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At least 1,729 records · Page 96Linked to original sources
PubMed1996

Effects of angiotensin I and angiotensin II in blood vessels: greater influence of converting enzyme activity in the rabbit basilar artery.

We investigated the constrictor effects of Angiotensin I (Ang I) and Angiotensin II (Ang II) on rabbit peripheral (aorta, carotid artery, mesenteric artery, saphenous artery) and cerebral (basilar artery) vessels and in rat aorta in functional organ bath studies. The effect of angiotensin converting enzyme (ACE) inhibition by captopril was also assessed in these preparations. Ang II elicited concentration-dependent contractions with comparable potency in rabbit and rat endothelium-free vascular rings (pD2 about 8.5) which indicates a lack of species and regional variation in the contractile responses to Ang II. The responses to Ang II were reduced by the presence of a functional endothelium in rabbit mesenteric artery and in rat aorta. Since ACE determines the plasma and tissue conversion of Ang I to active Ang II, we calculated the ratio R (EC50 Ang I-induced contraction: EC50 Ang II-induced contraction) as an indicator of the tissue ACE effectiveness. In the aorta without endothelium, Ang I was found to be much less potent than Ang II in the rabbit (R = 44) compared with the rat (R = 3.5). This species difference in the aortic conversion of Ang I to Ang II was confirmed by the use of captopril. Captopril (10(-6) M) shifted the Ang I concentration/ response curve by 2- and 14-fold to the right in rabbit and rat respectively. In other rabbit blood vessels, the rank order of potency to Ang I in endothelium denuded rings was basilar artery > > carotid artery > or = aorta > or = saphenous artery. In addition, the R value was the lowest for the basilar artery (R = 2.5). This is in agreement with the highest rightward shift (78-fold) of the Ang I concentration/response curve by captopril for basilar artery in comparison with only 3-, 8- and 3-fold shifts observed in carotid artery, saphenous artery and aorta respectively. In conclusion, our data provide evidence for a greater influence of ACE in rabbit basilar artery than in peripheral vessels.

Angiotensin I↗
PubMed1987

The effect of uropathogenic bacteria on ureteral motility.

The effect of bacterial products of various strains obtained from patients with urinary tract infections was tested on peristalsis of sheep ureteral rings. In 55-70% spontaneous rhythmic contractions were inhibited by addition of small amounts of growth supernatants from Escherichia coli, Pseudomonas aeruginosa and Klebsiella pneumoniae. The isolates were also tested on mesenteric artery ring preparations. In these vessels the isolates induced tonic contractions, particularly when the vessel had been depolarised and precontracted with a 40 mM KCl solution. This response is characteristic of a calcium ionophore, known to occur in some bacterial toxins. The active principle of the bacterial ureteroplegic factor (BUF) is heat sensitive and distinct from endotoxins which speed up peristalsis. It is suggested that the ureteroplegic action depends on an exotoxin with ionophoric properties.

Animals↗
PubMed1997

Role of maxi-K+ channels in endothelin-induced vasoconstriction of mesenteric and submucosal arterioles.

The action of endothelin in small intestinal resistance vessels of the guinea pig was studied by examining submucosal arteriole vasoactivity in vitro and electrical properties of mesenteric arteriole smooth muscle cells. Endothelin-1 (ET-1) constricted submucosal arterioles with a half-maximal effective concentration of 170 pM. ET-3 caused detectable constriction with a minimum of 20 nM. The ET-1 response was prolonged, with a time to 90% relaxation of 41 +/- 2.8 min after washout. The ETA antagonist BQ-123 (200 nM) decreased the sensitivity to ET-1 approximately 40-fold. Arterioles preconstricted with prostaglandin F2 alpha did not relax when superfused with ET-1, ET-3, or an ETB agonist, IRL-1620, and pretreatment with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine was ineffective in countering ET-1-induced constriction, indicating the absence of functional ETB receptors. Resting membrane potential in isolated cells was characterized by transient hyperpolarizing spikes (THs). ET-1 (20 nM) increased TH frequency and caused the emergence of a larger amplitude population. Under voltage clamp, spontaneous transient outward currents (STOCs) were seen that reversed at the K+ equilibrium potential. ET-1 increased STOC frequency and amplitude. Iberiotoxin (IBTX; 200 nM), a maxi-K+ channel antagonist, blocked the ET-1-induced THs and reduced STOC activity. IBTX or tetraethylammonium increased the rate and extent of ET-1-induced arteriole constriction. We suggest that ET-1-induced vasoactivity of ileal resistance arterioles involves ETA receptor-mediated early activation of maxi-K+ channels that serves to counter strong constriction.

Animals↗
PubMed1995

Two-dimensional time-of-flight magnetic resonance angiography in the coronal plane for abdominal disease: its usefulness and comparison with conventional angiography.

Using two-dimensional time-of-flight magnetic resonance angiography (2D-TOF MRA) in the coronal plane, 54 cases of arterial disease and 46 cases of venous disease were evaluated. The results were compared with those of conventional angiography to establish their relative usefulness for diagnosing abdominal diseases. Using 2D-TOF MRA, relatively large vessels such as the splenic artery, the trunks of the superior mesenteric artery (SMA) and the renal artery were clearly visualized. However, smaller vessels such as the gastroduodenal artery, main hepatic artery, branches of the SMA and the renal artery were not clearly imaged. The diameters of stenotic arteries correlated well with their images on conventional angiography (r = 0.953). In the venous system, the splenic, renal and portal veins and the first branches of the portal vein bilaterally were clearly imaged. Veins, normal or abnormal, less that 5 mm in diameter were not clearly imaged using 2D-TOF MRA. 2D-TOF MRA in the coronal plane provided useful diagnostic information, especially regarding venous diseases, tumour thrombi in the portal vein, renal vein or inferior vena cava (IVC), collateral vessels or shunts, vascular malformations, and the relationships between the portal and hepatic veins. Limitations encountered in arterial disease did not interfere with evaluations of venous disease.

Abdomen↗
PubMed1995

Effluxes of 3,4-dihydroxyphenylalanine, 3,4-dihydroxyphenylglycol, and norepinephrine from four blood vessels during basal conditions and during nerve stimulation.

Effluxes of 3,4-dihydroxyphenylalanine, 3,4-dihydroxyphenyglycol, and norepinephrine from four superfused canine blood vessels (saphenous and portal veins and mesenteric and pulmonary arteries) were studied under basal conditions and during nerve stimulation. From quantification of the compounds a series of indices of activities at neuroeffector junctions are proposed. These are (a) basal overflow of 3,4-dihydroxyphenylglycol as an index of vesicular-cytoplasmic translocation of norepinephrine, (b) the increase in 3,4-dihydroxyphenyglycol overflow attributable to nerve stimulation as an index of neuronal reuptake of norepinephrine released by stimulation, (c) the sum of the increases in overflows of norepinephrine and 3,4-dihydroxyphenylglycol attributable to nerve stimulation as an index of evoked release of norepinephrine, and (d) the efflux of 3,4-dihydroxyphenylalanine as an index of the activity of tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of norepinephrine. There were clear differences between these indices in the vessels. Correlation coefficients of the indices among vessels indicated that a high tissue norepinephrine level was associated with high biosynthetic capacity and high vesicular-cytoplasmic exchange but not with high release. There was no evidence suggesting feedback inhibition of synthesis by neuroplasmic norepinephrine--whether arising from vesicular-cytoplasmic translocation or from reuptake from the junctional cleft. The major value of these indices will probably be in determining the integrated effects of pharmacologic agents at neuroeffector junctions in different blood vessels.

Animals↗
PubMed1999

Heterogeneity of vascular smooth muscle alpha-adrenoceptors in canine blood vessels.

1. For the past decade, using radioligand binding, contractility and immunohistochemical techniques, we have been characterizing vascular smooth muscle (VSM) adrenoceptors in four functionally different canine blood vessels, namely the dog aorta (DAO), dog mesenteric artery (DMA), dog mesenteric vein (DMV) and dog saphenous vein (DSV). 2. This communication briefly reviews our findings (with a special emphasis on alpha-adrenoceptor subtypes), which showed that none of the four canine vessels showed the same complement of alpha-adrenoceptor subtypes. 3. All four vessels elicited alpha 1-adrenoceptor contractile responses (antagonized by prazosin), but alpha 2-adrenoceptor responses (sensitive to rauwolscine), were found only in DMV and DSV. 4. Pharmacological characterization using alpha 1-adrenoceptor subtype-selective antagonists showed that DAO contains mainly alpha 1B-adrenoceptors (some alpha 1D-adrenoceptors) and DMA has primarily alpha 1A/1L-adrenoceptors, alpha 1-Adrenoceptors in DMV are primarily of the alpha 1D subtype, but either a new or unusual alpha 1-adrenoceptor subtype was revealed in the DSV.

Adrenergic alpha-Antagonists↗
PubMed2000

Possible role of P-450-derived metabolites in endothelium-dependent relaxation of rat small mesenteric arteries.

We reported previously that acetylcholine (ACh)-induced endothelium-dependent relaxation of rat mesenteric microvessels depended both on nitric oxide (NO) and on a charybdotoxin (CTX)-sensitive endothelium-derived hyperpolarizing vasodilator. Cytochrome P450 (CYP)-dependent arachidonic acid metabolites act in some systems as hyperpolarizing vasodilators. We sought to quantitate contributions of such metabolites to the CTX-sensitive component of ACh-induced vasodilation in isolated rat mesenteric resistance arteries. ACh relaxed these vessels nearly completely (93.3+/-1.2%, n = 71); cyclooxygenase inhibition with indomethacin did not diminish this response (94.3+/-11.4%, n = 9). NO synthase inhibition with Nitro-L-arginine (NNLA) reduced relaxation by 30% (n = 54, p<0.05). Pretreatment of vessels with CYP inhibitors, either clotrimazole (CTM) or 17-octadecynoic acid (17-ODYA), or with selective K+ channel inhibitors, either tetraethyammonium acetate (TEA) or CTX, each led to similar small reductions in maximal relaxation (17%, 22%, 16%, and 9% respectively, n = 3-6). Combined pretreatment with NNLA + either (CTM or 17-ODYA) or (TEA or CTX) each led to similar maximal relaxations (52.2+/-4.8%, 50.6+/-9.2, 37.6+/-8.6%, and 44.1+/-11.5%, respectively, n = 6-35; p<0.05 for NNLA+[CTM or TEA or CTX] vs NNLA alone). Combined pretreatment with NNLA+CTM+(CTX or TEA) led to similar maximal relaxations (43.0+/-7.3%, 43.7+/-15%, n = 6-11) that did not differ from values in vessels pretreated with either NNLA+CTM or NNLA+(CTX or TEA). We conclude that the ACh-induced vasodilation was insensitive to cyclooxygenase inhibition, partially sensitive to NO synthase inhibition, and that the K+ channel blockers TEA and CTX identified the same minor component of ACh relaxation as did the CYP inhibitor CTM.

Acetylcholine↗
PubMedDate not supplied

Outcomes after redo procedures for failed mesenteric revascularization.

This report examines results of mesenteric revascularization following a failed splanchnic revascularization. Patients undergoing repeat mesenteric revascularization from January 1985 to July 2002 were identified from a prospectively maintained registry. Data recorded included procedures performed, perioperative mortality, complications, and operative indications. Patients who had embolic events were excluded. Eighty-six patients underwent 105 mesenteric interventions in this time period; 22 patients underwent 33 repeat mesenteric revascularization procedures. There were 25 single-vessel bypasses, 3 multivessel reconstructions, 3 angioplasty procedures (1 open, 2 percutaneous), and 2 graft thrombectomies. Complications occurred in 33.3%. Perioperative mortality was 6.1%, all in patients with acute mesenteric ischemia. One- and 4-year primary patency for repeat mesenteric revascularization was 73.5% and 62.2%, respectively, and survival for repeat mesenteric revascularization was 85.9% and 75.5%, respectively. Patients surgically treated for mesenteric ischemia can require additional interventions. Repeat revascularization effectively prolongs survival when an earlier intervention fails.

Adult↗
PubMed1996

[Hydrosonography of the pancreas. Initial results of a pilot study].

PURPOSE: To evaluate a new ultrasonographic imaging technique of the pancreas (hydrosonography), based on a combination of chemical intestinal paralysis and water distension of the stomach and duodenum, regarding its significance for tumor detection, staging and assessment of tumor resectability. MATERIAL AND METHODS: In an open prospective study 51 patients with suspected pancreatic neoplasm were examined between July 1995 and October 1995. The technique of hydrosonography included intravenous injection of 40 mg N-butyl-scopolaminiumbromid (Buscopan) and maximum gastric and duodenal wall distension by oral administration of an average of 11 warm tap water (0.5-1.51). A detailed evaluation form was used to assess (1) overall imaging quality; (2) accuracy of identification of the pancreas in its various anatomic regions and of peripancreatic vessel structures relevant for resectability, such as splenic, superior mesenteric, and portal veins, celiac trunk, and superior mesenteric, splenic and hepatic arteries; and (3) tumor size, sonographic structure and level of organ and vessel infiltration. As gold standards for positive tumor detection and description, surgery and microscopic diagnosis were used, and for negative tumor detection, event-free survival of 6 months. RESULTS: All examinations were diagnostic. Identification of the pancreas was complete in all 51 patients with an excellent overall imaging quality in 53%. In 86% of cases the various examined organ and vessel structures were depicted with either good or average imaging quality. In 48 of the 51 patients diagnosis positive for tumor or other organ pathology was made. A total of 16 pancreatic carcinomas and 5 benign tumors were diagnosed. Twenty-seven patients had pathology not related to a pancreatic neoplasm. For tumor detection, sensitivity was 82% and specificity 100%. For correct assessment of tumor resectability, sensitivity was 86% and specificity 100%. CONCLUSION: The new technique of hydrosonography combines the value of routine non-invasive abdominal ultrasound with increased sensitivity and specificity for tumor detection and assessment of resectability by improved imaging accuracy.

Adult↗
PubMed2006

Modulation of sympathetic neurotransmission by neuropeptide Y Y2 receptors in rats and guinea pigs.

We have investigated the effect of the Y2 receptor agonist (Y2 agonist; N-acetyl [Leu28,31] NPY 24-36), on contractions evoked by transmural electrical stimulation of sympathetic nerves of isolated arteries from a range of vascular beds in rats and guinea pigs. Contractions evoked by transmural stimulation of the rat renal, mesenteric and femoral arteries were significantly attenuated in the presence of the Y2 agonist. In these arteries, contractions were significantly inhibited in the presence of an alpha-adrenoceptor antagonist (76-97%). So we conclude that these responses were primarily mediated by noradrenaline and that the Y2 agonist attenuates the release of noradrenaline via presynaptic Y2 receptors. Contractions of the rat carotid artery were not attenuated by the Y2 agonist but were completely abolished in the presence of an alpha-adrenoceptor antagonist suggesting that in this artery the Y2 agonist has no effect on release of noradrenaline. In the guinea pig, carotid arteries contractions evoked by transmural nerve stimulation were attenuated in the presence of the Y2 agonist and inhibited by an alpha-adrenoceptor antagonist 75-87% suggesting that the Y2 agonist attenuates the release of noradrenaline via presynaptic Y2 receptors in this vessel. In the guinea pig femoral artery contractions evoked by transmural stimulation were not modified in the presence of the Y2 agonist but were completely abolished in the presence of an alpha-adrenoceptor antagonist. This suggests that the Y2 agonist does not modify noradrenaline release in this vessel. Contractions of the guinea pig mesenteric artery were significantly potentiated by the Y2 agonist, possibly by potentiation of neuropeptide Y (NPY) at the Y1 receptor. The Y1 antagonist inhibited more than 70 % of the response, indicating that the majority of the contraction was mediated by NPY. The current study demonstrates heterogeneity of neurotransmitter substances in sympathetic nerves supplying vascular beds within and across species and in subsequent functional response.

Adrenergic alpha-Antagonists↗
PubMed2005

Diabetes induces Na/H exchange activity and hypertrophy of rat mesenteric but not basilar arteries.

Experimental hyperglycemia produces a marked hypertrophic response in rat mesenteric arteries, accompanied by activation of Na/H exchange (NHE) in medial smooth muscle. This study asked if other vascular beds are similarly affected by examining the hypertrophic and NHE response of the basilar artery. Sections of mesenteric and basilar arteries from adult rats were analysed by standard morphometric techniques at 1 and 3 weeks after streptozotocin injection. NHE activity was assessed as changes in intracellular pH in isolated intact vessels using concurrent myography and fluorescence spectroscopy. Mesenteric arteries showed a significant increase in lumenal (47%), medial (51%) and adventitial (17%) area. In contrast, these parameters were not increased in basilar arteries from the same set of animals. Maximal NHE activity was significantly increased at 1 week (24%) and 3 weeks (20%) in mesenteric arteries, but in basilar arteries there was no change in basal intracellular pH, maximal NHE activity or kinetic properties of the transporter. NHE plays a central role in vascular changes in diabetes. As the mesenteric hypertrophy is amenable to therapeutic intervention these findings add further to the potential of NHE as a therapeutic target for ameliorating vascular disease in diabetes.

Animals↗
PubMed1997

Role of cytosolic Ca2+ and protein kinase C in developing myogenic contraction in isolated rat small arteries.

Cytosolic Ca2+ and protein kinase C (PKC) may regulate the myogenic contraction of arterial myocytes. The role of these second messengers is examined in skeletal muscle small arteries, which have strong myogenic activity, and mesenteric small arteries, which have weak myogenic activity. The vessels were isolated and cannulated. The inner diameter was measured with a video-digitizing system. Cytosolic Ca2+ concentration was assessed by fura 2. Skeletal muscle small arteries dilated from 122 +/- 6 to 153 +/- 6 microm immediately after the transmural pressure change from 40 to 100 mmHg and constricted to 121 +/- 5 microm (myogenic contraction) with an increase in the 340/380 fluorescence ratio (by approximately 33%) in control vessels. Nifedipine abolished myogenic contraction and the increase in the fluorescence ratio. PKC inhibitors (H7 and staurosporine) abolished myogenic contraction but did not depress the increase in the fluorescence ratio. In mesenteric small arteries, myogenic contraction was insignificant in control vessels. A relatively low dose of PKC activator (4.4 +/- 1.4 nmol/l) elicited myogenic contraction, but a higher dose (21 +/- 6 nmol/l) depressed it. Thus the cytosolic Ca2+ increase and PKC activity may cooperatively act on the myogenic contraction of skeletal muscle small arteries. The activity of PKC should play an important role in myogenic contraction of rat small arteries.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMedDate not supplied

[Anatomic and physiopathologic basis for the diagnosis and treatment of intestinal ischemia].

Changes of circulatory parameters in splanchnic territory lead to gut ischemia in an acute or chronic form (postprandial abdominal stroke). The implicated factors in intestinal ischemia are the timing and kind of onset, countercurrent vascularization and the eventuality of anastomotic subsystems for becoming hypertrophic. Superior mesenteric artery (SMA) is the "key" blood vessel implicated in the production of chronic intestinal ischemia, the atherosclerotic lesion being localized more frequent near SMA's ostium or even at ostium itself. Nonoclusif ischemia is induced by another stimulus that provokes mesenteric vasoconstriction, status that affects more the antimesenteric intestinal border, with a larger expansion at mucosa level. The most reseed diagnostic methods are selective angiographies and ultrasound examination. Usually chronic intestinal ischemia is clinically asymptomatic and becomes clinical evident just in the presence of an acute superposed factor or when at least two digestive arteries are affected. Revascularization methods are different, based on the type, mechanism and site of obstruction, each with its advantages and disadvantages. The most used method is retrograde aortomesenteric by-pass, at infrarenal aortic level (that is more accessible than the supraceliac aorta) and SMA reimplantation.

Humans↗
PubMed2004

Prolongation of the intestinal viability using oxygenated perfluorocarbon in an experimental model of acute intestinal ischemia.

OBJECTIVES: Liquid perfluorocarbons (PFCs) are well known for their capability to carry respiratory gases. The aim of this study was to evaluate the effectiveness of oxygenated F-Decalin on the intestinal viability, in an experimental model of acute intestinal ischemia. MATERIAL AND METHODS: Thirty-six rabbits were subjected to 8h intestinal ischemia by ligation of the superior mesenteric artery (subgroups 1), the mesenteric vein (subgroups 2) or both vessels (subgroups 3). The animals were divided into three groups: (a) Control (ischemia alone), (b) PFC-O2 (ischemia plus infusion of oxygenated F-Decalin) and (c) PFC (ischemia plus infusion of not-oxygenated F-Decalin). Intestinal biopsies from four different sites and blood samples for serum enzymes measurements were taken at 2, 4, 6 and 8 h. All tissue sections were examined blindly under light microscope. Sections from the specimens were taken at 4 and 8 h, and examined blindly under the electron microscope. Statistical analysis was performed by non-parametric Kruskal Wallis test. RESULTS: Using light microscope, the observed intestinal damages to the sections from Control and PFC groups were severe at 4 h and destructive after 8 h. On the contrary, minimal injuries were observed in the biopsies from PFC-O2 group at 4 and even after 8 h of ischemia. These findings were confirmed by the electron microscope study and correlated to the serum enzymes measurements. CONCLUSIONS: These results suggest that intestinal viability could be prolonged after acute ischemia using oxygenated perfluorocarbons and this could be a promising pretreatment modality for a variety of mesenteric ischemic forms.

Acute Disease↗