Mesenteric revascularization: an operative decision.
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Aorta, Abdominal↗
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Responses of saphenous and mesenteric veins to administration of dopamine.
Others have observed that dopamine (3,4-dihydroxyphenylethylamine) constricts resistance vessels in skin, but dilates these vessels in the mesentery. We studied the effects of dopamine on cutaneous and mesenteric veins of dogs to see if this agent also produced qualitatively different effects on the tone of capacitance vessels (veins) in these vascular beds. The lateral saphenous or the left colic vein was perfused at constant flow with blood from a femoral artery. Pressures at the tip of the perfusion cannula and at the tip of a catheter 15 cm downstream were recorded continuously. Increases in the pressure gradient between these two points indicated venoconstriction; decreases indicated venodilatation. Dopamine and norepinephrine injected into the perfusion tubing caused constriction of both veins. The constriction was antagonized by blockade of alpha receptors. A dilator action of dopamine was not seen, even after alpha receptor blockade or in the presence of increased venous tone produced by serotonin, norepinephrine, or nerve stimulation. Reserpine and cocaine did not alter responses to dopamine in the saphenous vein; this suggests that the venoconstrictor action of dopamine results mainly from a direct effect on alpha receptors and that uptake into sympathetic nerve endings may not be important in regulating the amount of dopamine available to receptors in the saphenous vein.
Adrenergic alpha-Antagonists↗
Mast-cell secretion and angiogenesis, a quantitative study in rats and mice.
The activation of the autogenous mast cells (MCs) in situ in intact mesenterial windows was elicited by the intraperitoneal injection of the MC secretagogue Compound 48/80 over a period of 1, 3 and 5 days in Sprague-Dawley rats and in C57 BL/6 and CBA/Ca mice. As a probe of MC secretion, the release of histamine was quantified fluorometrically at predetermined intervals during the treatment. Fourteen days after the start of the treatment, the angiogenic response was quantified histologically as the number of vessel profiles per unit length of mesenteric window. Both the MC-activating and the angiogenic effect of the 48/80-treatment was greater in the rats than in the mice. The occurrence of MC-mediated angiogenesis in the mouse is demonstrated here for the first time. In the rat, 48/80-induced MC mediated angiogenesis increased in a distinctly dose-dependent manner. Two daily doses of 48/80 was the most efficient angiogenic protocol tested; a single day's treatment increased the number of vessels almost fivefold. The remarkable potency of the angiogenic reaction following MC secretion supports our previous notion that MC-mediated angiogenesis may have therapeutic implications in poorly vascularized tissues.
Animals↗
Role of NAD(P)H oxidase on vascular alterations in angiotensin II-infused mice.
OBJECTIVES: Angiotensin (Ang) II stimulates vascular reactive oxygen species generation via NAD(P)H oxidase activation. We investigated whether vascular NAD(P)H oxidase influences structure and function of resistance arteries from Ang II-infused mice. METHODS: Mice received Ang II alone (400 ng/kg per min, subcutaneously), Ang II + apocynin (NAD(P)H oxidase inhibitor, 2.5 mg/day, in the food), apocynin alone or Ang II + hydralazine (50 mg/kg per day) for 14 days. Systolic blood pressure (SBP) was measured by tail-cuff methodology and function and structure of small mesenteric arteries were studied in pressurized vessels. Vascular collagen type I/III content was evaluated by confocal immunofluorescence microscopy and by immunoblotting. RESULTS: The rise in SBP induced by Ang II (P < 0.001) was prevented by apocynin and hydralazine. Media/lumen ratio increase in Ang II-infused mice (P < 0.01) was prevented by apocynin. Acetylcholine-mediated relaxation, which was impaired in Ang II-infused mice (P < 0.001), was improved by apocynin. Confocal microscopy and immunoblotting demonstrated increased collagen type I/III content in mesenteric arteries from Ang II-infused mice. Apocynin, but not hydralazine, prevented the increase in collagen abundance in Ang II-infused mice. The increase in vascular NAD(P)H oxidase activity by Ang II (P < 0.001) was prevented by apocynin. CONCLUSIONS: The NAD(P)H oxidase inhibitor apocynin reduced blood pressure elevation and prevented structural alterations, endothelial dysfunction, and collagen deposition in the media of small arteries in Ang II-infused mice. Although hydralazine also decreased blood pressure, it had no effects on vascular collagen content. Our findings suggest that NAD(P)H oxidase activity plays an important role in vascular functional and structural changes and in the composition of the vascular wall in Ang II-dependent hypertension.
Acetophenones↗
Smooth muscle dysfunction in resistance arteries of the staggerer mouse, a mutant of the nuclear receptor RORalpha.
Retinoic acid receptor-related orphan receptor alpha (RORalpha) is a member of the nuclear receptor superfamily. The mouse mutant staggerer (sg/sg) carries a deletion within the RORalpha gene. RORalpha plays a major role in cellular differentiation during development and growth. In the present study, we found a lower mean arterial blood pressure in sg/sg than in +/+ mice (80.1+/-1.2 and 87.0+/-0.9 mm Hg, respectively; P<0.0002) and a smaller increase in blood pressure after in vivo injections of phenylephrine. To elucidate the mechanisms responsible for this phenotype, we investigated the vascular reactivity of large vessels (aorta and carotid arteries) and small resistance mesenteric arteries in response to mechanical forces or vasoactive agents. Arteries from sg/sg and +/+ mice were studied in vitro in arteriographs. Vascular responses of large vessels to all stimuli were similar in both groups. However, we found a markedly altered vascular function in mesenteric arteries from sg/sg mice. Flow-induced dilation, pressure-induced myogenic tone, responses to endothelium-dependent or -independent vasodilators, and responses to vasoconstrictors were significantly reduced in sg/sg compared with +/+ mice. We also determined by Western blot analysis the expression of smooth muscle (SM)-myosin, calponin, and heavy (h)-caldesmon, in large and small arteries of sg/sg and +/+ mice, and found a marked decrease in the expression of these contractile proteins in mesenteric arteries of sg/sg mice. Our findings provide the first evidence that functional RORalpha is required for normal contractile phenotype of smooth muscle cells (SMCs) in small resistance arteries and suggest that RORalpha might be involved in the differentiation of SMCs in mesenteric arteries.
Animals↗
Endothelium-dependent relaxation is not uniformly impaired in chronic heart failure.
Abnormalities of vasomotor tone are characteristic of heart failure. This study was designed to assess the effects of chronic heart failure on endothelium-dependent relaxation in both large conduit arteries and small resistance vessels and to determine whether or not impaired nitric oxide (NO) production is involved. Segments of pulmonary artery (PA), abdominal aorta (AA), and small mesenteric artery (MA) were harvested from rats with heart failure resulting from coronary artery ligation and from sham-operated controls. Organ-bath experiments done in the presence of indomethacin to avoid the influence of vasodilatory prostanoids demonstrated that relaxation to acetylcholine (ACh) was impaired in the PA but not the AA or MA of the group with heart failure. Endothelium-independent relaxation to nitroglycerin was not significantly affected by the development of heart failure. Constriction to prostaglandin (PG) F(2alpha) was enhanced in PA but not in AA or MA segments. Preincubation with N(omega)-nitro-L-arginine (NNA) to inhibit the production of NO increased baseline force in vessels from all three beds, but the effect was greatest in the PA. Although relaxation to ACh was significantly diminished by NNA in the PA, it was not completely abolished. Furthermore, ACh-mediated relaxation in the presence of NAA was still impaired in the group with heart failure compared with the sham-operated control group. NNA had only mild effects on ACh-mediated relaxation in MA. These results demonstrate that (a) the mediators of endothelium-dependent relaxation may vary throughout the arterial circulation, (b) the contribution of NO to endothelium-dependent relaxation is substantial in PA and minimal in mesenteric resistance vessels, (c) endothelium-dependent relaxation is not uniformly impaired throughout the arterial bed by the development of heart failure, and (d) although a defect in NO production may account for enchanced vasoconstriction seen in response to PGF(2alpha), it does not account for the diminished vasodilatory response to ACh in this experimental model of heart failure.
Acetylcholine↗
Carcinoid tumors of the alimentary tract. II. Angiographic diagnosis of small intestinal and colonic lesions.
The angiographic findings of five small intestinal and two colonic carcinoids are described and illustrated, together with a review of the pertinent literature. It is pointed out that the demonstration of a complex of angiographic findings related to the primary site, mesentery, and liver is highly specific. It helps in the preoperative diagnosis as well as in the localization and stage of development of the gastrointestinal carcinoid. The triad of findings is composed of: (a) faint to moderate staining at the primary site; (b) narrowing, obstruction of the distal mesenteric arcade, cluster of irregular kinked vessels, and encasement in the more central areas of mesentery; and (c) hypervascular liver metastasis. The colonic lesions examined are unique in the literature, and exhibited angiographic findings similar to the small bowel carcinoids.
Adult↗
Endothelium-dependent vasodilatation in Sprague-Dawley rats with postinfarction hypertrophy: lack of endothelial dysfunction in vitro.
The hypothesis was tested whether postinfarction hypertrophy/congestive heart failure in rats is associated with endothelial dysfunction and increased vascular generation of reduced oxygen species. Myocardial infarction was induced in Sprague-Dawley rats by ligation of the left coronary artery. After 16 weeks, endothelium-dependent (with acetylcholine) and -independent (with sodium nitro-prusside) relaxations were studied in isolated aortic rings, and isolated rings from the femoral and mesenteric arteries. The generation of superoxide, hydrogenperoxide, and peroxynitrite was measured in arteries using lucigenin- and luminol-enhanced chemiluminescence techniques. Systolic blood pressure decreased over the 16 week study period as compared to shamoperated control rats; organ weights (lungs, right and left ventricles) significantly increased in coronary artery ligated rats indicating development of congestive heart failure. Surprisingly, concentration response curves with acetylcholine and sodium nitroprusside were almost identical in myocardial infarction rats as compared to control animals, irrespective of which type of vessel was studied (aorta, femoral or mesenteric arteries). In addition, no differences in the production of reduced radical species were found in aortic tissue from heart failure rats as compared to control rats.
Acetylcholine↗
Modulation of leukocyte adhesion in rat mesenteric venules by aspirin and salicylate.
Erythrocyte velocity, vessel diameter, leukocyte rolling velocity, and number of adherent and emigrated leukocytes were measured in postcapillary venules both before and during superfusion of rat mesentery with either aspirin or sodium salicylate. In some experiments, animals were treated with either a leukotriene (LT)-synthesis inhibitor (L-663,536), an LTD4 antagonist (MK-571), an LTB4 antagonist (SC-41930), misoprostol, or prostaglandin (PG) I2, then the aspirin protocol was repeated. Superfusion of aspirin but not sodium salicylate resulted in increased leukocyte adherence and a reduced leukocyte rolling velocity but did not affect leukocyte emigration. Aspirin-induced leukocyte adhesion was effectively prevented by the LT-synthesis inhibitor and LTB4 antagonist but not by the LTD4 antagonist. Misoprostol and PGI2 also prevented the aspirin-induced adhesion responses. Superfusion of the mesentery with either platelet-activating factor (PAF) or LTB4 enhanced leukocyte adherence and emigration while reducing leukocyte rolling velocity. Sodium salicylate prevented all of the adhesion responses elicited by LTB4. Although salicylate did not affect the PAF-induced leukocyte adherence and rolling responses, it completely prevented the increased leukocyte emigration. These results indicate that aspirin promotes, whereas sodium salicylate inhibits, leukocyte-endothelial cell adhesive interactions at therapeutically relevant concentrations.
Animals↗
The effect of external Ca2+ concentration on the contractility of bovine mesenteric lymphatics.
Spontaneous isometric contractions of isolated lymphatic vessels were studied in the single sucrose gap apparatus. Contractions were also elicited by applying single electrical pulses either within the Krebs solution (field stimulation) or across the sucrose gap (gap stimulation), or by means of high-K+ Krebs. Reductions in the calcium concentration increased the frequency but decreased the force of spontaneous contractions and ultimately abolished them. The loss of mechanical activity in calcium free solution was associated with failure of action potential firing. Increasing external [Ca2+] had no apparent effect on the force of spontaneous contractions but these became less frequent and finally stopped. The calcium antagonist D600 decreased the force of spontaneous contractions without increasing their frequency. The contractions elicited by electrical stimulation and by high-K+ Krebs were less readily abolished by calcium removal. This was particularly true of field stimulation where contractions could still be elicited up to 40 min after exposure to a calcium-free solution. It is concluded that calcium ions are important for the control of pacemaking, for the propagation of the impulse, and for the contractile response itself in these bovine lymph vessels.
Animals↗
Aberrations of cyclic nucleotide metabolism in the hearts and vessels of hypertensive rats.
In the aortas and mesenteric arteries from spontaneous hypertensive rats and in the aortas from stress- and desoxycorticosterone-acetate-hypertensive rats, the intracellular cGMP: cAMP ratios were significantly elevated when compared to the ratios in the aortas of the respective controls. Decreases in the intracellular cAMP or cGMP levels were consistently associated with increased activity of the cyclic-nucleotide-specific low K(m) phosphodiesterase (3':5'-cAMP 5' nucleotidohydrolase, EC 3.1.4.17). Increases in intracellular cGMP levels were associated with elevated guanylyl cyclase [GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2] activity. Furthermore, adenylyl cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] activity was less sensitive to stimulation by the beta-adrenergic stimulant isoproterenol in both the aortas and the hearts of the hypertensive animals. These changes could provide the biochemical basis for the (a) increased vascular smooth muscle tone and peripheral resistance observed in these animals, (b) increased reactivity to norepinephrine, and (c) decreased ability of aortas from hypertensive rats to relax. The presence of these same effects in different etiologic types of hypertension indicates that this aberration in cyclic nucleotide metabolism may represent a common metabolic defect basic to the hypertensive syndrome irrespective of etiology.
Adenylyl Cyclases↗
Influence of age on relaxation of rat blood vessels to atriopeptin II.
The ability of atriopeptin II to relax isolated ring segments of the thoracic aorta and renal, mesenteric and carotid arteries was studied in Fischer 344 rats aged 6, 12, 20 and 24 to 27 months. Vessels were precontracted with norepinephrine (aorta, mesenteric and carotid arteries) or serotonin (renal artery) in concentrations that produced approximately 50% of the maximal contractile response. Agonist concentrations used and magnitude of induced tone did not change with age, except in the carotid artery, where tone induced in vessels from the oldest group of animals was significantly greater. Thus it was possible to obtain contractile responses that were relatively stable with age in order to test the effect of age on relaxation responses effectively. There were significant differences in sensitivity to atriopeptin II and maximum relaxation among the vessels studied when comparisons were made within a single age group. Thus the thoracic aorta and carotid artery were more sensitive to atriopeptin II and had greater maximum relaxation responses than the renal and mesenteric arteries. In terms of the influence of age, for the most part neither sensitivity to atriopeptin II nor maximum relaxation response changed with age. However, there were some exceptions. Particularly in the thoracic aorta at several concentrations of atriopeptin II, relaxation in vessels from animals 12 months of age was significantly greater than in the other age groups. This difference is most likely due to an effect of maturation, as there was no further alteration in atriopeptin sensitivity into senescence.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Prevention of hypertension and vascular changes by captopril treatment.
Treatment of female spontaneously hypertensive rats (SHR) and control Wistar-Kyoto (WKY) rats with captopril was carried out by the addition of the drug in the drinking water throughout pregnancy and lactation and after weaning. At 28 weeks of age, average systolic blood pressure of treated SHR was 113 +/- 3 mm Hg, which was below that of control SHR (188 +/- 3 mm Hg) and WKY rats (124 +/- 3 mm Hg). Body weight and heart rate of the SHR were not affected by the treatment. Tissue level of catecholamines was increased by captopril treatment in the superior cervical ganglia but remained unchanged in the plasma, heart, mesenteric arteries, and the adrenal glands of both SHR and WKY rats. Left ventricular weight, wall thickness, and internal diameter of the left ventricle in the SHR were reduced by the treatment. Morphometric measurements of the mesenteric arteries showed that vascular alterations present in the control SHR were prevented by the treatment. In the superior mesenteric artery and large mesenteric artery, smaller lumen size at maximal relaxation found in the control SHR was normalized to the level of the WKY rats. Hypertrophy of the medial wall in the superior mesenteric, large and small mesenteric arteries, and an increase in the number of smooth muscle cell layers in the large mesenteric artery of the SHR were prevented by the treatment. Perfusion study of the mesenteric vascular bed showed that reactivity of these vessels to norepinephrine was reduced, and sensitivity to norepinephrine (as determined by the effective dose that causes 50% of maximal response) was increased in the SHR by captopril treatment. Sensitivity of the tail artery in response to norepinephrine was not altered by the treatment. We conclude that long-term treatment with captopril of SHR before and after birth prevented the development of hypertension, structural and functional alterations of the mesenteric arteries, and cardiac hypertrophy.
Animals↗
Enhancement by vasopressin of adrenergic responses in human mesenteric arteries.
Vasopressin not only acts directly on blood vessels through V1-receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vitro and in vivo. The aim of the present study was to investigate whether subpressor concentrations of vasopressin could modify the constrictor responses to norepinephrine and electrical stimulation of the perivascular nerves in human mesenteric arteries. Human mesenteric artery rings (3-3.5 mm long, 0.8-1.2 mm OD) were obtained from 38 patients undergoing abdominal operations. The arterial rings were suspended in organ bath chambers for isometric recording of tension. Vasopressin (3 x 10(-11) M) enhanced the contractions elicited by electrical stimulation at 2, 4, and 8 Hz (by 100, 100, and 72%, respectively) and produced a leftward shift of the concentration-response curves to norepinephrine (half-maximal effective concentration decreased from 2.2 x 10(-6) to 5.0 x 10(-7) M; P < 0.05) without any alteration in maximal contractions. Vasopressin also potentiated KCl- and calcium-induced contractions. The V1-receptor antagonist 1-[beta-mercapto-beta,beta-cyclopentamethylenepropionic acid-2-O-methyl-tyrosine, 8-arginine]vasopressin (10(-6) M) prevented the potentiation evoked by vasopressin in all cases. The calcium antagonist nifedipine (10(-6) M) did not affect the potentiation of electrical stimulation and norepinephrine induced by vasopressin but abolished KCl-induced contractions. The results suggest that vasopressin, in addition to its direct vasoconstrictor effect, strongly potentiates the responses to adrenergic stimulation and KCl depolarization. Both the direct and indirect effects of vasopressin appear to be mediated by V1-receptor stimulation. The amplifying effect of vasopressin on constrictor responses may be relevant in those clinical situations characterized by increased plasma vasopressin levels.
Adult↗
Ruptured atherosclerotic aneurysm of the superior mesenteric artery with celiac axis occlusion.
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Aneurysm, Infected↗
[Successful aorto-superior mesenteric artery shunt in acute mesenteric thrombosis].
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Acute Disease↗
Differences in responses to TC-81 among various arteries in dogs.
The vasodilation induced by TC-81 was investigated in vitro and in vivo. In helical strips of dog arteries precontracted with 65.4 mM KCl, TC-81, nicardipine, nifedipine, diltiazem, and papaverine produced concentration-dependent relaxation. The potencies of TC-81 were in the following order: basilar > coronary > femoral > renal > mesenteric arteries. The other drugs also showed a similar property of greater response in basilar and coronary arteries than in renal and mesenteric arteries. However, the difference in reactivity to TC-81 was greater. On the other hand, TC-81, nicardipine, and papaverine dose-dependently increased the blood flow in vertebral, coronary, and femoral arteries in anesthetized dogs. However, the blood flow in renal and mesenteric arteries was not changed or decreased. The decreases in vessel resistance induced by TC-81 were in the following order: vertebral > coronary > femoral > renal = mesenteric arteries, agreeing with the experimental results in vitro. These results suggest that Ca2+ antagonists have the pharmacological property of vasodilating cerebral and heart blood vessels more selectively than other arteries, and this property of TC-81 might be an advantage compared with other drugs.
Animals↗
The nitrate ester ITF 296 relaxes isolated canine arteries and veins.
Experiments were designed to compare the relaxant activity of the new nitrate ester ITF 296 in isolated arteries and veins of the dog and to determine the extent of modulation by the endothelium of the response to the compound. Rings (with and without endothelium) of coronary, basilar, mesenteric, and femoral arteries and of mesenteric, femoral, and saphenous veins were suspended in organ chambers for measurement of changes in isometric tension. In all blood vessels without endothelium, ITF 296 caused concentration-dependent relaxation. The order of potency (from measurements of ED50) was: basilar artery > or = coronary artery > femoral artery > mesenteric vein > femoral vein > saphenous vein > mesenteric artery. The maximal relaxation to ITF 296 was greater in the arteries (with the exception of the mesenteric) than in veins. In all blood vessels except for the basilar artery, nitroglycerin caused larger relaxations than ITF 296: The ED50 for nitroglycerin was comparable in all blood vessels studied except for the mesenteric artery, where it was less. ITF 296 did not cause hyperpolarization of vascular smooth muscle in coronary arteries either with or without endothelium. The presence of endothelial cells blunted the relaxation to ITF 296 in basilar and coronary arteries, but not in the other blood vessels studied. These results demonstrate that ITF 296 has a direct inhibitory effect on vascular smooth muscle, which is most pronounced in coronary and cerebral arteries. These findings are in line with the vascular selectivity profile reported for the compound in vivo.
Animals↗