine (1 mM). In contrast, the endothelium-dependent relaxation induced by ACh in phenylephrine-contracted mesenteric resistance arteries (MRA, unstretched luminal diam 200 microns) was not blocked by hemoglobin, methylene blue, or NG-monomethyl-L-arginine. KCl (25 mM) partially inhibited the ACh-dependent relaxation in MRA. Furthermore, the ACh-dependent relaxation in MRA was selectively inhibited by the Ca(2+)-activated K+ channel blocker charybdotoxin (0.1 microM). In contrast, the ATP-sensitive K+ channel blocker glibenclamide (50 microM) did not block the ACh-dependent relaxation in MRA. We conclude that 1) NO is a major component of the ACh-dependent relaxation in SMA and 2) the ACh-dependent relaxation of MRA is resistant to NO inhibitors but sensitive to a Ca(2+)-activated K+ channel blocker. This suggests that an endothelium-derived hyperpolarization factor may be involved in the relaxation of MRA.

Acetylcholine↗

PubMed1989

Comparison of peptidergic mechanisms in different parts of the guinea pig superior mesenteric artery: immunocytochemistry at the light and ultrastructural levels and responses in vitro of large and small arteries.

The presence and distribution of peptide-containing nerve fibres and axon terminals have been studied in the proximal part of the superior mesenteric artery (SMA) (i.e. conductance vessel) and in the finer ramifications of the SMA close to the intestine (outer diameter 200 microns, i.e. resistance vessel). Light microscopic immunocytochemistry revealed that the proximal part of the SMA possessed a rich supply of neuropeptide Y (NPY)- and tyrosine hydroxylase (TH)-immunoreactive nerve fibres, forming a loose perivascular network which increased in density distally. The vasoactive intestinal peptide (VIP) immunoreactivity was moderate in the proximal artery and only a few VIP fibres could be identified in the distal portion of the SMA. Calcitonin gene-related peptide (CGRP)-, neurokinin (NK)- and substance P (SP)-immunoreactive fibres had an intermediate density in both arterial regions, but their distribution pattern varied. Electron microscopic immunocytochemistry showed that NPY-immunoreactive nerve terminals were close to the smooth muscle cells of the medial layer in both parts of the SMA, indicative of a vasomotor role. Although the VIP-immunoreactive terminals had a similar localization they were seen less frequently. CGRP-, NK- and SP-immunoreactive axons had an identical distribution in the two vascular regions. Interestingly, they were usually seen more distant from the medial layer, localized in the adventitia. Examination of vasomotor responses to perivascular peptides revealed significant regional differences: NPY produced only weak contractions (13 +/- 3%) of proximal vessel segment of the conductance type, while strong concentration-dependent contractions were seen in distal parts of the SMA (resistance vessel). In neither region was any interaction with noradrenaline demonstrated. Proximal segments of the SMA revealed a stronger and more potent response to VIP and peptide histidine isoleucine than did distal segments, while on the other hand acetylcholine was more potent and elicited stronger effects in distal segments. CGRP, NKA and SP relaxed precontracted arteries by 50-75% and there was no significant difference in responsiveness to these peptides in the two regions of the SMA.

Animals↗

PubMed1969

The effects of endotoxin on vascular endothelium.

This study was undertaken to develop a technique for the preparation of sheets of endothelial cells and to investigate the effects of bacterial endotoxin on large numbers of cells from continuous sheets of vascular endothelium. Rabbits were divided into one control and two experimental groups. The experimental animals received intracardially an LD(50) dose of Escherichia coli endotoxin. 1 and 24 hr postinjection, the vessels of the animals were perfused with glutaraldehyde in Millonig's buffer with methylene blue as a marker. Pieces of mesentery containing arteries were postfixed in buffered glutaraldehyde, dehydrated, and placed in acetone (to remove fat deposits). The surrounding connective tissue was stripped from the mesenteric arteries, and segments of the vessels were slit longitudinally, flattened out, and firmly affixed to a sheet of cork with fine mounting pins. A 3% solution of Formvar in ethylene dichloride was pipetted onto the luminal surfaces of the vessels. The endothelial cells were impregnated with and adhered to the Formvar and, after soaking overnight in 10 N NaOH, could be stripped from the vessel walls as monolayers. Sheets of Formvar-impregnated cells were temporarily mounted on glass slides in aqueous methylene blue and examined by phase and bright-field microscopy. Methylene blue stained the nuclei a deep blue and the cytoplasm faintly, but cell outlines were indistinct. Endothelial sheets from control rabbits had smooth, elliptical nuclei oriented parallel to the longitudinal axis of the cells and irregularly distributed over a smooth background with faint longitudinal striations. Essentially every cell in endothelial sheets from endotoxin-injected animals appeared to be severely damaged. Cell sheets from 24 hr posttreatment animals exhibited the same type of, but more extensive, damage than that observed in 1 hr posttreatment animals. The most prominent features of the damaged endothelium were distorted nuclei, apparent nuclear vacuolization, and missing nuclei. Unstained platelets and plaques were present on the surfaces of the specimens from the experimental animals only. Stained and unstained red blood cells were also dispersed over the luminal surfaces of the endotoxin-treated vessels.

Animals↗

PubMed1992

Effects of enalapril and hydralazine treatment and withdrawal upon cardiovascular hypertrophy in stroke-prone spontaneously hypertensive rats.

OBJECTIVE: To test the hypothesis that effects of angiotensin converting enzyme (ACE) inhibitors upon resistance vessel structure are responsible for their ability to cause long-term reduction in blood pressure. DESIGN: Stroke-prone spontaneously hypertensive (SHRSP) and Wistar-Kyoto (WKY) rats were treated with enalapril or hydralazine from 4 to 15 weeks of age. Effects upon tail-cuff blood pressure, left ventricular hypertrophy and structural indices of the superior mesenteric artery (SMA) and its resistance vessels were assessed at 11 weeks of treatment and up to 11 weeks post-treatment. METHODS: Left ventricular hypertrophy was assessed by left ventricular weight:body weight ratios. Evidence of vascular structural change was obtained from tissue weight:body weight ratios, levels of RNA, DNA and expression of alpha-actin and elastin messenger (m)RNA. RESULTS: The effects of enalapril and hydralazine upon left ventricular hypertrophy in SHRSP were consistent with their respective effects upon blood pressure. Both drugs prevented the development of medial hypertrophy in SMA and resistance vessels. This was accompanied by substantial reductions in RNA:DNA ratios. Alpha-actin mRNA levels were not affected by either drug but elastin mRNA levels were reduced by both drugs. During the first 12 days post-treatment there was evidence of structural change in SMA accompanying the increases in blood pressure but importantly not in the resistance vessels. CONCLUSION: The effects of enalapril upon left ventricular hypertrophy and mesenteric arterial hypertrophy are totally consistent with responses to blood pressure and the persistence of structural changes post-treatment does not underlie the ability of the ACE inhibitors to persistently suppress hypertension.

Animals↗

PubMed1991

Calcium dependence of effects of endothelin on rat mesenteric microvessels.

We investigated the calcium dependence of the effects of endothelin (ET) on resistance vessels (less than 300 microns lumen diameter) from the mesenteric vascular bed of the rat, mounted on a wire myograph. ET-1 induced a potent sustained contraction with an ED50 of 12 nmol/L. The response to ET-3 and big ET at the maximum concentrations used (100 nmol/L) was less than 40% of that to ET-1, with an estimated ED50 of 45 nmol/L. Relaxation of the ET-1-induced contraction was slow, and resulted in a reduction of the maximum response to a second challenge with ET-1 to 60% of the initial contraction after 3 h. Long-lasting tachyphylaxis to arginine vasopressin (AVP) induced contraction also occurred. The response to 100 nmol/L ET-1 produced an active tension 88% greater than that induced by 124 mmol/L KCl, and similar to that produced by norepinephrine and AVP. The response to 100 nmol/L ET-1 in the absence of calcium + 1 mmol/L EGTA in the medium for 30 min resulted in a maximum contraction of 43% of the response in the presence of calcium, followed by a faster relaxation rate. The addition of calcium produced a further contraction, and stimulation with 100 nmol/L ET-1 at this point did not result in further response. The calcium channel blocker nitrendipine in concentrations of 1-10 mumol produced increasing reductions of the responses to 100 nmol/L ET-1 to 35% at the higher concentration. Nitrendipine (3 mumol/L) partially blocked the response to calcium after ET-1 was added in the absence of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Morphology of the constricted arteriolar wall: physiological implications.

Microvessels undergo complex shape changes during constriction that could have profound implications for control of resistance. We exploited in vitro cannulation techniques in combination with electron microscopy to assess the effects of physiological degrees of vasoconstriction on the size and form of the lumen of isolated rat mesenteric arterioles. Photomicrographs of vasoconstricted vessels revealed that the luminal surface is folded and thrown into longitudinal ridges several hundred microns long. These ridges begin to form and encroach on the lumen as the vessel is constricted. Ridge height may increase to 5-10 microns, and as many as 50 ridges were observed around the circumference of a 70-microns vessel. Ridges are comprised of endothelial cells, basal elastic lamina, and portions of the smooth muscle cytoplasm including thick filaments. The ridges are major determinants of the relationships among stress on smooth muscle contractile elements, intraluminal pressure, and luminal diameter. The ridges may also limit the precision of measurement of microvessel diameter in situ since it is not known whether the apex or the base of the ridge is measured under typical conditions of in vivo microscopy. Our findings emphasize the need for additional detailed study of wall morphology to fully understand the regulation of microvessel flow resistance by smooth muscle function.

Animals↗

PubMed1997

Structural properties of rat mesenteric small arteries after 4-wk exposure to elevated or reduced blood flow.

We determined the structure of mesenteric small arteries after chronic elevation and chronic reduction of blood flow. In 6-wk-old rats, we ligated second-order side branches of every other first-order side branch of the superior mesenteric artery. This persistently reduced blood flow (-90%) in the vessels feeding into the ligated trees and elevated blood flow (+80%) in the nonligated mesenteric artery side branches. Four weeks after surgery, vessels that had been exposed to high blood flow (HF) or low blood flow (LF) and vessels from sham-operated rats (Sham) were isolated and mounted in a pressure myograph system. At an intraluminal pressure of 100 mmHg, the internal diameter at rest was larger in HF (533 +/- 23 microm) and smaller in LF (262 +/- 14 microm) than in Sham vessels (427 +/- 15 microm). Also, wall and media cross-sectional areas were larger in HF and smaller in LF than in Sham vessels (media: 22 +/- 1, 11 +/- 2, and 16 +/- 1 x 10(3) microm2, respectively), but circumferential wall stress did not differ among groups. DNA content was significantly increased in HF vessels (+100%) and was not modified in LF vessels. Maximal vasoconstrictions elicited by high potassium or norepinephrine were slightly increased in HF vessels but were reduced by 50% in LF vessels. Thus chronic changes in blood flow give rise to structural changes that normalize circumferential wall stress. Elevated blood flow resulted in outward hypertrophic remodeling involving hyperplasia. Reduced blood flow resulted in inward hypotrophic remodeling accompanied by hyporeactivity of the arterial smooth muscle.

Animals↗

PubMed2004

Effects of des-aspartate-angiotensin I on the actions of angiotensin III in the renal and mesenteric vasculature of normo- and hypertensive rats.

An earlier study showed that des-aspartate-angiotensin I (DAA-I) attenuated the pressor action of angiotensin III in aortic rings of the spontaneously hypertensive rat (SHR) but not the normotensive Wistar Kyoto (WKY) rat. The present study investigated similar properties of DAA-I in isolated perfused kidneys and mesenteric beds of WKY and SHR. In the renal vasculature, angiotensin III induced a dose-dependent pressor response, which was more marked in the SHR than WKY in terms of significant greater magnitude of response and lower threshold. DAA-I attenuated the pressor action of angiotensin III in both the WKY and SHR. The attenuation in SHR was much more marked, occurring at doses as low as 10(-15) M DAA-I, while effective attenuation was only seen with 10(-9) M in WKY. The effects of DAA-I was not inhibited by PD123319 and indomethacin, indicating that its action was not mediated by angiotensin AT2 receptors and prostaglandins. However, the direct pressor action of angiotensin III in the SHR but not the WKY was attenuated by indomethacin suggesting that this notable difference could be due to known decreased response of renal vasculature to vasodilator prostaglandins in the SHR. Pressor responses to angiotensin III in the mesenteric vascular bed was also dose dependent, but smaller in magnitude compared to the renal response. The responses in the SHR, though generally smaller, were not significantly different from those of the WKY. This trend is in line with the similar observations with angiotensin III and II by other investigators. In terms of the effect of DAA-I, indomethacin and PD123319 on angiotensin III action, similar patterns to those of the renal vasculature were observed. This reaffirms that in the perfused kidney and mesenteric bed, where the majority of the vessels are contractile, femtomolar concentrations of DAA-I attenuates the pressor action of angiotensin III. The attenuation is not indomethacin sensitive and does not involve the angiotensin AT2 receptor. The findings suggest that DAA-I possesses protective vascular actions and is involved in the pathophysiology of hypertension.

Angiotensin I↗

PubMed1988

Comparative healing of mesenteric and antimesenteric incisions in the bovine jejunum.

Paired incisions (n = 6 pairs) were made in the jejunum of each of 8 Holstein cows. Pairs consisted of 2-cm transverse incisions, 35 cm apart, at the antimesenteric region and at the mesenteric region. Bursting-wall tension was used to test mechanical strength, and cellular and vascular events of healing were evaluated using histologic examination and microangiography. Healing was evaluated at postoperative hour (POH) 48 in 4 of the cows (group 1) and at POH 96 in the remaining 4 (group 2). Evidence of leakage of intestinal contents was not found in any of the cows. At POH 48 and 96, bursting-wall tension was significantly (P less than 0.001) greater in the intestinal segments with antimesenteric incisions than in those segments with mesenteric incisions. Disruption of normal vasculature was seen at mesenteric and antimesenteric sites; ingrowth of vessels, reformation of vascular plexuses, and development of collateral circulation were observed at POH 96. Granulation tissue was observed at POH 96 at the antimesenteric and mesenteric sites, and early stages of mucosal reepithelialization were seen in several sections at POH 48. Better apposition of tissue layers was seen in antimesenteric incisions, but mucosal eversion was evident in several mesenteric incisions. Some sections examined from cows at POH 96 had complete bridging of mucosa, submucosa, and muscularis layers at the antimesenteric location. Inflammatory cells were observed along the incision and at the mucosal and serosal surfaces in many of the sections. Deposition of new collagen was not appreciable in any section at POH 48 or 96.

Animals↗

PubMed2001

Comparative effects of the novel vasotocin analogue F-180 vs. vasopressin and terlipressin on systemic and splanchnic isolated vessels from portal hypertensive rats.

F-180 has been proposed as a new vasopressin analogue for the treatment of portal hypertension. This study investigates the contractile profile of F-180 compared to vasopressin and its analogue terlipressin on isolated systemic and splanchnic vessels from sham-operated and partial portal vein ligated (PPVL) rats. F-180 (10(-9)-10(-6) M), vasopressin (10(-11)-10(-8) M) and terlipressin (10(-9)-10(-4) M) induced contraction of the mesenteric vein, aorta, iliac, tail and mesenteric arteries. The order of potency in these vessels was vasopressin (pD2 approximately 9) > F-180 (pD2 approximately 8) > terlipressin (pD2 approximately 6). Significant (P<0.01) differences between sham-operated and PPVL rats were noticed exclusively in the mesenteric vein, being the maximal effect of the three agonists at least twice greater in PPVL rats than in sham-operated rats. The order of sensitivity to the vasoconstrictors in vessels from PPVL rats was aorta < mesenteric artery << iliac artery approximately equal tail artery approximately equal mesenteric vein. The contractile profile of these peptides in each vessel from PPVL animals was quite similar, except in the mesenteric vein and the aorta. F-180 showed higher efficacy (P<0.01) than terlipressin in the mesenteric vein and lower (P<0.05) efficacy than vasopressin in the aorta. These findings suggest the existence of a vasoconstrictor territorial selectivity for vasopressin and its analogues, which could justify the efficacy of these drugs in portal hypertension therapy. In particular, F-180 appears to be a viable alternative to the classic vasopressin analogues.

Animals↗

PubMed2004

Hyperpolarization of murine small caliber mesenteric arteries by activation of endothelial proteinase-activated receptor 2.

Activation of endothelial proteinase-activated receptor 2 (PAR-2) relaxes vascular smooth muscle (VSM) and causes hypotension by nitric oxide (NO)-prostanoid-dependent and -independent mechanisms. We investigated whether endothelium-dependent hyperpolarization of VSM was the mechanism whereby resistance caliber arteries vasodilated independently of NO. VSM membrane potentials and isometric tension were measured concurrently to correlate the electrophysiological and mechanical changes in murine small caliber mesenteric arteries. In uncontracted arteries, the PAR-2 agonist, SLIGRL-NH2 (0.1 to 10 micromol/L), hyperpolarized the VSM membrane potential only in endothelium-intact arterial preparations. This response was unaltered by treatment of arteries with inhibitors of NO synthases (L-NAME), soluble guanylyl cyclase (ODQ), and cyclooxygenases (indomethacin). L-NAME, ODQ, and indomethacin also failed to inhibit SLIGRL-NH2-induced hyperpolarization and of cirazoline-contracted mesenteric arteries. However, in blood vessels that were depolarized and contracted with 30 mmol/L KCl, the effects of the SLIGRL-NH2 on membrane potential and tension were not observed. SLIGRL-NH2-induced hyperpolarization and relaxation was inhibited completely by the combination of apamin plus charybdotoxin, but only partially inhibited after treatment with the combination of barium plus ouabain, suggesting an important role for SKCa and IKCa channels and a lesser role for Kir channels and Na+/K+ ATPases in the hyperpolarization response. We concluded that activation of endothelial PAR-2 hyperpolarized the vascular smooth muscle (VSM) cells of small caliber arteries, without requiring the activation of NO synthases, cyclooxygenases, or soluble guanylyl cyclase. Indeed, this hyperpolarization may be a primary mechanism for PAR-2-induced hypotension in vivo.

Animals↗

PubMed1984

An experimental model of calcification in the vessel wall.

Multiple angiolytic changes of the mesenteric arteries due to administration of vast amounts of Na2EDTA into the peritoneal cavity of guinea pigs have already been demonstrated by Yamaguchi et al. (1981 a, b). In this experiment, one week after Na2EDTA administration calcium lactate was administered in the same manner. As a result calcium deposition was observed in the intimal elastic fibers, in and at the collagenous fibers and intermuscular spaces of lytic and ensuing dilatated areas of the vascular wall. This suggests that dystrophic calcification might be induced by conjugation of calcium ions to the free negative charges of acid mucopolysaccharides (aMPS) which are the main component of the above structural elements.

Aneurysm↗

PubMed1993

Oxygen radicals, lipid peroxidation, and permeability changes after intestinal ischemia and reperfusion.

This study examined the effects of a 21-aminosteroid, U-74389, on lipid peroxidation [determined by plasma and tissue malondialdehyde (MDA) levels], intestinal permeability (plasma-to-luminal clearance of 51Cr-labeled EDTA), and intestinal blood flow (laser Doppler) during and after intestinal ischemia [superior mesenteric artery (SMA) and collateral vessel occlusion for 20 min with atraumatic clip]. Untreated ischemia increased EDTA clearance (from 0.050 +/- 0.005 to 0.169 +/- 0.040 ml.min-1.100 g-1; n = 16, P = < 0.05), reduced SMA flow 88% (P < 0.05), and increased plasma MDA (0.340 +/- 0.120 to 4.030 +/- 0.86 nmol/ml; n = 8, P = 0.01); 2 h of reperfusion further increased EDTA clearance (0.323 +/- 0.060 ml.mg-1.100 g-1). EDTA clearance remained unchanged from baseline throughout the experimental period in sham ischemic rats (n = 12, 0.060 +/- 0.006 ml.min-1.100 g-1). Aminosteroid treatment at ischemia (n = 10) or with reperfusion (n = 11) returned EDTA clearance to near baseline (baseline 0.071 +/- 0.023; reperfusion 0.091 +/- 0.014 ml.min-1.100 g tissue-1) and reduced the ischemia-reperfusion-associated rise in tissue MDA. Two hours after reperfusion, SMA blood flow was above baseline values in all experimental groups. Our data suggest that oxygen-derived free radicals produced during intestinal ischemia and reperfusion contribute to 1) lipid peroxidation of cell membranes and 2) increases in intestinal mucosal permeability, potentiating bacterial translocation and sepsis.

Animals↗

PubMed1985

Adrenergic nervous control of resistance and capacitance vessels. Studies on isolated blood vessels from the rat.

A systematic comparison of neurogenic responses from consecutive sections of the cardiovascular system has not yet been performed under the well-defined conditions that an in-vitro system can offer. The present investigation aimed at analysing the neuroeffector properties of different isolated vessels, mounted in a myograph, where isotonic and isometric responses to transmural nerve stimulation could be determined. The vessels investigated were the abdominal aorta and caval vein, the superior mesenteric artery and vein, and 200-micron arteries and corresponding veins from the mesenteric arcades, the latter representing true resistance and capacitance vessels, respectively. Further, the vascular adrenergic innervation was visualized by Hillarp-Falck's formaldehyde fluorescence technique as well as immunohistochemical methods. In all vessels the innervation was confined to the adventitio-medial border. The responses to single neurogenic impulses differed markedly between the vessels, being distinct and rapid in the small, slow in the intermediate vessels, and absent in the aorta and the caval vein. This was in contrast to the responses to direct electrical activation of the muscle, which were quite rapid in all vessels. The organisation of the neuromuscular transmission thus has a marked influence on the effector response. The maximal neurogenic responses parallelled the innervation density, being greatest in the small arteries and least in the abdominal aorta. The frequency for half-maximal response appeared to depend also on other factors, such as velocity of contraction and relaxation of the smooth muscle. Of the small vessels, the veins were relatively more activated by low frequencies. Stimulation with an irregular impulse pattern, derived from human sympathetic nerve discharge, had greater effects than the corresponding constant-frequency stimulation on the resistance arteries; the small veins responded equally to either pattern. This difference could be related to the observed frequency-response relations around the average frequency used. The effects of inhibition of neuronal amine uptake on neurogenic responses and on responses to exogenous noradrenaline differed considerably, particularly in the resistance arteries. Here the magnitude of the neurogenic responses were hardly affected by this inhibition, whereas responses to exogenous noradrenaline were strongly enhanced. On its own, blockade of prejunctional adrenergic alpha 2-receptors had little effect on either response, but blocking both alpha 2-receptors and reuptake clearly potentiated the neurogenic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗

PubMed1998

Regional variation in appearance of vascular contractile endothelin-B receptors following organ culture.

OBJECTIVE: The aim of this study was to investigate the appearance of contractile endothelin (ET)-B receptors following organ culture in different vascular regions. METHOD: The contractile responses of vascular smooth muscle induced by ET-1 and the selective ETB receptor agonist sarafotoxin 6c (S6c) were investigated in circular segments representing eight vascular regions in the rat (aorta, femoral artery, mesenteric artery, branch of the mesenteric artery, proximal and distal parts of the caudal artery, femoral and mesenteric veins). To allow the ETB receptor to be expressed, the segments were placed in organ culture for 1 to 5 days. Pharmacological characterisation of the ET receptors was performed in mesenteric arterial segments. All contractile responses were measured in percentage of K(+)-induced contraction. RESULTS: ET-1 induced strong concentration-dependent contractions of all fresh (not cultured) segments. S6c had negligible effects on all fresh vessels with the exception of the mesenteric vein, where a small contraction was seen. After 1 day of organ culture all tested segments, with the exception of aorta and the proximal part of the caudal artery, showed concentration-dependent contractile responses to S6c which were further augmented after 5 days of culture. The ET-1-induced responses were only slightly affected by organ culture. Contractions induced by S6c were more enhanced in small arteries and veins than in larger arteries. Furthermore, the S6c-induced response was more pronounced in the mesenteric region as compared to the hindlimb. In fresh mesenteric arterial segments FR139317 (ETA receptor antagonist) and bosentan (ETA/ETB receptor antagonist) but not IRL 2500 (ETB receptor antagonist) shifted the ET-1-induced concentration-response curve in parallel to the right. In contrast, after organ culture the S6c-induced concentration-response curves were shifted parallel to the right in the following potency order: IRL 2500 > bosentan > FR139317. CONCLUSION: During normal conditions, the ETA receptor is the dominating mediator of endothelin-induced contraction in eight different vascular regions. Furthermore, this study indicates that most of the vessels have the ability to develop contractile ETB receptors and that this plasticity differs in vascular regions.

Animals↗

PubMed1978

[Occlusion of the three unpaired aortic branches with the development of an extensive Riolan's anastomosis (author's transl)].

A 60-year-old patient with occlusion of the inferior and superior mesenteric arteries and the coeliac axis developed a collateral circulation from the iliac arteries through the rectal vessels, the ascending ramus of the inferior mesenteric artery and the medical colic branch of the superior mesenteric artery. These collaterals were able to ensure survival of all three vascular territories. Along the medial wall of the descending colon and the sigmoid a second, less well developed collateral circulation could be demonstrated by iliac arteriography. The branches of the superior mesenteric artery and of the coeliac axis were only partly demonstrated, or failed to fill, during a free aortic injection and a counter current arteriogram. Clinically the occlusion of the unpaired aortic branches manifested itself as periumbilical pain after food. The involvement of the visceral aortic branches to this extent in the presence of generalised vascular disease is related to an attack of dysentry 38 years previously.

Celiac Artery↗

PubMedDate not supplied

Color duplex ultrasonography of the superior mesenteric artery after placement of endografts with suprarenal stents.

After endovascular repair of abdominal aortic aneurysm with endografts with suprarenal stents, the proximal uncovered stent may cross the origin of the superior mesenteric artery. Effects on splanchnic circulation are unknown and may include development of stenosis at the vicinity of the stent. The criteria of high-grade superior mesenteric artery stenosis using color duplex ultrasonography have been previously reported. The purpose of this study is to examine the incidence of high-grade superior mesenteric artery stenosis in patients with endografts with suprarenal stents using color duplex ultrasonography. Candidates for the study were patients who had placement of an aortic endograft with a suprarenal stent and were able to undergo ultrasonography of the superior mesenteric artery. After reviewing computed tomography scans, patients who had the origin of the superior mesenteric artery crossed by the suprarenal stent underwent color duplex ultrasonography of this vessel. Presence of turbulence or narrowing of the superior mesenteric artery, or a peak systolic velocity greater than 2.75 m/sec, or an end-diastolic velocity greater than 0.45 m/sec were considered significant for the presence of high-grade superior mesenteric artery stenosis. There were 24 patients (21 males, three females), median age 71 years (range, 59-83). The suprarenal stent was crossing the superior mesenteric artery in 17 of 24 patients (71%). Color duplex ultrasound was technically successful in 13 of 17 (76%). The test was performed after a median follow-up of 9 months (range, 3 days to 34 months). No patient had evidence of turbulence or narrowing of the superior mesenteric artery during ultrasonography. The median peak systolic velocity was 0.92 m/sec (range, 0.53-1.21 m/sec). No patient had peak systolic velocity greater than 2.75 m/sec. The median end-diastolic velocity was 0.10 m/sec (range, 0.09-0.14 m/sec). No patient had end-diastolic velocity greater than 0.45 m/sec. Color duplex ultrasonography did not demonstrate the presence of high-grade superior mesenteric artery stenosis during early follow-up of patients with endografts with suprarenal stents. Longer follow-up of larger series of patients is needed to determine the long-term effects of suprarenal stents on splanchnic circulation.

Aged↗

PubMed1993

Resection for adenocarcinoma of the body and tail of the pancreas.

Adenocarcinoma of the pancreatic body and tail often presents late and is widely regarded as incurable by surgical resection; long-term survivors are rare. Thirteen patients underwent left resection (n = 7) or total pancreatectomy (n = 6) in a consecutive series of 105 patients with carcinoma of the body or tail of the pancreas. Comparison was made with 17 patients with locally advanced or metastatic disease. Preoperative computed tomography predicted irresectable disease when a large perivascular lymph node mass was demonstrated. Preoperative angiography predicted irresectable disease when there was encasement or obliteration of the coeliac axis or its major branches, or of the superior mesenteric artery or vein. Splenic vessel involvement was sometimes compatible with resection. After resection, median survival was 13 (range 3-50) months, with a minimum follow-up of 2 years. Five patients survived more than 2 years, and three are still alive 30, 43 and 50 months after resection. Resection of carcinoma of the body or tail of the pancreas was possible in 12 per cent of patients and long-term survival was observed in some of these.

Adenocarcinoma↗