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PubMed1986

Aggressive long-term antihypertensive therapy with pinacidil does not cause regression of cardiovascular hypertrophy in the spontaneously hypertensive rat.

After dosage titration from the age of 1 month to the age of 3 months, spontaneously hypertensive rats (SHR) were treated with pinacidil 10 mg/kg daily until the age of 6 or 12 months. Morphometric data were obtained from the treated SHR as well as from untreated age-matched SHR and normotensive Wistar-Kyoto rats (WKY) at these two developmental stages. Heart:body weight ratios and media:lumen ratios for resistance vessels were determined. Vessels obtained from the mesenteric region were investigated on a myograph. Vessels from heart, kidney and lung were investigated by morphometric analysis of histological sections, only specimens from 12-month-old rats were used. In SHR no effects of either ageing or treatment were detectable, although their blood pressure had been effectively held at normotensive levels throughout the life of the treated animals from the age of 3 months. With the exception of the media index of the pulmonary vessels, which was not statistically different from treated or control SHR, the WKY morphological parameters were significantly lower. In conclusion, pinacidil normalized blood pressure without complications, but this did not affect SHR cardiovascular structure. It is suggested that development of this strain-specific enlargement can only be modified if blood pressure is kept at hypotensive levels, or if the effect of a hitherto unidentified causative factor is antagonized by more-specific pharmacological treatment.

Animals↗

PubMed1987

Mechanical, morphological and pharmacological properties of oesophageal varices and small mesenteric veins in portal hypertensive rabbits.

The properties of isolated small oesophageal and mesenteric veins were investigated in a rabbit model subjected to a 4-week period of portal vein stenosis. The animals developed oesophageal varices and these together with the small mesenteric veins were mounted on a myograph. Compared with sham-operated controls portal hypertension resulted in an increased normalized inner radius and media thickness of the oesophageal veins resulting in a non-significant increase in the media to lumen ratio, while the inner radius decreased as media thickness increased in mesenteric veins resulting in a significant (P less than 0.01) increase in the media to lumen ratio. When activated, the active wall tension of both the oesophageal and mesenteric veins was increased following portal hypertension, but the active media stress was unchanged. The EC50 for noradrenaline and angiotensin II did not change in portal hypertensive vessels compared with controls and was equal in oesophageal and mesenteric vessels. The ability of isoprenaline and serotonin to relax pre-contracted vessels of both types was reduced by the portal hypertension. The results of these studies suggest that the development of oesophageal varices is not only due to increased portal venous pressure.

Angiotensin II↗

PubMed1994

Characterization of the alpha-1 adrenoceptors in the mesenteric vasculature from deoxycorticosterone-salt hypertensive rats: studies on vasoconstriction, radioligand binding and postreceptor events.

The vasoconstrictor responses to alpha-1 adrenoceptor agonists, binding behavior of alpha-1 adrenoceptors and postreceptor events in the mesenteric vasculature from deoxycorticosterone acetate-salt hypertensive rats were studied. The reactivity of perfused mesenteric artery to norepinephrine (NE) and phenylephrine, but not KCl, was enhanced significantly in the hypertensive rats compared with control rats. Prazosin antagonized the pressor response to NE more effectively in the hypertension than in the control. [3H]Prazosin binding was saturable and a single class of specific sites. Scatchard analysis revealed that the dissociation constant for [3H]prazosin was lower and the maximum binding capacity was greater in the hypertensive rats than in the control rats. The NE-stimulated phosphatidylinositol hydrolysis, estimated by measuring inositol 1,4,5-triphosphate (IP3) accumulation, was greater in the hypertensive rat artery compared with the control one. The IP3-induced contraction in the beta-escin-treated mesenteric large resistance vessel was smaller in the hypertensive rats. The vasoconstrictor response to phorbol 12,13-dibutyrate of the perfused mesenteric artery was larger in the hypertensive animals than in the control. Staurosporine antagonized the phorbol 12,13-dibutyrate-induced vasoconstriction in preparations from both rats. These results suggest that the increases in the number and affinity of alpha-1 adrenoceptors may result in an enhanced phosphatidylinositol hydrolysis accounting for an increased vascular reactivity to alpha-1 adrenoceptor agonists in deoxycorticosterone acetate-salt hypertensive rats. Furthermore, the enhancement of vasoconstrictor mechanism mediated by protein kinase C pathway may also contribute to vascular hyper-reactivity to NE, whereas the decreased IP3-induced contraction may function to minimize the hyper-reactivity observed in this model of experimental hypertension.

Animals↗

PubMed1995

Vascular and myocardial protective effects of converting enzyme inhibition in experimental heart failure.

Systemic vasoconstriction due to stimulation of the sympathetic and renin-angiotensin-aldosterone systems is a hallmark of heart failure and this is accompanied by impaired endothelium-dependent relaxations at the level of large arteries. This study investigated, in a rat model of heart failure, whether such an endothelial dysfunction also exists at the level of the resistance artery, and whether this is associated with morphologic changes, as well as the effects of chronic treatment with the angiotensin-converting enzyme inhibitor perindopril (2 mg/kg/day). After 12 months, arterial pressure, left ventricular (LV) end diastolic pressure (LVEDP), and LV dP/dt were measured in anesthetized rats. Responses to acetylcholine and nitroprusside were determined in isolated and perfused mesenteric artery segments (diameter: 280 +/- 15 microns). After fixation, vessel diameter, media cross-sectional area, and media collagen and elastin densities were measured by image analysis. After 12 months, untreated rats showed signs of heart failure, i.e., reduced LV dP/dt, and increased LVEDP, heart weight/body weight, LV cavity circumference, and myocardial collagen density. In mesenteric vessels the endothelium-dependent vasodilator response to acetylcholine was impaired, whereas the response to the nitric oxide donor nitroprusside was unaffected. Heart failure did not affect vascular morphological parameters. Perindopril decreased blood pressure and LVEDP without any modification of LV dP/dt, and prevented cardiac remodeling. At the vascular level, perindopril improved the response to acetylcholine and reduced media cross-sectional area and collagen density without affecting internal vessel diameter or elastin density. Thus, heart failure decreases endothelium-dependent vasodilator response to acetylcholine without modification of vessel structure.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed2006

Pancreatic adenocarcinoma: signs of vascular invasion determined by multi-detector row CT.

The purpose of this study was to analyse multi-detector row CT (MDCT) signs of peripancreatic arterial and venous invasion in pancreatic carcinoma. Among 101 patients with pancreatic carcinoma examined by MDCT, 54 candidates for surgery were pre-operatively evaluated for vascular invasion based on MDCT signs. The peripancreatic major vessels (including superior mesenteric artery, coeliac artery, common hepatic artery, superior mesenteric vein and portal vein) were examined carefully by surgeons during the operation. At surgical exploration, 78 of 224 vessels were invaded by tumour. The invaded peripancreatic major arteries (n = 29) and veins (n = 49) presented different MDCT signs: 43% of invaded veins (18/42, except for 7 occluded veins) were surrounded by tumour less than 50% of the vessel circumference compared with 97% (28/29) of the invaded arteries, which were surrounded by tumour more than 50% of the vessel circumference or were embedded in tumour (p<0.001). 69% (34/49) of the invaded veins had vascular stenosis or obliteration, compared with 41% (12/29) of the invaded arteries (p<0.05). Irregularity of the vein wall, 74% (31/42, except for 7 occluded veins); occurred more often than that of the artery wall, 45% (13/29) (p<0.05). In conclusion, the MDCT signs of peripancreatic arterial and venous invasion have different characteristics, which should be considered in pre-operative evaluation.

Adenocarcinoma↗

PubMed2005

Further characterization of the time-dependent vascular effects of delta9-tetrahydrocannabinol.

We have previously shown that over time (2 h), the active ingredient of cannabis, Delta(9)-tetrahydrocannabinol (THC), produces peroxisome proliferator-activated receptor (PPAR) gamma-mediated vasorelaxation of conduit arteries. We have now investigated whether incubation with THC affects agonist-stimulated contractile (methoxamine) and endothelium-dependent vasorelaxant (acetylcholine) responses in the rat superior mesenteric artery (G0) and aorta by myography. We have also investigated whether similar responses are observed in isolated resistance (G3) vessels of the mesenteric bed. In both the aorta and G0, incubation with 10 microM THC for 2 h, but not 10 min, significantly attenuated the contractile responses to methoxamine. This effect of THC was abolished in the presence of the enzyme catalase, which breaks down H(2)O(2), and was reduced in the presence of the superoxide dismutase inhibitor diethyldithiocarbamate (DETCA), but it was not PPARgamma-mediated. THC also inhibited calcium influx in a H(2)O(2)-dependent manner. In G0, but not the aorta, incubation with 10 muM THC for 2 h significantly enhanced endothelium-dependent vasorelaxation. This was inhibited by a PPARgamma antagonist, 2-chloro-5-nitro-N-phenylbenzamide (GW9662), catalase, and DETCA, but not by the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester. By contrast, in G3, no time-dependent vasorelaxation of precontracted arteries to THC was observed, and incubation with THC led to potentiation of contractile responses and blunting of vasorelaxation to acetylcholine, which seems to involve inhibition of endothelium-derived hyperpolarizing factor (EDHF) production, and agonist-stimulated production of EDHF. These data demonstrate further the time-dependent vascular actions of THC and also highlight the heterogenous effects of THC in different arterial types.

Animals↗

PubMed1978

[Significance of the state of the celiac and mesenteric arteries in the treatment of occlusive lesions of the abdominal aorta and iliac vessels].

The status of the celiac and mesenteric arteries in 124 patients with occlusive injuries to the abdominal aorta and iliac arteries has been studied by means of the antero-posterior and lateral translumbar abdominal aortography. Clinical picture and symptoms of pathological conditions with the regard to the localization of occlusion are described. Some practical recommendations are given.

Aorta, Abdominal↗

PubMed1975

Dopamine induced relaxation of isolated canine renal, mesenteric, and femoral arteries contracted with prostaglandin F2-alpha.

The purpose of this investigation was to develop a system for studying the effects of dopamine on isolated blood vessels. Canine renal, mesenteric, and small femoral arteries (less than 1 mm outside diameter) were exposed to phenoxybenzamine 10-5 M for one hour and contracted with prostaglandin F2-alpha. Cumulative concentrations of dopamine ranging from 10-6 to 10-4 M caused dose-related relaxation of the arteries. Propranolol 10-6 M did not affect the relaxation in concentrations which markedly antagonized the effects of isoproterenol. Large femoral arteries (greater than 1 mm outside diameter) did not relax with similar concentrations of dopamine. N-methyldopamine (epinine) produced similar relaxation; 3-methoxytyramine was inactive. Specific antagonism could not be demonstrated by the postulated dopamine antagonists-haloperidol, chlorpromazine, apomorphine, or bulbocapnine-in concentrations up to 10-5 M. Higher concentration of these agents could not be used because they caused the arteries to relax. This study demonstrated that PGF2-alpha-contracted arteries pretreated with phenoxybenzamine are suitable for further investigations of putative dopamine agonists and antagonists.

Adrenergic beta-Antagonists↗

PubMed2000

Endogenous calcitonin gene-related peptide (CGRP) mediates adrenergic-dependent vasodilation induced by nicotine in mesenteric resistance arteries of the rat.

1. The mechanisms underlying vasodilator effect of nicotine on mesenteric resistance blood vessels and the role of calcitonin gene-related peptide (CGRP)-containing (CGRPergic) vasodilator nerves were studied in the rat. 2. Mesenteric vascular beds isolated from Wistar rats were perfused with Krebs solution, and perfusion pressure was measured with a pressure transducer. 3. In preparations with intact endothelium and contracted by perfusion with Krebs solution containing methoxamine, perfusion of nicotine (1 - 100 microM) for 1 min caused a concentration-dependent vasodilator response without vasoconstriction. 4. The nicotine-induced vasodilation was markedly inhibited by hexamethonium (nicotinic cholinoceptor antagonist, 10 microM) and blocked by guanethidine (adrenergic neuron blocker, 5 microM). 5. Either denervation by cold storage (4 degrees C for 72 h) or adrenergic denervation by 6-hydroxydopamine (toxin for adrenergic neurons, 2 mM for 20 min incubation, twice) blocked the nicotine-induced vasodilation. 6. Neither endothelium removal with perfusion of sodium deoxycholate (1.80 mg ml(-1), for 30 s) nor treatment with N(omega)-nitro-L-arginine (nitric oxide synthase inhibitor, 100 microM), atropine (muscarinic cholinoceptor antagonist, 10 nM) or propranolol (beta-adrenoceptor antagonist, 100 nM) affected the nicotine-induced vasodilation. 7. In preparations without endothelium, treatment with capsaicin (depleting CGRP-containing sensory nerves, 1 microM) or human CGRP[8 - 37] (CGRP receptor antagonist, 0.5 microM) markedly inhibited the nicotine-induced vasodilation. 8. These results suggest that, in the mesenteric resistanc artery of the rat, nicotine induces vasodilation, which is independent of the function of the endothelium and is involved in activation of CGRPergic nerves. It is also suggested that nicotine stimulates presynaptic nicotinic cholinoceptors on adrenergic nerves to release adrenergic neurotransmitters, which then act on CGRPergic nerves to release endogenous CGRP from the nerve.

Animals↗

PubMed1986

Histamine level changes in the plasma and tissues in hemorrhagic shock.

Histamine (H) levels have been reported during various types of shock, but there is a paucity of such data during hemorrhagic shock. The present study demonstrates a rapid, severalfold increase of radioenzymatically measured plasma H in conscious and anesthetized dogs subjected to experimental hemorrhagic shock. Shock was elicited by bleeding to a mean arterial blood pressure of 5.3 kPa, and maintained until 20% of the maximal bleeding volume (MBV) was taken back by the animal. The corresponding figures in the anesthetized group were 4 kPa and 30% uptake. The increased H level persisted in both groups during hypovolemia and remained above the control value following reinfusion. Survival was examined in the conscious group. At MBV, survivors had significantly higher H levels and H/norepinephrine and H/renin activity ratios in the plasma than nonsurvivors. The H level increased in the liver, lungs, spleen, left atrium and ventricle, and blood vessel walls (superior mesenteric artery, small jejunal arteries and veins, femoral artery and vein). The H/norepinephrine ratio increased in the left ventricle and blood vessel walls. The increase of H in the blood plasma and blood vessels during hemorrhagic shock may exemplify a counterregulation against excessive vasoconstriction and could be a positive factor in survival.

Animals↗

PubMed1994

Diabetes mellitus-induced enhancement of prostaglandin F2 alpha-responses is inhibited by lipoxygenase- but not cyclooxygenase-inhibitors in mesenteric veins and arteries of mouse and rat.

The mechanisms responsible for diabetes mellitus-induced enhancement of prostaglandin (PG) F2 alpha response were investigated in vascular smooth muscles isolated from diabetic mice and rats. Streptozocin (150 mg/kg, i.v. bolus, 6 week-elapsed)-ddY mice and (60 mg/kg, i.v. bolus)-Wistar rats and genetically diabetic GK-rats were used. The responses to PGF2 alpha were enhanced in small blood vessels such as mesenteric arteries (diabetic rats) and veins (diabetic mice) and they were reduced in large blood vessels such as the aorta and vena cava (diabetic rats). The enhanced response to PGF2 alpha in diabetic blood vessels was significantly inhibited by nordihydroguaiaretic acid (NDGA) (0.03 mM) and phenidone (0.05 mM), lipoxygenase inhibitors, cycloheximide (1 mg/kg, i.v.), a protein synthesis inhibitor and actinomycin D (2.8 mg/kg, i.v.), a RNA polymerase inhibitor, but neither inhibited by cyclooxygenase inhibitors, a thromboxane antagonist, nor Ca2+ antagonists. The PGF2 alpha response was also enhanced with aging alone, whereas the extent of enhancement was less than that with diabetes mellitus, and not significantly blocked by NDGA. These results demonstrate that diabetes mellitus-induced imbalance in the regulation of the eicosanoid metabolic pathways (suppressed cyclooxygenase and accelerated lipoxygenase) may cause the enhancement of PGF2 alpha-induced responses in small blood vessels.

Aging↗

PubMed1991

Morphological and functional alterations of mesenteric small resistance arteries in early renal hypertension in rats.

We investigated the structure and reactivity of small resistance arteries of two-kidney, one-clip (2K,1C) and one-kidney, one-clip (1K,1C) Goldblatt hypertensive rats within 4-6 wk of development of hypertension. Blood vessels from the mesenteric vascular bed with lumen diameter less than 300 microns were mounted on a wire myograph. The media of the vessel wall was significantly increased and lumen diameter was decreased in 2K,1C and 1K,1C rats. External diameter of blood vessels was reduced in both 2K,1C and 1K,1C rats, whereas cross-sectional area of the wall was increased significantly in 1K,1C rats. Wall tension in response to KCl was significantly lower in 2K,1C and 1K,1C hypertensive rats, whereas tension in response to norepinephrine (NE) was reduced in 1K,1C hypertensive rats but was similar in 2K,1C rats and controls. Active tension in response to arginine vasopressin (AVP) was similar in all groups. As a consequence of the reduced lumen circumference of small arteries, effective pressure in response to NE was similar in hypertensive and control rats, whereas effective pressure in response to AVP was exaggerated in the hypertensive rats. The sensitivity to NE and AVP was similar in all groups. These results show the rapid development of functional and structural changes in small resistance arteries in renal hypertensive rats within 4-6 wk of hypertension, with significant reduction in external and lumen diameters, increased media width, and increased media-to-lumen ratio, which enhance vascular reactivity to vasoconstrictors, in particular NE and AVP.

Animals↗

PubMed2000

[Contrast-enhanced three-dimensional angiography].

Rapid advances in the techniques of contrast-enhanced MR angiography (MRA) have made it possible to evaluate the entire aorta and main arteries as well as small arteries and veins of the whole body. In this article, the technical aspects and clinical applications of contrast-enhanced MRA are reviewed. Dynamic contrast-enhanced three-dimensional (3D) MRA is a first-pass vascular imaging technique that uses the 3D fast field echo sequence with rapid bolus injection of contrast material. By repeating imaging sequences, it is possible to trace the dynamics of the injected contrast material over time and apply various postprocessing techniques, such as double subtraction and addition, to demonstrate arteries and veins separately and to display the arteries in a single image, even when circulation time is prolonged. This technique is flexible enough to be applied in a variety of clinical settings by optimizing the examination. The abdominal aorta and main arteries of the lower extremities are examined by two methods, dynamic subtraction 3D MRA (MRDSA) and the moving-bed method. Three bolus injections of contrast material are used in MRDSA. In contrast, a slow continuous injection of a large dose (20 ml or more) of contrast material is used in the moving-bed method, which is a convenient, useful method of contrast-enhanced MR angiography when the study must focus on arterial imaging. Clinical indications include atherosclerotic occlusive disease, Takayasu arteritis, aortic dissection, anti-phospholipid antibody syndrome, aneurysm, patent and occluded bypass graft, and deep vein thrombosis, among others. The problem with contrast-enhanced MRA is its difficulty in depicting small vessels such as mesenteric arteries, distal renal arteries, and peripheral small arteries. The nature of gradient-echo sequences has certain inherent problems for the imaging of small vessels. The fat-tissue interface becomes dark because of chemical shift artifact (which occurs both when the echo time is set in-phase and when it is set out-of-phase), reducing the ability to detect small arteries with contrast-enhanced MR angiography. The fat suppression technique is very useful for satisfactorily demonstrating small vessels by reducing chemical shift artifact. MR angiography remains an exciting and challenging field, and the best methods of contrast-enhanced MR angiography will be developed and established on the foundation of all previous work.

Adult↗

PubMed1987

Vascular structure and smooth muscle contractility in experimental hypertension.

The possible role of vascular structure as a pathogenetic factor in hypertension has been investigated by determining the media dimensions in resistance (mesenteric, renal, cerebral, and femoral) vessels taken from a variety of hypertensive rat models [spontaneously hypertensive (SHR), stroke-prone SHR (SHRSP), and one-kidney, one-clip renal hypertensive rats]. Resistance vessels from hybrid SHR/Wistar-Kyoto rats (WKYs) and from hybrid SHRSP/WKYs were also examined. In all cases, there was a correlation between media dimensions (media cross-sectional area or media/lumen ratio) of the resistance vessels (internal diameter of 100-300 microns) and the blood pressure of the rats concerned. Furthermore, the media of the SHR mesenteric resistance vessels were only increased in vessels larger than about 100 microns, indicating that structural changes were not to be expected in the microvasculature. These results suggest a causal relationship between blood pressure and the structure of the proximal resistance vasculature. Evidence that the increased structure is not solely a consequence of the increased pressure has been obtained from antihypertensive therapy experiments in which SHRs treated with hydralazine had resistance vessels with increased media/lumen ratios even though the animals had never become substantially hypertensive. The results point to a possible role for vascular structure in the development of hypertension.

Animals↗

PubMed1986

Discharge properties of mechanosensitive afferents supplying the retroperitoneal space.

Functional properties of lumbar mechanosensitive afferent fibres in the white rami L3 to L4 and the lumbar splanchnic nerves, which supply the retroperitoneal space were investigated. The receptive fields of these afferents, consisting of 1 to 3 mechanosensitive sites, were found on large vessels (aorta, inferior mesenteric artery, segmental arteries), on nerves, on the peritoneum, in fat lobules, on lymph nodes and on the vertebral column. Most afferent units were associated with small vessels. About 50% of the afferents had ongoing activity (about 0.1 to 2 imp/s). Two thirds of the afferents conducted at less than 2 m/s, the rest at 2 to 16 m/s. About 60% of the units were excited by local application of bradykinin and 75 to 90% by local application of hypertonic NaCl solution (4.5 and 9%) or KCl solution (60 and 155 mmol/l). About 50% of the afferent units with receptive fields on large arteries were activated by an increase in the arterial blood pressure. The function of these afferent fibres is unclear. However, it is conceivable that they are involved in nociception.

Animals↗

PubMed1995

[Operative management of retroperitoneal tumors involving major blood vessels: a report of 20 cases].

We report the experience of operative management in 20 patients with retroperitoneal tumors with major adjacent blood vessels involved, including portal vein inferior vena cava, abdominal aorta, iliac and renal vessels, and superior mesenteric vein. The diagnosis, preoperative preparation, intraoperative management and the postoperative complications were discussed. We emphasize the importance of radical resection of the tumors involving major blood vessels and vascular reconstruction.

Adult↗

PubMedDate not supplied

Necrotizing enterocolitis induced by local circulatory interruption in the ileum of neonatal piglets.

Occlusion of groups of vessels in the mesenteric vascular arcades of distal ileum for 48 h induced necrotizing enterocolitis lesions in low birth weight, spontaneously delivered, neonatal piglets. Lesion severity increased with numbers of adjacent groups of vessels occluded and with proximity to the ileocecal junction. A previously undescribed feature, "prepneumatosis," was confined to the lymphatic vessels of the submucosa and serosa. This feature closely resembled the position, shape, and distribution of classical pneumatosis intestinalis. Occlusion of vessels for 30 min followed by reperfusion did not induce any detectable changes 48 h later. Identical procedures (48-h occlusions) did not induce any detectable changes in 35-kg pigs.

Animals↗

PubMed1987

Collateral mesenteric circulation.

The origins of historical terms, such as "Arc of Riolan" and "marginal artery of Drummond" are traced herein with emphasis on the inherent confusion caused when these terms are used. Basic mesenteric anatomy is briefly mentioned and pathologic anatomy with its altered direction of blood flow induced by atherosclerosis is stressed. The significance of the meandering mesenteric artery as the main collateral vessel between the superior and inferior mesenteric artery is emphasized along with preoperative and intraoperative ways to ascertain whether or not the origin of this latter vessel can be safely ligated. Specific operations, such as abdominal aortic aneurysmorrhaphy and sigmoid colectomy, which can potentially interfere with blood flow in the meandering mesenteric artery, are discussed in an attempt to prevent postoperative necrosis of any portion of the intestine that may have deficient mesenteric blood flow.

Blood Vessel Prosthesis↗