PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MESENTERIC VESSELS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMed1986

Role of vascular structure in blood pressure development of the spontaneously hypertensive rat.

We measured the characteristics of isolated resistance vessels taken from mesenteric, renal and cerebral vascular beds of 14 to 18-week-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Mesenteric resistance vessels of SHR/WKY F2-hybrid rats were also investigated. All resistance vessels in the SHR had increased media:lumen ratios and increased media volumes when fully relaxed, while their contractility was increased. In the hybrid animals, preliminary analysis indicated a correlation between the resistance vessel media:lumen ratio and blood pressure, and also between vascular contractility and blood pressure. The results are consistent with the possibility that the abnormal structure of SHR resistance vessels is associated with one of the factors that produce hypertension in this animal.

Animals↗
PubMed1978

Binding of Trypanosoma congolense to the walls of small blood vessels.

The mesenteric microvasculature was studied in rats and rabbits infected with Trypanosoma congolense. By examining vessels in the living animals, trypanosomes were observed to adhere to vessel walls by their anterior ends. It was evident from stained preparations of the vessels that the microcirculation contained 4-1400 times as many trypanosomes as were free in the cardiac blood. Parasites were more numerous in very small vessels than in larger vessels, and they were clustered in groups within the small vessels. The localization of T. congolense in the microvasculature is demonstrated and it is shown that this localization is established by attachment of the organism to the vessel wall.

Animals↗
PubMedDate not supplied

[Angiodysplasia of the colon].

The authors present a case review of a congenital abnormality of the inferior mesenteric blood vessels which resulted in ischemia of the descending colon and rectosigmoid area. The resulting colitis is only very rarely secondary to a vascular congenital abnormality. In this case, rectosigmoidoscopy, barioum study of the large bowel and a biopsy of the rectal mucosa pointed towards the ischemic nature of the lesion. This led to the selective angiographic study of the inferior mesenteric vessels with findings of a dilated inferior mesenteric artery and angiodysplasia. Surgical treatment included tying off of the inferior mesenteric artery and resection of the descending and rectosigmoid colon followed by transverse colon-rectum anastomosis. The angiographic and histopathologic studies were of great importance in establishing the true nature of the patient's clinical syndrome. One must keep in mind that the rectosigmoidoscopic findings may be seen in other disease states which do not have a vascular origin. These include Crohn's disease, severe amoebiasis and penumatosis of the intestine.

Colitis↗
PubMed1995

Pathogenesis of ascites tumor growth: angiogenesis, vascular remodeling, and stroma formation in the peritoneal lining.

In the accompanying papers, we demonstrated that two murine ascites tumors (MOT and TA3/St) induced peritoneal lining blood vessels to become hyperpermeable to plasma proteins, leading to extravasation of fibrinogen and its clotting to cross-linked fibrin in peritoneal lining tissues (peritoneal wall, mesentery, and diaphragm). In solid tumors, vascular hyperpermeability and fibrin deposition lead to the generation of vascularized connective tissue. In order to determine whether fibrin had similar consequences in ascites tumors, the vasculature and stroma of peritoneal lining tissues were analyzed at successive intervals after i.p. tumor cell injection. In both MOT and TA3/St ascites tumors, the size and number of peritoneal lining microvessels increased significantly by 5-8 days. Subsequently, peritoneal lining vessels increased in cross-sectional area by as much as 15-fold and peritoneal vascular frequency increased by up to 11-fold. Incorporation of [3H]thymidine by mesenteric blood vessels was negligible in control animals but came to involve 20 and 40% of endothelial cells lining mesenteric vessels in MOT and TA3/St ascites tumor-bearing mice, respectively. After an early dramatic increase in cross-sectional area, peritoneal lining microvessels subsequently underwent a novel form of remodeling to smaller average size as the result of transvascular bridging by endothelial cell cytoplasmic processes. Thus, both of the ascites tumors studied here induced angiogenesis and stroma similar to that elicited when these same tumors were grown in solid form. However, stroma developed more slowly in ascites than in solid tumors and was entirely confined to a compartment (peritoneal lining tissues) that was distinct from that (peritoneal cavity) containing the majority of tumor cells and ascites fluid. These findings are consistent with the hypothesis that vascular hyperpermeability, induced in both solid and ascites tumors by tumor cell-secreted vascular permeability factor, is a common early step in tumor angiogenesis, resulting in fibrinogen extravasation, fibrin deposition, and likely other alterations of the extracellular matrix that together stimulate new vessel and fibroblast ingrowth.

Animals↗
PubMed1976

Acute mesenteric infarction caused by small vessel disease.

A case of acute mesenteric infarction caused by small vessel disease is reported. The patient recovered after 2 operations by which extensive bowel-resections were performed. The resected bowel showed intimal hyperplasia and atherosclerosis of the small mesenteric arteries. Since also thrombocytosis and increased platelet aggregation was demonstrated the main cause of thrombosis however is supposed to be hypercoagulability.

Acute Disease↗
PubMed1994

Diabetes-associated mesenteric vascular hypertrophy is attenuated by angiotensin-converting enzyme inhibition.

In experimental diabetes, the mesenteric vascular tree undergoes hypertrophy, and this is associated with an increase in mesenteric angiotensin-converting enzyme (ACE) levels. The aim of this study was to determine if inhibition of mesenteric ACE by ACE inhibition would influence diabetes-associated mesenteric vascular hypertrophy. Control or streptozocin-induced diabetic rats were randomized to receive no drug or the ACE inhibitor perindopril. In addition, other diabetic rats were randomized to receive either low-dose insulin that does not alter glycemic control or high-dose insulin, administered as a silastic pellet to achieve euglycemia. After 3 weeks, animals were killed for measurement of mesenteric ACE, vessel weight, and wall:lumen ratio. Diabetes was associated with increased mesenteric ACE levels, increased vessel weight, and an increase in the wall:lumen ratio. ACE inhibition, despite no effect on glycemic control, food intake, urinary urea excretion, or gut weight, prevented the increase in mesenteric ACE levels and attenuated mesenteric vascular hypertrophy as assessed by weight or wall:lumen ratio. The increase in staining by an antibody to the endothelial product, von Willebrand factor, in diabetic rats was totally prevented by perindopril treatment. Euglycemia but not low-dose insulin therapy in the diabetic rats normalized mesenteric vessel ACE, weight, and wall:lumen ratio. In conclusion, ACE inhibition may have a specific role in preventing diabetes-associated vascular hypertrophy, an important process in the genesis of micro- and macrovascular diabetic complications.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Endothelium-derived relaxing factor and the effects of acetylcholine and histamine on resistance blood vessels.

1. The role of endothelium-derived relaxing factor (EDRF) in the action of vasodilator (acetylcholine, histamine, nitroprusside) and vasoconstrictor (noradrenaline, vasopressin) drugs on vascular resistance in the isolated perfused kidney and mesentery of the rat was studied. 2. Acetylcholine (EC50 = 0.18 +/- 0.05 nmol and 3.1 +/- 0.06 nmol, n = 8) and histamine (EC50 = 31.2 +/- 4.9 nmol and 46.2 +/- 3.9 nmol, n = 8) produced dose-related vasodilatation in noradrenaline-preconstricted (i.e. 'high tone') rat renal and mesenteric blood vessels. The response to both vasodilators (but not nitroprusside) was abolished by infusion of CHAPS (4.7 mg ml-1, 30 s). By use of an immunocytochemical staining procedure CHAPS was demonstrated to remove vascular endothelial cells lining intrarenal blood vessels. 3. Gossypol (3 microM), metyrapone (10 microM) and nordihydroguaiaretic acid, (NDGA, 30 microM), presumed inhibitors of EDRF biosynthesis, reduced or abolished the response to acetylcholine and histamine in perfused kidney and mesentery of the rat without affecting vasodilatation due to nitroprusside. Mepacrine (10 microM) similarly abolished the response to acetylcholine and histamine but in addition, reduced the response to nitroprusside in both preparations. 4. Methylene blue (100 microM), a presumed antagonist of the effect of EDRF, abolished vasodilatation due to acetylcholine and histamine and reduced the response to nitroprusside in perfused rat kidney and mesentery. Superoxide dismutase, SOD (15 u ml-1), was without effect. 5. While CHAPS treatment significantly augmented the vasoconstrictor response to both noradrenaline and vasopressin in perfused renal and mesenteric vessels this effect was not mimicked by metyrapone or gossypol suggesting that the enhanced effect of vasopressor agents in CHAPSperfused rat organs is due to the removal of a permeability barrier rather than impaired EDRF formation. 6. Responses to vasoconstrictor and vasodilator drugs in the perfused kidney and mesentery were obtained in the presence of indomethacin (8 microM) which produced in excess of 90% inhibition of prostacyclin (PGI2) release as measured by radioimmunoassay of 6-oxo-prostaglandin F1 alpha,. (6-oxo- PGF1 alpha) in the Krebs effluent. 7. We provide evidence that EDRF mediates the vasodilator response to acetylcholine and histamine in resistance blood vessels in perfused rat kidney and mesentery. The possibility that EDRF has a physiological role to play in regulating the calibre of resistance blood vessels is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

[Cardiohemodynamics and blood circulation in the mesenteric and intra mural vessels of the stomach and intestines in victims of traumatic shock during general anesthesia].

The angiotensiometric method was used for studying blood pressure in mesenteric and intramural vessels of the gastrointestinal tract in 63 patients with traumatic shock and 167 patients with surgical and oncological diseases during laparotomy under conditions of general anesthesia. The value of hypotension in the intestinal vessels was found to depend on the degree of shock established before the beginning of antishock therapy and narcosis in spite of satisfactory indices of systemic hemodynamics.

Abdominal Injuries↗
PubMed2001

The vasoconstrictor response of uterine and mesenteric resistance arteries is differentially altered in the course of pregnancy.

OBJECTIVES: The purpose of the present study was to test the hypothesis that pregnancy is associated with an attenuation of the vasoconstrictor response not only in the uterine, but also in the systemic circulation. Decreased vascular reactivity should be characterized by an early onset to account for the rapid fall in peripheral resistance which was observed during the first third of gestation. STUDY DESIGN: Dose-response curves for phenylephrine hydrochloride (PE), angiotensin II (ANG II), and endothelin 1 (ET 1) were recorded from isolated pressurized uterine and mesenteric arterioles. Vessels were obtained from virgin, early (day 7-9) pregnant (EP) and late (day 19-21) pregnant (LP) rats. RESULTS: (1) In uterine resistance arteries, the response to PE and ANG II decreased early, but for ANG II the reduction did not persist. ET 1 sensitivity was unchanged in early, and diminished in late gestation; (2) in mesenteric vessels, sensitivity to ET 1 was enhanced in early pregnancy and did not differ from the non-pregnant level in late gestation. Sensitivity to PE and ANG II was unchanged in early, and reduced in late pregnancy. CONCLUSIONS: The vasoconstrictor response is not uniformly blunted during pregnancy. Changes in vascular reactivity are differentially regulated with respect to the agonist, to their time course, and. to the origin of the vessel. The relative increase of vasoconstrictor sensitivity in the splanchnic circulation during early pregnancy may prevent hypotensive dysregulation, while concentrations of endogenous vasodilators rise and the vascular filling state normalizes only gradually.

Angiotensin II↗
PubMed1998

Gastrointestinal cancer metastasis and lymphogenous spread: viewpoint of animal models of lymphatic obstruction.

Primary gastrointestinal cancer frequently spreads to the mesentery, omentum and other parts of the peritoneum and these deposits are generally considered to be induced by intraperitoneal seeding from the primary lesion. In this work, we examined the spread of gastrointestinal cancer from the viewpoint of lymphogenous metastasis using a rat model of mesenteric lymph vessel obstruction. With these models, we carried out mesenteric lymphangiography on the fourth and sixth postoperative days (five animals each) to examine morphological changes in the lymph vessels and lymph flow. In model animals with mesenteric lymph vessel obstruction, re-celiotomy, performed on the fourth postoperative day, revealed marked mesenteric edema and enlargement of the mesenteric lymph nodes, suggestive of lymph retention. We also carried out mesenteric lymphangiography and obtained images of extensive mesenteric lymph vessels and reflux of lymph distal to the obstruction point in all five animals. On the sixth postoperative day, we obtained lymphangiographic images of lymphatico-venous communication in the mesentery in all five animals. Thus in animals with lymph vessel obstruction, the lymph flow appeared to change to lymphatico-venous communication or reverse lateral flow. In clinical cases, it is conceivable that lymph retention and reflux of lymph induced by lymph vessel obstruction sometimes play a role in the mechanism of intraperitoneal cancer dissemination and hematogenous metastasis.

Animals↗
PubMed1988

Possible role of vascular oscillatory activity in the development of high blood pressure in spontaneously hypertensive rats.

Many investigators have shown that vascular smooth muscle from hypertensive individuals shows oscillatory activity, i.e., spontaneous or rhythmic contractions. This paper reviews work performed in the author's laboratory designed to determine if the oscillatory activity of mesenteric resistance vessels taken from spontaneously hypertensive rats (SHR) is associated with the cause of the high blood pressure in these animals, as well as to determine the mechanism producing the oscillatory activity. Cross-breeding of SHR and normotensive control Wistar-Kyoto rats (WKY) was used to produce F2-SHR/WKY rats. In the F2-SHR/WKY rats, there was a correlation between systolic blood pressure and mesenteric resistance vessel oscillatory activity, but no correlation between systolic blood pressure and mesenteric resistance vessel calcium sensitivity. The oscillatory activity appeared to be associated with changes in membrane potential and is inhibited by inhibitors of potential-dependent calcium channels. This is consistent with reports from other laboratories that the oscillatory activity could be associated with an interaction between potential-dependent calcium channels and calcium-dependent potassium channels. The results suggest that the increased oscillatory activity of the mesenteric resistance vessels of the SHR is associated with a cause of high blood pressure in these animals and may be due to an abnormal activity of the calcium-dependent potassium channels.

Animals↗
PubMed1986

Neonatal sympathectomy of normotensive Wistar-Kyoto and spontaneously hypertensive rats with 6-hydroxydopamine: effects on resistance vessel structure and sensitivity to calcium.

6-Hydroxydopamine (6-OHDA) was injected on alternate days from birth to 3 weeks of age into spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) control rats. The effects of this neonatal treatment on cardiovascular structure and mesenteric resistance vessel calcium sensitivity was studied in young (6 week) and adult (5 month) rats. Mean arterial pressure of treated SHRs and WKYs was reduced by 10% compared with control rats, but the heart:body weight ratio was unaffected by treatment. Both pharmacological and histological studies suggested that at 6 weeks of age, mesenteric resistance vessels from treated WKYs were completely denervated, but that vessels from treated SHRs still had sparse innervation. At 5 months all vessels from the treated rats had some adrenergic innervation, but less than the control rats. In the WKYs, treatment was associated with reduced media:lumen ratio and reduced calcium sensitivity of the mesenteric resistance vessels, while no such changes were observed in the SHR vessels. The results indicate that the sympathetic nervous system in SHRs is more resistant to chemical denervation than the sympathetic nervous system of the WKYs. The results also suggest that sympathetic innervation of mesenteric resistance vessels may affect vessel structure and sensitivity.

Animals↗
PubMed2002

A comparative study of the effects of Cl(-) channel blockers on mesenteric vascular conductance in anaesthetized rat.

There is evidence to suggest that niflumic acid is capable of selectively inhibiting Ca(2+)-dependent Cl(-) channels. Furthermore, it has been demonstrated that niflumic acid is capable of antagonizing contractile responses due to activation of alpha(1)-adrenoceptor in mesenteric vasculature. Here, we have examined the effects of three Cl(-) channel blockers, niflumic acid, indanyloxyacetic acid 94 (IAA-94) and diphenylamine-2-carboxylic acid (DPC) on cirazoline-mediated vasoconstriction in mesenteric blood vessel in vivo. Infusion of cirazoline produced a dose-dependent increase in blood pressure, decrease in superior mesenteric blood flow, mesenteric vascular conductance and heart rate. While niflumic acid and IAA-94 did not have any impact on cirazoline-induced changes in blood pressure, DPC accentuated the pressor effect of cirazoline. Neither agent affected cirazoline-mediated reflex reduction in the heart rate. Niflumic acid, IAA-94 and DPC attenuated alpha(1)-adrenoceptor mediated decrease in mesenteric blood flow and vascular conductance. Based on the profile of the actions of these compounds, it may be suggested that IAA-94 did not appear to act as selective inhibitor of Ca(2+)-activated Cl(-) channels when compared to niflumic acid in the mesenteric blood vessels. In addition, while DPC seems to be as effective as niflumic acid in its effects on mesenteric blood vessels, its actions may be attributed to other pharmacological effects.

Animals↗
PubMed1982

Effects of Ca antagonists on Ca fluxes in resistance vessels.

We have examined contractions and 45Ca fluxes induced by norepinephrine (NE) and 80 mM potassium (high K) depolarization and their inhibition by diltiazem in rabbit mesenteric resistance vessels. Contraction induced by both NE and high K depended almost completely on extracellular Ca. Dose-response curves for diltiazem inhibition of NE (10(-5) M) and high K contractions showed ED50 values of 1 X 10(-8) and 6 X 10(-7) M, respectively, indicating that the receptor-operated channel (ROC) was more sensitive than the potential-operated channel (POC) to the action of diltiazem. Diltiazem (10(-6) M) was shown to inhibit NE- and 80 mM K-stimulated 45Ca influx effectively by 87 +/- 15 and 85 +/- 10%, respectively. Comparison of these data to those obtained from aorta suggest that although the sensitivity of the POC is approximately the same in aorta and mesenteric resistance vessels, the sensitivity of the ROC is much greater in the latter. This increased sensitivity is paralleled by a greatly decreased role of intracellular Ca release in NE contraction in mesenteric resistance vessels.

Animals↗
PubMed1987

Evidence for endothelium-dependent vasodilation of resistance vessels by acetylcholine.

In the perfused mesenteric arterial vasculature of the rabbit, vasodilation by acetylcholine (ACh) was almost completely blocked after a 15-min perfusion of the vasculature with 0.2% collagenase, an enzyme capable of removing endothelial cells. In the perfused mesenteric arterial vasculature of the rat, vasodilation by ACh was markedly, though not completely, inhibited by hemoglobin (10 microM), an agent which can inactivate endothelium-derived relaxing factor (EDRF). These results suggest that a major component of vasodilation of mesenteric resistance vessels in rabbit and rat by ACh is mediated by EDRF.

Acetylcholine↗
PubMed2001

Inferior mesenteric artery as outflow vessel in endoleaks after abdominal aortic stent-graft implantation: 36-month follow-up CT study.

The aim of this study was to determine the role of the inferior mesenteric artery (IMA) as an outflow vessel in endoleaks after abdominal aortic stent-graft implantation. Forty consecutive patients in whom abdominal aortic aneurysms (AAA) had been treated with stent-graft implantation were evaluated retrospectively. Spiral-CT examinations and angiographies up to 36 months after implantation were analyzed. In 29 (73%) of the 40 patients the IMA was perfused prior to implantation. In 5 (17%) of these 29 cases, the artery remained perfused after stent-graft insertion. In all 5 cases, endoleaks were detected; however, in none of these cases was the IMA the sole cause. In 3 of these 5 cases, angiography showed antegrade flow in the IMA. Implantation of extension stent grafts caused thrombosis of the aneurysmal sac and the IMA. There were no secondary endoleaks caused by the IMA at the 36-month follow-up examinations. The majority of IMAs which are patent prior to intervention occlude after successful stent-graft insertion. In cases with leaks and angiographically proven antegrade flow in the IMA, implantation of extension stent grafts is a therapeutic alternative to embolization. In this study, the IMA was not responsible for secondary endoleaks.

Aged↗
PubMed1975

[Effect of dopamine on perfusion pressure in rat peripheral blood vessels].

Rat mesenteric and hind limb arteries were perfused with the rat's own blood under constant perfusion rate, in situ. The effect of dopamine (DA) administered intraarterially was investigated and compared with effects of norepinephrine (NE), tyramine (Tyr), and phenylephrine (PHE). The magnitude of the vasoconstrictive maximum response of both vasculatures to NE and PHE was larger than those to DA and Tyr, and those to DA were larger than those to Tyr in hind limb, but those to Tyr were more potent than those to DA in the mesenteric artery. The vasoconstriction evoked by celiac ganglionic stimulation was much the same to that evoked by NE and PHE. Under cocaine infusion, the rise in perfusion pressure of both vasculatures evoked by NE and PHE. Under cocaine infusion, the rise in perfusion pressure of both vasculatures evoked by NE was slight, but the duration was markedly potentiated. However, the effect of Tyr was suppressed and that of DA was not changed. In rats on alpha-methyl-rho-tyrosine, the responses of both vasculatures to Tyr were reduced and those to NE and DA were not changed. In the reserpinized rat, the effect of NE was not changed and that of Tyr was reduced, while that of D was more evident in both vasculatures. After phenoxybenzamine treatment, vasoconstrictive effect of DA was reversed in mesenteric and reduced in hind limb artery. Vasodilating effect of DA after phenoxybenzamine, was not changed by treatment with propranolol, atropine, and diphenhydramine but was reduced with reserpine and abolished with haloperidol. These results suggest that the vasoconstrictive effect of DA depends partly on indirect sympathomimetic action, and after phenoxybenzamine, DA acts by vasodilating the DA receptor. Potentiation with reserpine may depend on a post-synaptic mechanism and increase in dopamine-beta-hydroxylase activity.

Animals↗