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PubMed1991

Hemorrhagic shock and bacterial translocation in a swine model.

Bacterial translocation is proposed as an explanation for sepsis associated with hemorrhagic shock. This study attempted to document these events in a large animal model. Male swine were randomly assigned to control (n = 10) or experimental (n = 10) groups. Animals were anaesthetized, and the bladder, portal vein, and a mesenteric lymphatic vessel cannulated. Experimental animals were bled 40% of blood volume. Over the next six hours maintenance fluids were given, and cultures of portal blood and mesenteric lymph taken. Before the swine were killed, cultures were taken from portal and systemic blood, mesenteric lymph, and lymph nodes, and a portion of terminal ileum was resected for histologic study. Experimental animals experienced significant shock as demonstrated by changes in hemodynamic and biochemical variables. Cultures and histologic examination of the terminal ileum showed no significant difference between control and experimental animals. In an unresuscitated swine model, significant bacterial translocation was not demonstrated within six hours of hemorrhagic shock.

Animals↗
PubMed1995

Comparative study of elgodipine and nisoldipine on the contractile responses of various isolated blood vessels.

The effects of elgodipine, a new dihydropyridine derivative, were compared to those of nisoldipine on contractile responses in various isolated artery rings and on mechanical activity in portal vein segments. Arteries used were: rabbit aorta, mesenteric (fifth branch), femoral and basilar, and sheep coronary arteries. Elgodipine and nisoldipine (10(-16)-3 x 10(-6) M) produced a concentration-dependent inhibition of the contractile responses induced by high K+ (80 mM), 5-hydroxytryptamine (10(-5) M) or noradrenaline (10(-6) M or 10(-4) M) in all the arteries studied. The inhibitory effect of elgodipine was greater in mesenteric resistance vessels (IC50 = 8.0 +/- 2.1 x 10(-12) M and 2.0 +/- 0.5 x 10(-13) M for the depression of high K(+)- and agonist-induced contraction, respectively), and in coronary arteries (IC50 = 2.6 +/- 0.3 x 10(-10) M and 9.0 +/- 1.4 x 10(-8) M for the inhibition of high K(+)- and agonist-induced contraction, respectively). In addition, the action of elgodipine in peripheral resistance vessels and in the coronary artery was more prominent than in aorta or femoral arteries, and this tissue selectivity was more apparent for elgodipine than for nisoldipine. In rat portal vein elgodipine (IC50 = 6.5 +/- 0.9 x 10(-8) M) and nisoldipine (IC50 = 8.5 +/- 1.3 x 10(-8) M) reduced in a concentration-dependent manner the development of mechanical activity. Furthermore, contractile responses produced by the addition of Ca2+ (1-5 mM) to Ca(2+)-free high K+ solution were also concentration dependently inhibited by elgodipine. However, elgodipine did not modify noradrenaline-induced contractions attributed to intracellular Ca2+ release. The results of this study indicate that elgodipine has potent vasodilator properties and vascular selectivity. The mechanisms through which elgodipine relaxes vascular smooth fibres seem to be related to its ability to inhibit the entry of extracellular Ca2+ into the cell.

Animals↗
PubMed1997

Functional electrical properties of the endothelium in lymphatic vessels of the guinea-pig mesentery.

1. The resting and agonist-stimulated properties of endothelial cells and electrical communication between the endothelium and smooth muscle were investigated in open segments of guinea-pig mesenteric lymphatic vessels using intracellular microelectrodes. 2. Endothelial cells had a mean resting membrane potential (RMP) of -71.5 +/- 0.5 mV (n = 100) which was significantly different from the value of -60.8 +/- 1.1 mV (n = 75) recorded in smooth muscle. 3. Acetylcholine (ACh, 5-10 microM) generally evoked an initial hyperpolarization followed by depolarization (mean 3.4 +/- 0.5 mV and 15.4 +/- 1.0 mV, respectively, n = 75). 4. Ca(2+)-activated K+ channels were likely to underlie the ACh-induced hyperpolarization as this response exhibited an increased in membrane conductance, was larger in 0.5 mM K+ solution and was blocked by charybdotoxin (50 nM). 5. The endothelium did not exhibit a response to nitric oxide (NO) as the NO-donor sodium nitroprusside did not alter the RMP and the electrical responses to ACh were not affected by the NO-synthase inhibitor N omega-nitro L-arginine at a concentration which markedly inhibited smooth muscle hyperpolarization. 6. Electrical coupling between the endothelium and smooth muscle was not functional as there was extremely limited electrical continuity (1 in 12, endothelial/smooth muscle cell simultaneous recordings) and bradykinin, noradrenaline and isoprenaline caused different electrical responses in the two cell types. 7. These results provide the first description of RMP and electrical responses to various agonists in the lymphatic endothelium and its lack of functional electrical coupling with the smooth muscle.

Acetylcholine↗
PubMed1993

Relaxing actions of corticotropin-releasing factor on rat resistance arteries.

1. Although it well established that corticotropin-releasing factor (CRF) injected i.v. can cause hypotension and vasodilatation, there is no in vitro evidence that CRF acts as a vasodilator. We have therefore tested the hypothesis that the hypotensive effect of i.v. CRF is due to a direct vasodilator action by carrying out experiments in vitro on rat resistance arteries (i.d. 150-300 microns). 2. Initial in vivo experiments confirmed that CRF (1.5 nmol.kg-1) injected i.v. caused hypotension in rats, this being partially antagonized by the CRF analogue CRF9-41. 3. For the in vitro experiments, vessels were taken from the mesenteric, cerebral and femoral vascular beds, and mounted as ring preparations in an isometric myograph. The vessels were pre-contracted with one of 3 agonists (prostaglandin F2 alpha, arginine vasopressin or noradrenaline) or with a high-potassium solution (K+). 4. With maximal concentrations of the agonists, CRF caused relaxation of mesenteric and cerebral vessels with 10 nM, and near complete relaxation with 100 nM. Femoral vessels pre-constricted with agonists and all vessels pre-constricted with K+ were less affected by CRF. In the mesenteric vessels, with sub-maximal levels of pre-constriction, CRF caused substantial relaxation at 1 nM and could cause complete relaxation at 10 nM. 5. The relaxant effect of CRF on contractions of mesenteric vessels was antagonized by 100 nM CRF9-41. Neither tetraethyl ammonium (30 mM) nor glibenclamide (3 microM) antagonized the relaxant effect of CRF. 6. The relaxant effect of CRF on mesenteric small arteries was found to be unaffected by removal of the endothelium. 7. The results indicate that CRF causes an endothelial-independent vasodilatation of rat resistance arteries under in vitro conditions at concentrations which are consistent with this being an important cause of the hypotension observed with i.v. injection of CRF.

Animals↗
PubMed1985

Effect of felodipine on resistance vessels from spontaneously hypertensive and normotensive rats.

We have investigated the effect of felodipine [4-(2,3,-dichlorophenyl)-1,4-dihydro-2, 6-dimethyl-3-ethoxycarbonyl-5-ethoxycarbonylpyridine] on the calcium concentration response relations of noradrenaline-activated mesenteric resistance vessels from 3-mo-old spontaneously hypertensive (SHR) and age-matched Wistar-Kyoto (WKY) rats. SHR vessels were more sensitive to calcium (ED50 approximately equal to 5.49 X 10(-5) M) than WKY vessels (ED50 approximately equal to 1.01 X 10(-4) M) in control condition. Also, maximal active tension development in SHR vessels was greater (3.14 N/m) than in WKY vessels (2.22 N/m). Felodipine (10(-12) M) decreased calcium sensitivity in vessels from both strains and also decreased maximal active tension development of SHR vessels. In a higher concentration (5 X 10(-10) M), the calcium sensitivity of both SHR and WKY vessels became similar. The active tension development was equally reduced in both rat strains. The results indicate that at least part of the antihypertensive effect of felodipine is due to a direct vasodilation, and also that vessels from SHRs may be more sensitive to felodipine than those from WKY rats.

Animals↗
PubMed2002

Magnetic resonance angiographic techniques for the diagnosis of arterial disease.

Magnetic resonance angiography (MRA) techniques use inherent magnetization properties of tissues in combination with pharmacologic contrast agents, such as gadolinium, that shorten T1 relaxation time. The availability of powerful magnetic field gradients along with a variety of post-processing algorithms make MRA possible. MRA is widely used for the diagnosis of disease in a variety of vessels, including aorta, carotids, renals, mesenteric, and peripheral vessels. Performance of high-quality 3D contrast MRA requires appropriate understanding of MRA methodologies, including the critical dependence of bolus timing and ways to optimize it. Additionally, recognition of artifacts and learning to avoid them is important.

Aorta, Abdominal↗
PubMed1983

Effects of arachidonic acid and its cyclo-oxygenase and lipoxygenase products on lymphatic vessel contractility in vitro.

Lymphatic vessels exhibit rhythmical contractility in vivo and in vitro and this activity appears to regulate lymph flow. A technique for measuring the circular muscle contractions of isolated bovine mesenteric lymphatic vessel segments has been devised and utilized to study the pharmacological properties of these vessels. Non-contracting lymphatic vessels can be induced to contract rhythmically with a variety of mediators, the most potent being a stable PGH2 analogue (compound U46619), and the leukotrienes B4, C4 and D4 (threshold concentrations in the nanomolar range). Prostaglandin F2 alpha, noradrenaline, serotonin and histamine also elicited rhythmical activity but much higher concentrations were required. PGE2 and PGE1 were potent inhibitors of spontaneous contractions or those induced with U46619. In keeping with the diverse pharmacological effects of the metabolites of arachidonic acid, the addition of arachidonate to an isolated lymphatic vessel generated both stimulatory and inhibitory activities. It is concluded that arachidonic acid products (produced in the lymphatic vessel or entering the vessel in lymph draining the tissues) regulate lymph flow through their effects on lymphatic smooth muscle.

Alprostadil↗
PubMed1978

Ion transport in tonic and phasic vascular smooth muscle and changes during deoxycorticosterone hypertension.

The washout of radioisotopes was studied in aorta, femoral artery and portal mesenteric vein from controls and rats made hypertensive with injection of deoxycorticosterone (DOC) acetate. Experiments were also conducted on tonic (pulmonary artery) and phasic (portal mesenteric vein) smooth muscle from rabbits. The rate constants for the washout of 42K, 36Cl and 24Na from aorta were significantly elevated in the DOC hypertensives. Acute removal of extracellular K slowed the washout of 24Na by 50%, however, the rate constant for the DOC group remained higher than the controls. Increased turnover of 42K was also observed in the femoral artery and in a vessel (portal mesenteric vein) not exposed to the effects of high blood pressure in the rat. The rate constants for the washout of 42K, 36Cl and 24Na from phasic smooth muscle in rabbit were greater than the tonic type. Ouabain significantly slowed 24Na washout, however, the rate constant for the portal mesenteric vein remained higher than the pulmonary artery. DOC hypertension was associated with increased ion transport at several vascular sites. A similar change was observed for the phasic vascular smooth muscle from normal rabbits. A question is raised whether increased spontaneous activity of arteries reported to accompany DOC hypertension is the consequence of a membrane in transition from tonic to phasic behavior.

Animals↗
PubMed1994

Ileal carcinoid tumors and intestinal ischemia.

Three patients with carcinoid tumors of the ileum are presented; two had severe intestinal ischemia, one with infarction of the small intestine. In all three cases, histopathological examination revealed elastic vascular sclerosis (EVS) in the mesenteric blood vessels. Intestinal ischemia in the presence of a carcinoid tumor is probably due to a combination of tumoral secretion products, vascular changes, mesenterial retraction and nodal involvement. Selective superior mesenteric artery arteriography is diagnostic. All the reported carcinoid tumors with ischemic manifestations are ileal and invaded the mesentery or had positive nodes or metastases; two-thirds had EVS, and one-third mesenterial vascular luminal narrowing. Intestinal ischemia may be the underlying cause of vague symptoms in patients with a carcinoid tumor. This tumor may be small and must be looked for during laparotomy, mild intestinal ischemia or mesenterial thickening are important signs. Early resection can prevent intestinal complications. An aggressive attitude, including debulking of metastases, is justifiable.

Aged↗
PubMed2004

Effect of acute hypoxia in pregnant females on contractile activity of lymphatic vessels in the offspring.

Delayed consequences of acute hypoxia were studied in 60-day-old rat pups. The animals were exposed to acute hypobaric hypoxia on day 10 of embryogenesis. The offspring of intact females served as the control. Reactivity of mesenteric lymphatic vessels to norepinephrine was studied by vital microscopy. The frequency and duration of lymphatic vessel contractions in males significantly increased compared to the control. In females the duration of norepinephrine-induced lymphatic vessel contractions increased, while the frequency and amplitude of contractions and basal vascular tone did not differ from the control.

Animals↗
PubMed1984

Lymphatic endothelial and smooth-muscle cells in tissue culture.

Endothelial and smooth-muscle cells from bovine mesenteric lymphatic vessels have been collected and cultured in vitro. The endothelial cells grew as a monolayer exhibiting a "cobblestone" appearance with individual cells tending to be more flattened at confluence than their blood vascular counterparts. Approximately 30% of these cells expressed Factor VIII antigen compared with bovine mesenteric artery or human umbilical-vein endothelium in which the majority of cells were positive. The lymphatic smooth-muscle cells exhibited focal areas of multilayering and were Factor VIII negative. The availability of lymphatic endothelial and smooth-muscle cells in culture will provide a new tool for the investigation of the biological properties of the lymphatic vessels and their role in homeostasis.

Animals↗
PubMed2005

Effects of chronic portal hypertension on agonist-induced actin polymerization in small mesenteric arteries.

The ability of arterial smooth muscle to respond to vasoconstrictor stimuli is reduced in chronic portal hypertension (PHT). Additional evidence supports the existence of a postreceptor defect in vascular smooth muscle excitation contraction coupling. However, the nature of this defect is unclear. Recent studies have shown that vasoconstrictor stimuli induce actin polymerization in smooth muscle and that the associated increase in F-actin is necessary for force development. In the present study we have tested the hypothesis that impaired actin polymerization contributes to reduced vasoconstrictor function in small mesenteric arteries derived from rats with chronic prehepatic PHT. In vitro studies were conducted on small mesenteric artery vessel rings isolated from normal and PHT rats. Isometric tension responses to incremental concentrations of phenylephrine were significantly reduced in PHT arteries. The ability to polymerize actin in portal hypertensive mesenteric arteries stimulated by phenylephrine was attenuated compared with control. Inhibition of cAMP-dependent protein kinase (PKA) restored agonist-induced actin polymerization of arteries from PHT rats to normal levels. Depolymerization of actin in arteries from normal rats reduced maximal contractile force but not myosin phosphorylation, suggesting a key role for the dynamic regulation of actin polymerization in the maintenance of vascular smooth muscle contraction. We conclude that reductions in agonist-induced maximal force development of PHT vascular smooth muscle is due, in part, to impaired actin polymerization, and prolonged PKA activation may underlie these changes.

Actin Cytoskeleton↗
PubMed1996

Selective expression of c-mas proto-oncogene in rat cerebral endothelial cells.

Northern blot analysis of cultured endothelial cells derived from rat cerebral resistance vessels demonstrated the presence of c-mas mRNA. This is the first description of mas expression in non-neuronal cells. c-mas message was not detectable in cultured endothelial cells derived from other vascular beds, including rat aorta and mesenteric resistance vessels. Since c-mas has been purported to regulate the proliferation response to angiotensin, the growth properties of all three endothelial cell cultures were examined. The data indicated no differences in either basal or angiotensin-stimulated cell growth among brain, mesenteric or aortic-derived endothelial cells. These data suggest that c-mas is selectively expressed in brain endothelial cells and that this proto-oncogene does not regulate cell proliferation in this cell type.

Angiotensin II↗
PubMed2001

The mesenteric hemodynamic response to circulatory shock: an overview.

The mesenteric hemodynamic response to circulatory shock is characteristic and profound; this vasoconstrictive response disproportionately affects both the mesenteric organs and the organism as a whole. Vasoconstriction of post-capillary mesenteric venules and veins, mediated largely by the alpha-adrenergic receptors of the sympathetic nervous system, can effect an "autotransfusion" of up to 30% of the total circulating blood volume, supporting cardiac filling pressures ("preload"), and thereby sustaining cardiac output at virtually no cost in nutrient flow to the mesenteric organs. Under conditions of decreased cardiac output caused by cardiogenic or hypovolemic shock, selective vasoconstriction of the afferent mesenteric arterioles serves to sustain total systemic vascular resistance ("afterload"), thereby maintaining systemic arterial pressure and sustaining the perfusion of non-mesenteric organs at the expense of mesenteric organ perfusion (Cannon's "flight or fight" response). This markedly disproportionate response of the mesenteric resistance vessels is largely independent of the sympathetic nervous system and variably related to vasopressin, but mediated primarily by the renin-angiotensin axis. The extreme of this response can lead to gastric stress erosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepatitis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock can produce decreased or increased mesenteric perfusion, but is characterized by an increased oxygen consumption that exceeds the capacity of mesenteric oxygen delivery, resulting in net ischemia and consequent tissue injury. Mesenteric organ injury from ischemia/reperfusion due to any form of shock can lead to a triggering of systemic inflammatory response syndrome, and ultimately to multiple organ dysfunction syndrome. The mesenteric vasculature is therefore a major target and a primary determinant of the systemic response to circulatory shock.

Animals↗
PubMed2003

Effect of tetrahydrobiopterin on blood pressure in rats after subtotal nephrectomy.

BACKGROUND: Previous studies have shown that endothelial dysfunction after 5/6 nephrectomy (5/6 Nx) in rats is associated with decreased nitric oxide (NO) bioavailability and increased vascular superoxide production. Blood pressure is significantly increased by day 10 after surgery. Tetrahydrobiopterin (BH4) is a key cofactor of NO synthase. Suboptimal levels of BH4 result in uncoupling of NO synthase, low NO synthesis and augmented production of superoxide anions. The aim of this study was to evaluate whether BH4 supplementation may improve NO production and prevent the increase of blood pressure after 5/6 Nx. METHODS: Three groups were evaluated: 5/6 Nx (untreated rats), BH4 (5/6 Nx rats treated with BH4, 10 mg/day i.p. for 10 days) and L-ARG (5/6 Nx rats treated with L-arginine, 260 mg/kg BW, p.o for 10 days). Systolic blood pressure (SBP), urinary nitrate excretion (UNO(3)) and creatinine clearance (CCR) were measured before surgery and on days 3 and 10 after surgery. Endothelial NO synthase (eNOS) protein content of mesenteric resistance vessels was measured at the end of the study. RESULTS: SBP increased from 107 +/- 2 to 127 +/- 4 mm Hg in untreated 5/6 Nx rats (p < 0.01). By contrast, rats treated with BH4 or L-ARG remained normotensive. Ten days after 5/6 Nx, creatinine clearance decreased similarly in all groups. Both BH4 and L-ARG supplementation markedly increased UNO(3) excretion. The mesenteric vascular expression of eNOs protein was significantly higher in BH4 but not in L-ARG, compared with Nx rats. CONCLUSIONS: BH4 supplementation prevents the earlier increase in blood pressure observed in rats after 5/6 Nx, possibly by upregulating eNOS in resistance vessels.

Animals↗
PubMed1993

Endothelium-derived relaxing factor activates calcium-activated potassium channels of resistance vessel smooth muscle cells.

Direct observation was made by using the patch-clamp technique with a specially designed microperfusion system to investigate the effect of acetylcholine (Ach 10(-6) mol/L) elicited endothelium-derived relaxing factor (EDRF) on the calcium-activated potassium channel (IK(Ca)) in the smooth muscle cells of mesenteric resistance vessels in Wistar rats. Activation of IK(Ca) was firstly observed by inducing the elicited EDRF or sodium nitroprusside (SNP 10(-8) mol/L) under various clamping voltages in cell-attached configuration. While the pipette solution contained KCl 126 mmol/L and the bath solution contained KCl 5.9 mmol/L, two types of conductances of calcium-activated potassium current being 76.4 +/- 2.3 pS (mean +/- S.E. n = 7) and 160.3 +/- 7.5 pS (mean +/- S.E. n = 7) were recorded during the EDRF activation, one type of conductance being 100.5 +/- 2.8 pS (mean +/- S.E. n = 6) was activated by nitric oxide (NO) which is an effective component from SNP. Differences in kinetic characteristics of these channels between EDRF and NO activation were found, particularly the probability of the channel being open in EDRF activation was obviously greater than that in NO stimulation. It has been shown that the potassium channel mechanisms involved in the EDRF and NO actions might be different.

Animals↗
PubMed2005

Angiotensin II infusion alters vascular function in mouse resistance vessels: roles of O and endothelium.

We hypothesized that prolonged angiotensin II (AngII) infusion would alter vascular reactivity by enhancing superoxide anion (O-.2) generation. Male C57BL/6 mice were infused with AngII at 400 ng/kg/min (n=16, AngII mice) or vehicle (n=16, sham mice) for 2 weeks via subcutaneous osmotic minipumps. Contraction and relaxation of mesenteric resistance vessels (MRVs) were assessed using a Mulvany-Halpern myograph. AngII infusion increased systolic blood pressure, MRV NADPH oxidase activity and expression of p22phox mRNA. Contraction to norepinephrine was unchanged, but AngII infusion increased contractile responses to AngII (41+/-5 vs. 10+/-4%, p<0.001) and endothelin-1 (ET-1; 95+/-10 vs. 70+/-9%, p<0.05), which was normalized by tempol (10(-4) M, a stable membrane-permeable superoxide dismutase mimetic) and ebselen [10(-5) M, a peroxynitrite (ONOO-) scavenger]. Endothelium removal enhanced MRV contraction to AngII and ET-1 in sham mice but blunted these contractile responses in AngII mice. Relaxation to ACh was impaired in AngII mice (60.1+/-8.8 vs. 83.2+/-3.5%, p<0.01), which normalized by tempol, whereas relaxation to sodium nitroprusside was similar in both groups. N-nitro-L-arginine (NNLA, a nitric oxide synthase inhibitor), partially inhibited acetylcholine relaxation of vessels from sham mice but not from AngII mice. The residual endothelium-dependent hyperpolarizing-factor-like relaxation was not different between groups. In conclusion,the AngII slow pressor response in mouse MRVs consisted of specific contractile hyperresponsiveness and impairment in the NO-mediated component of endothelium-dependent relaxation, which was mediated by O-.2 and ONOO- in the vascular smooth muscle cell.

Angiotensin II↗