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At least 433 records · Page 24Linked to original sources
PubMed1965

Observations on "lung shift" after chemotherapy in mice infected with Schistosoma mansoni.

It is known from work with Puerto Rican strains of Schistosoma mansoni that in experimental bilharziasis in laboratory animals there may be a shift of flukes from the mesenteric vessels to the lungs, and that this occurs both in untreated animals and in those given chemotherapy. The work reported in this paper was undertaken to study this phenomenon with an Egyptian strain of S. mansoni.With but one exception, no schistosomes were found in groups of untreated mice autopsied 6-12 weeks after infection. Some were found in the lungs of a few mice treated 6 weeks after infection and more in the lungs of those treated 10 weeks after infection.A shift of flukes to the lungs appears to be dependent upon a number of linked factors. In the study reported, the important factor was the effect of an active compound which resulted in a passive shift of flukes from their normal sites in the mesenteric vessels. Possible routes by which schistosomes may reach the lungs are discussed.

Animals↗
PubMed1999

Hsp90 regulation of endothelial nitric oxide synthase contributes to vascular control in portal hypertension.

The molecular chaperone, heat shock protein 90 (Hsp90), acts as an intermediate in the signaling cascades leading to activation of endothelial nitric oxide synthase (eNOS). In this study, we examine the participation of this pathway in nitric oxide (NO)-dependent vasodilation in the rat mesentery in vitro. In normal animals, immunoprecipitation of eNOS from intact mesentery coimmunoprecipitates Hsp90 and, additionally, both eNOS and Hsp90 colocalize to the endothelial lining of mesenteric vessels. In the perfused mesenteric vasculature of normal animals, geldanamycin (GA), a specific inhibitor of Hsp90 signaling, attenuates ACh-dependent vasodilation but does not affect vasodilation in response to sodium nitroprusside. Next, studies were performed in animals with experimental portal hypertension induced by portal vein ligation (PVL). In PVL animals, NOS catalytic activity is markedly enhanced in mesenteric tissue and the perfused mesentery is hyporesponsive to the vasoconstrictor methoxamine (MTX). GA significantly potentiates MTX-induced vasoconstriction after PVL, thereby partially reversing the hyporeactivity to this agent exhibited in the mesenteric vasculature after PVL. These studies suggest that Hsp90 can act as a signaling mediator of NO-dependent responses in the mesenteric circulation and indicate that the excessive NO production observed in portal hypertension is mediated in part through Hsp90 signaling.

Acetylcholine↗
PubMed1977

Uptake of 3H-norepinephrine in rabbit mesenteric blood vessels.

The uptake of traited norepinephrine in isolated rabbit mesoduodenal blood vessels was measured. Neuronal uptake was estimated utilizing the inhibitory effect of cocaine, and expressed on the basis of wet and dry tissue weights as well as circumferential area of the vascular wall. This area was presumed to approximate the area of the adrenergic nerve terminal plexus. The wet weight of smaller tissues was apt to be underestimated due to excessive drying during weighing; dry weight was more consistent over a wide range of tissue size. Either on the basis of weight or circumferential are, neuronal uptake in arteries increased as the diameter diminished, but uptake was practically constant in all segments of the veins. Arterial uptake per unit circumferential area was greater than in the accompanying veins, but this was not necessarily the case when uptake was expressed per unit weight. Neuronal norepinephrine may be a useful index of adrenergic nerve density. On this basis it is suggested that the adrenergic neural vasoconstriction increases with decrease in diameter of both arteries and veins in rabbit mesoduodenum.

Adrenergic Fibers↗
PubMed2004

Non-esterified fatty acids impair endothelium-dependent vasodilation in rat mesenteric resistance vessels.

Elevated circulating levels of NEFAs (non-esterified fatty acids) are associated with states of insulin resistance and increased risk of vascular disease. Previous animal and human studies have demonstrated NEFA-induced endothelial dysfunction of large conduit arteries, reversible by the antioxidant ascorbic acid. We therefore investigated the effect of NEFAs on carbachol-induced endothelium-dependent vasodilation of rat resistance arteries in vitro using the technique of wire myography. In addition, we investigated the effect of co-incubation of NEFAs and ascorbic acid. Cumulative concentration-response curves to carbachol (endothelium-dependent vasodilation) and SNAP (S-nitroso-N-acetyl-DL-penicillamine; endothelium-independent vasodilation) were constructed. Those to carbachol were repeated following a 30 min incubation with either oleic acid (10(-4) M) or palmitic acid (10(-4) M), demonstrating significant impairment of endothelium-dependent vasodilation with both [P<0.05, comparison of pD2 values (the negative log concentration of agonist required to effect a 50% response)]. A cumulative concentration-response curve to carbachol was repeated following co-incubation with palmitic acid (10(-4) M) and the antioxidant ascorbic acid (10(-5) M), demonstrating an abolition of the previously observed endothelial dysfunction induced by palmitic acid. There was no impairment of vasodilation to SNAP following NEFA incubation. We conclude that NEFAs directly impair endothelial function in rat resistance arteries via an increase in oxidative stress at the vascular endothelium.

Animals↗
PubMedDate not supplied

Endovascular treatment of chronic mesenteric ischemia: report of five cases.

PURPOSE: To evaluate the midterm results of percutaneous transluminal angioplasty (PTA) and stent placement in stenotic and occluded mesentesic arteries in five consecutive patients with chronic mesenteric ischemia. METHODS: Five patients with 70%-100% obliterations of all mesenteric vessels resulting in chronic mesenteric ischemia (n = 4) and as a prophylactic measure prior to abdominal aortic aneurysm repair (n = 1) underwent PTA of celiac and/or superior mesenteric artery (SMA) stenoses (n = 2), primary stenting of ostial celiac occlusions (n = 2), and secondary stenting of a SMA occlusion (n = 1; recoil after initial PTA). All patients underwent duplex ultrasonography (US) (n = 3) and/or angiography (n = 5) during a median follow-up of 21 months (range 8-42 months). RESULTS: Clinical success was obtained in all five patients. Asymptomatic significant late restenoses (n = 3) were successfully treated with repeat PTA (n = 2) and stenting of an SMA occlusion (n = 1; celiac stent restenosis). Recurrent pain in one patient was interpreted as secondary to postsurgical abdominal adhesions. Two puncture-site complications occurred requiring local surgical treatment. CONCLUSIONS: Endovascular techniques may be attempted prior to surgery in cases of stenotic or short occlusive lesions in patients with chronic mesenteric ischemia. Surgery may still be preferred in patients with long occlusions and a low operative risk.

Adult↗
PubMed2004

Characterisation of the vasorelaxant properties of the novel endocannabinoid N-arachidonoyl-dopamine (NADA).

1. We have investigated the vascular effects of N-arachidonoyl-dopamine (NADA), a novel endocannabinoid/vanilloid. NADA caused vasorelaxant effects comparable to those of anandamide in small mesenteric vessels (G3), the superior mesenteric artery (G0) and in the aorta. 2. In G3, addition of N(G)-nitro-l-arginine methyl ester (300 microm) or the dopamine (D(1)) receptor antagonist (SCH23390, 1 microm) did not affect responses to NADA. In the presence of 60 mm KCl, after de-endothelialisation, or after K(+) channel inhibition with charybdotoxin (100 nm) and apamin (500 nm), relaxant responses to NADA were inhibited. 3. In G3, pretreatment with the vanilloid receptor (VR) agonist capsaicin (10 microm) or the VR antagonist capsazepine (10 microm) reduced vasorelaxation to NADA. 4. In G3, application of the CB(1) antagonist SR141716A at 1 microm but not 100 nm reduced the potency of NADA. Another CB(1) antagonist, AM251 (100 nm and 1 microm), did not affect vasorelaxation to NADA. After endothelial denudation, SR141716A (1 microm) did not reduce the responses further. A combination of capsaicin and SR141716A (1 microm) reduced vasorelaxation to NADA further than with capsaicin pretreatment alone. The novel endothelial cannabinoid (CB) receptor antagonist O-1918 opposed vasorelaxation to NADA in G3. 5. In the superior mesenteric artery (G0), vasorelaxation to NADA was not dependent on an intact endothelium and was not sensitive to O-1918, but was sensitive to capsaicin and SR141716A or AM251 (both 100 nm). 6. The results of the present study demonstrate for the first time that NADA is a potent vasorelaxant. In G3, the effects of NADA are mediated by stimulation of the VR and the novel endothelial CB receptor, while in G0, vasorelaxation is mediated through VR(1) and CB(1) receptors.

Animals↗
PubMed2004

Proteinase-activated receptor 2 activation modulates guinea-pig mesenteric lymphatic vessel pacemaker potential and contractile activity.

Lymphatic vessels rhythmically constrict to avoid fluid and protein accumulation in the interstitial space. This activity is critical during inflammation to prevent excessive oedema. Lymphatic pumping is intrinsic to the smooth muscle in the vessel wall and is due to the spontaneous occurrence of action potentials, the pacemaker of which is proposed to be spontaneous transient depolarizations (STDs). This function is highly susceptible to the fluid load and modulated by chemical agents, amongst which inflammatory mediators are important players. Activation of proteinase-activated receptors (PARs) has been involved in inflammation and affects vascular smooth muscle tone. The present study aims to investigate the role of PAR2, a member of the PAR family, in lymphatic vessel pumping. RT-PCR experiments revealed that PAR2 message is present in lymphatic vessels of the guinea-pig mesentery. Agonists of PAR2 such as trypsin and the activating peptide, SLIGRL-NH2, caused a decrease in the contractile activity of intraluminally perfused lymphatic vessels. Moreover, intracellular microelectrode recordings from isolated vessels revealed that PAR2 activation hyperpolarized the lymphatic smooth muscle membrane potential and altered STD amplitude and frequency. The decreases in constriction frequency and STD activity as well as the hyperpolarization were dependent on a functional endothelium, not affected by NO synthase or guanylyl-cyclase inhibition, but mimicked by PGE2 and iloprost and blocked by indomethacin (10 microM) and glibenclamide (1 microM). These results show that PAR2 activation alters guinea-pig lymphatic vessel contractile and electrical activity via the production of endothelium-derived cyclo-oxygenase metabolites.

Animals↗
PubMed1979

Effects of distension on mesenteric blood flow and O2 saturation of venous blood in the dog intestinal loop.

Arterial and venous blood flow and oxygen saturation of the venous blood in the mesenteric vessels arising from single mesenteric artery and vein to the intestinal loop in anesthetized dogs were measured simultaneously with systemic arterial blood pressure during distension of this loop. Mesenteric arterial blood flow decreased to the zero level, while mesenteric venous outflow increased to about twice the quiescent level at the onset of elevation of intraluminal pressure. However, during distension, the decreased arterial blood flow tended to increase, but the increased venous flow was reduced to one half of the quiescent level. Oxygen saturation of venous blood diminished initially and then increased progressively during distension. At the end of distension venous outflow stopped temporarily. After suspension of distension, arterial and venous flow and oxygen saturation increased beyond the quiescent level. These results may suggest that there is a by-pass or A-V anastomosis which cannot be compressed mechanically by elevation of intraluminal pressure.

Animals↗
PubMed2006

CT diagnosis of 52 patients with lymphoma in abdominal lymph nodes.

AIM: To assess CT manifestations and its diagnostic value for lymphoma in the abdominal lymph nodes (LALN). METHODS: CT findings in 52 cases of LALN proved by surgery or biopsy, including Hodgkin's disease (HD) in 16 cases and non-Hodgkin's lymphoma (NHL) in 36 cases, were retrospectively analyzed. RESULTS: (1) CT manifestations based on distribution of the lesions of LALN: Solitary mass type was found in 10 cases, including solitary, round, uniform-density, enlarged lymph nodes in 3 cases; and multiple, enlarged lymph nodes fusing into singular lobular mass in 7 cases. Thirty-four cases of multiple-nodular type showed multiple, round, enlarged lymph nodes with uniform density and clear margins. Vessels-embedded signs, including mesenteric vessels, renal vessels, abdominal aorta or inferior vena cava, were seen in 6 cases, and duodenum-embedded signs were seen in 2 cases. Eight cases of diffuse type showed characteristic "cobblestone signs". (2) CT manifestations correlated with pathological type: CT manifestations of 12 cases of HD were different from those of 40 cases of NHL in distribution, size, quantity and fused lesion of enlarged lymph nodes. (3) Twenty-eight cases of 52 patients were accompanied with extra-nodal lymphoma in the abdomen, especially gastrointestinal lymphoma, which had characteristic CT findings. (4) In follow-up examinations, CT images showed uniform, heterogeneous or rim enhancement in 15 cases, and occasional calcifications accompanied with reduction of the lesion size and quantity in 12 cases, whereas the lesions disappeared in 3 cases after treatment. CONCLUSION: CT images show many characteristic manifestations valuable for qualitative diagnosis of LALN, and it is also helpful for pathological classification of LALN and therapeutic evaluation in follow-up of patients.

Abdomen↗