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PubMed1983

Sodium metabolism in rat resistance vessels.

Using 22Na we have investigated the Na metabolism in rat mesenteric resistance vessels (internal diameter about 200 micron). The intracellular Na content was determined by washing the vessels at 0 degrees C in saline with Li substituted for Na, and was related to smooth muscle volume determined from measurements of media thickness and internal diameter using light microscopy. On this basis an internal Na concentration of 13.7 mmol l-1 cells was found. The efflux of Na into saline at 37 degrees C consists of two phases, a fast one and a slow one, where the slow phase was considered to be intracellular. It had a rate constant of 0.137 min-1, which was decreased by 50% if 1 mM-ouabain was added to or K withdrawn from the efflux medium. The gain of cell Na after addition of 1 mM-ouabain was much faster than would be expected from the decrease in efflux, indicating that 1 mM-ouabain increases the permeability to Na.

Animals↗
PubMed1996

Beta-adrenoceptor-mediated hyperpolarization in lymphatic smooth muscle of guinea pig mesentery.

Intracellular microelectrode recordings were performed to investigate the consequences of beta-adrenoceptor activation in smooth muscle of guinea pig mesenteric lymphatic vessels. Isoproterenol (Iso) hyperpolarized the membrane with an associated increase in membrane conductance and decreased the amplitude of spontaneous transient depolarizations. Iso effects were mimicked by forskolin (FSK), 3-isobutyl-1-methylxanthine, and two adenosine 3',5'-cyclic monophosphate (cAMP) derivatives. Iso- and FSK-induced hyperpolarizations were inhibited by H89, an inhibitor of cAMP-dependent protein kinase A, increased in K+-free solution, but were not affected by ouabain or by the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine. They were partially inhibited by 20 mM tetraethylammonium (approximately 40%) or by 2.5 mM 4-aminopyridine (approximately 55%). The-Iso-induced hyperpolarization was partially inhibited by iberiotoxin (20 nM) and charybdotoxin (40 nM), whereas the FSK-induced hyperpolarization was less affected. In cells where the Iso-induced hyperpolarization was decreased by 40 microM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, acetoxymethyl ester form, the FSK-induced hyperpolarization was little changed. Our results indicate that in guinea pig mesenteric lymphatic vessels, beta-adrenoceptor stimulation activates a protein kinase A-dependent K+ conductance, involving more than one channel type.

Animals↗
PubMed2005

[The changes in the tumor necrosis factor alpha, interleukin-6 and interleukin-8 levels in the lymph and of the dynamics of the lymphokines during shock stage of rats with major burns].

OBJECTIVE: To study the dynamic changes in the lymphokines and the changes in tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-8 (IL-8) levels in the lymph during shock stage of rats with major burns. METHODS: Forty-two male adult Wistar rats were randomly divided into burn resuscitation group (A, n = 18), burn non-resuscitation (B, n = 18) and the control (C, n = 6) groups. The TNF-alpha, IL-6 and IL-8 levels in the lymph were determined with radioimmunoassay at 6, 24, 48 postburn hours (PBH). The lymphokines in the mesenteric lymphatic vessels was observed at 6, 24 and 48 PBH with inverted microscopy and digital image processing, and the contraction frequency of the lymphatic was calculated. The lymph was collected by cannulation of the chylous cistern, and its speed of flow was calculated. RESULTS: The lymphatic contents of TNF-alpha and IL-6 in both A and B groups began to increase at 6PBH, reaching the peak values at 24 PBH (TNF-alpha in A and B groups were 1.61 +/- 0.27 ug/L and 1.86 +/- 0.34 ug/L, respectively; IL-6 in A and B groups were 398 +/- 67 ng/L and 572 +/- 97 ng/L, respectively), and they were significantly higher than those in C group at each time points (P < 0.01), meanwhile there was also obvious difference in them between A and B groups (P < 0.01). The lymphatic contents of IL-8 in A and B groups began to increase at 24 PBH, and continued to increase till 48PBH (540.29 +/- 0.32 ng/L in A group, 863.48 +/- 105.16 ng/L in B group), which were evidently higher than those in C group (P < 0.01). There was significant difference in IL-8 contents between A and B groups (P < 0.01). The contraction frequency of the mesenteric lymphatic vessels in A and B groups were decreased, especially so at 24 PBH (P < 0.01). The speed of lymphatic flow in A and B groups was increased at each time points (P < 0.01). The central chylous vessels in the villi of the small intestine were extremely dilated as seen under microscope. CONCLUSION: After burn injury, the lymphatic vessels dilated, with its motility decreased and speed of flow increased, and the contents of TNF-alpha, IL-6 and IL-8 in lymph were increased during the shock stage of burn rats. Fluid resuscitation could improve the lymph circulation.

Animals↗
PubMed1993

Nitric oxide-mediated changes in vascular reactivity in pregnancy in spontaneously hypertensive rats.

1. To examine the mechanisms which may account for pregnancy-induced vasodilatation in spontaneously hypertensive rats (SHR), we have investigated the changes in vascular reactivity and the effects of endothelial nitric oxide (NO) inhibition in the in situ blood-perfused, mesenteric resistance vessels of 18-20 day pregnant SHR. The effects of NG-nitro-L-arginine (L-NOARG) were compared in pregnant and nonpregnant SHR and gestation matched normotensive Wistar-Kyoto (WKY) rats. 2. Intra-arterial mean blood pressures (MBP) were similar in pregnant and nonpregnant SHR. Basal perfusion pressures (BPP) were decreased in pregnant compared with nonpregnant SHR. Pregnant WKY had lower MBP and BPP than either pregnant or nonpregnant SHR. 3. Vasoconstrictor responses to electrical stimulation (ES) and intra-arterial noradrenaline (NA) were decreased in pregnant compared with nonpregnant SHR. These responses were still greater in pregnant SHR when compared with pregnant WKY. Vascular reactivity to angiotensin II (AII) in pregnant SHR was reduced to a similar level to that in pregnant WKY. 4. L-NOARG (5 mg kg-1, i.v.), an inhibitor of nitric oxide synthase, increased MBP and BPP in all groups. After L-NOARG, BPP were equalized between pregnant and nonpregnant SHR. Pregnant WKY still showed lower MBP and BPP than SHR groups. 5. L-NOARG potentiated vascular responses to ES, NA and AII in all groups. The blunted vascular responses to NA and ES were normalized and the reactivity to AII was only partially reversed in pregnant SHR compared with nonpregnant SHR. Pregnant WKY still had much lower vascular responses to ES and NA than either pregnant or nonpregnant SHR. L-NOARG enhanced vascular responses to All to a greater extent in pregnant SHR than in pregnant WKY.6. These results demonstrate that blunted responses to NA and ES were NO-dependent, while diminished reactivity to AII was only partially dependent on NO in the in situ blood perfused mesenteric resistance vessels of pregnant SHR.7. The present results in pregnant SHR differ from our previous finding with pregnant normotensive WKY, in which blunted responses to NA, but not to ES, were equalized by L-NOARG. Pregnancy induced vasodilatation in hypertensive rats appears to be more dependent on endothelial NO than in normotensive WKY. A defect of the endothelial NO generating pathway which promotes vasodilatation in pregnancy may contribute to the predisposition of women with essential hypertension to develop pre-eclampsia.

Animals↗
PubMed1997

Blockage of mesenteric lymphatic flow in rats.

An experimental model of blockage of the mesenteric lymphatic flow (MLF) in rats was designed, and morphologic changes of mesenteric lymphatic vessels (MLV) and lymph nodes were investigated by mesenteric lymphangiography and histopathologic examination. Body weight in rats with blockage of MLF did not increase normally. Mesenteric lymphangiography revealed dilation of the MLV, reverse flow into the peripheral MLV, and leakage of contrast medium, resulting in chylous ascites. Remarkable dilation of the lymphatic sinuses and dilated and increased rough endoplasmic reticulum in lymphocytes in the mesenteric lymph nodes due to lymph stagnation were observed by light and electron microscopic examination, respectively.

Animals↗
PubMed2004

Gut and vessel alterations induced by mesenteric ischaemia/reperfusion in rats.

A rat model of transient occlusion of the superior mesenteric artery was used to study the intestinal and vascular injury induced by ischaemia/ reperfusion (I/R). A pronounced intestinal injury was observed, ranging from hyperaemia to severe haemorrhagic necrosis and bleeding. The length of the damaged intestinal segments reached 58.6% of the small intestine with a decrease of the wet weight in the I/R group. Sham operation resulted in 100% survival, I/R decreased survival to 40% after 24 h. Following I/R a significant increase of vascular permeability was observed in the small intestine. Gamma-glutamyl transpeptidase activity decreased aborally in sham operated rats and I/R reduced it further in all parts of the small intestine. I/R resulted in damaged endothelium-dependent relaxation of mesenteric artery rings. This was manifested by decreased maximal responses of arterial preparations to acetylcholine as well as decreased pD2 values. The results confirmed and specified the presumed effect of I/R on the small intestine and on vascular functions.

Analysis of Variance↗
PubMed1999

Relationship between hypercholesterolaemia, endothelial dysfunction and hypertension.

OBJECTIVES: We have previously shown that in the rat a diet high in cholesterol and deficient in vitamin E and selenium results in hypercholesterolaemia and increased lipid oxidation. We utilized this model to determine whether rats given this diet develop impaired endothelium-dependent relaxation mediated by nitric oxide (NO) in mesenteric and in renal vessels. In addition, we tested whether the impairment is due to (i) decreased endothelial NO synthase activity, (ii) increased NO inactivation and/or (iii) increased production of the endothelium-derived constricting factors thromboxane A2/prostaglandin H2 and endothelin-1. We also investigated whether endothelial dysfunction induced by dyslipidaemia increases the sensitivity for the development of hypertension in response to high dietary salt. METHODS: Male Dahl salt-sensitive (DSS) rats were divided into three groups and received a standard diet (control group), a high (4%) cholesterol diet (HChol), or a high cholesterol diet deficient in the anti-oxidants vitamin E and selenium (HChol-Def). The NaCl content of these diets was 0.5%. After 18 weeks we studied endothelium-dependent relaxation in response to acetylcholine (ACh) in aortas and in isolated perfused preparations of mesenteric arteries and kidneys. In some experiments, ifetroban, a thromboxane A2/prostaglandin H2 receptor antagonist, was added to the organ bath or the perfusion buffer. Vascular responses to endothelin-1 as well as to BQ-123, an endothelin A receptor blocker, were studied in the isolated perfused kidneys. In addition, two extra groups of rats were fed a diet high in sodium chloride (2%): one of the groups received the normal cholesterol diet whereas the other group received the diet high in cholesterol and deficient in vitamin E and selenium. RESULTS: Compared to normocholesterolemic rats, responses to ACh were significantly impaired in aortas, mesenteric arteries and kidneys of HChol-Def rats (P < 0.01). Endothelial NO synthase activity (conversion of [14C]L-arginine to [14C]L-citrulline) was similar in aortas of control, HChol and HChol-Def rats; thus suggesting that impaired endothelium-dependent relaxation in the HChol-Def rats was not due to decreased cNOS catalytic activity. Ifetroban improved the impaired endothelium-dependent relaxation in mesenteric vessels, but not in aortas and kidneys. Endothelin-1 (ET-1: 10(-13)-10(-11) mol/l) elicited NO-mediated relaxations in kidneys of control rats but not in kidneys of HChol-Def; blockade of ET-1 with BQ-123, an ET(A) receptor blocker, did not improve NO-mediated relaxation of HChol-Def. Despite impaired endothelium-dependent relaxation in renal and mesenteric vessels, HChol-Def DSS rats failed to develop hypertension (systolic blood pressure 144 +/- 1 in control and 150 +/- 2 mmHg in HChol-Def) but manifested a significant increase in sensitivity to the pressor effects of a high (2% NaCl) dietary salt content during the initial 10 weeks of the study, although the final blood pressure at 18 weeks was similar in both groups. CONCLUSION: These studies support the notion that (i) products of lipid oxidation may reduce NO bioactivity without affecting endothelial NO synthase mass or catalytic activity, (ii) the mechanisms involved in the endothelial dysfunction induced by hypercholesterolaemia and oxidized lipids may differ among vascular beds, and (iii) decreased NO bioavailability does not necessarily result in systemic hypertension, but it may enhance the sensitivity to the hypertensinogenic effect of dietary salt.

Acetylcholine↗
PubMed1989

Microvascular circulation of the ascending colon in horses.

Microvascular circulation of the ascending colon in healthy horses was studied using microangiography, light microscopy, and scanning electron microscopy. The pelvic flexure with 30 cm of ventral and dorsal colon attached was removed from 14 adult horses immediately after horses were euthanatized. The lumen was flushed with warm water, and this section of the ascending colon was placed in a 37-C bath of isotonic NaCl. In sections from 8 horses, colic vessels were perfused with a radio-opaque medium for microangiography. After angiographic evaluation, tissue sections were prepared for light microscopic observation, using standard histologic methods. In sections from 6 horses, injection replicas were made by perfusing the vessels with 2 types of plastics. The results of microangiography, light microscopy, and scanning electron microscopy of vascular replicas were correlated, providing a comprehensive documentation of the microvasculature of the ascending colon at the pelvic flexure. Arteries branched from mesenteric colic vessels approximately every 2 cm toward the colonic tissue. Immediately after branching, arterial vessels formed an anastomotic plexus, the colonic rete. However, each branch from the colic vessel eventually continued into the colonic tissue. A second set of vessels originated from the colonic tissue. A second set of vessels originated from the colonic rete and supplied the mesenteric lymph nodes. Arterial vessels penetrated the tunica muscularis into the submucosa 3 to 4 cm toward the antimesenteric border forming a submucosal vascular network. From the submucosal arterioles, branching took place at right angles to supply the mucosal capillaries. Capillaries surrounded the colonic glands and anastomosed at the luminal surface, forming a superficial luminal honeycomb-appearing vascular plexus.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1982

Characterization of glutamic acid decarboxylase activity in cerebral blood vessels.

Glutamic acid decarboxylase activity associated with cerebral blood vessels appears to be part of a specific cerebrovascular system involving gamma-aminobutyric acid. This activity was characterized kinetically and pharmacologically and compared with that in brain and several nonneuronal tissues. Formation of gamma-aminobutyric acid from [14C]glutamate was measured in a soluble extract of pia-arachnoid blood vessels isolated from bovine brain. The vascular activity was like brain glutamate decarboxylase in that it required pyridoxal phosphate, was completely inhibited by aminooxyacetic acid, and had a similar affinity for glutamate. Cerebrovascular decarboxylase activity differed, however, from brain decarboxylase in that it was less sensitive to sulfhydryl reagents, was stimulated by 3-mercaptopropionic and cysteic acids, and was competitively inhibited by cysteine sulfinic acid. The glutamate decarboxylase activity of the cerebral vessels was similar to that in renal cortex and mesenteric blood vessels in its responses to sulfhydryl reagents and 3-mercaptopropionic acid. These findings are consistent with previous suggestions of a nonneuronal form of the enzyme and offer the possibility that synthesis of gamma-aminobutyric acid in cerebral blood vessels can be manipulated independently from that in neuronal tissue.

Animals↗
PubMed1983

Influence of extracellular calcium and calcium antagonists on contractions induced by potassium and prostaglandin F2 alpha in isolated cerebral and mesenteric arteries of the cat.

1 The effects of a number of calcium antagonists (diltiazem, nifedipine, nimodipine and verapamil) have been studied on feline isolated pial arteries contracted by potassium (127 mM) or prostaglandin F2 alpha (PGF2 alpha, 2.5 microM) and mesenteric arteries contracted by potassium (127 mM). 2 Withdrawal of Ca2+ from the extracellular medium for 30 min reduced the contractile response to potassium in cerebral vessels by 92% and in mesenteric vessels by 96%. Subsequent addition of Ca2+ caused reproducible contractions which were inhibited by both nifedipine and nimodipine. 3 The four calcium antagonists relaxed the isolated middle cerebral artery contracted either by potassium or PGF2 alpha, and mesenteric arteries contracted by potassium, in the following order of potency: nimodipine greater than nifedipine greater than verapamil greater than diltiazem. 4 Nimodipine was more potent than nifedipine in cerebral arteries, and more potent in cerebral than in mesenteric arteries. Otherwise, the potassium-contracted cerebral and mesenteric vessels showed no major differences in sensitivity to calcium antagonists.

Animals↗
PubMed2000

Regeneration of lymphatic vessels and lipometabolism in an experimental rat model of extensive dissection of the abdominal periaortic lymphatic vessels and lymph nodes.

The present study was conducted to analyze the regeneration of lymphatic vessels and lipometabolism in an experimental rat model of extensive dissection of the abdominal periaortic lymphatic vessels and lymph nodes from the renal artery to the mesenteric and celiac artery. Findings showing the regeneration of mesenteric lymphatic vessels were classified as complete, incomplete, or no regeneration. The incomplete regeneration of fine irregular lymphatic vessels was observed in all rats, 2 and 3 weeks postoperatively. At the same time, triglyceride (TG) was found to be significantly lower (P < 0.05) in the rats that were given extensive dissection than in the control group, due to chylomicron blockade after lymphatic dissection. The TG recovered to within the normal range around 4 weeks postoperatively following the growth of fine regenerated lymphatic vessels or collateral route formation.

Animals↗
PubMedDate not supplied

Effect of endothelial damage on prostaglandin synthesis by isolated perfused rabbit mesenteric vasculature.

Isolated perfused rabbit mesenteric blood vessels selectively metabolized arachidonic acid to prostacyclin (prostaglandin I2). However, the less lipid soluble prostaglandin endoperoxide (PGH2) administered exogenously was not metabolized by vascular prostacyclin synthetase but was partially degraded to prostaglandin E2 (PGE2). Peptide stimulation (e.g., angiotensin II, bradykinin) resulted in formation of both PGI2 and PGE2 from endogenous arachidonic acid. Denuding the blood vessels of their endothelial layer by perfusion with hypotonic fluid did not affect the metabolism of arachidonic acid or the response to peptide stimulation, suggesting that the cyclooxygenase, prostacyclin synthetase, and angiotensin II receptors are present and functional in the subendothelial smooth muscle cells of the vessel walls. In contrast, exogenous PGH2 either escaped completely unmetabolized or was converted to both PGI2 and PGE2 in the presence of vascular injury induced by hypotonic fluid.

Angiotensin II↗
PubMed1993

Effect of diameter variability along a microvessel segment on pressure drop.

In most microcirculatory studies, the diameter of a blood vessel is characterized by a single, average value, obtained from a projected two-dimensional microscopic view of the vessel. Such diameter values are often used to calculate microvascular hemodynamic variables (e.g., pressure drop along vessels). The validity, and some possible consequences, of the assumption that vessel diameter is constant along vessels were examined for (a) single capillaries of the hamster cremaster muscle and (b) a network model of blood flow in a rat mesenteric network. Vessel diameter was measured in cremaster microvessels of anesthetized golden hamsters (Nembutal, 70 mg/kg ip) at regular intervals along the lengths of individual vessels. The standard deviation of the diameter measurements (ranging from 0.2 to 4.0 microns) in each vessel increased with the average diameter (ranging from 4 to 27 microns, 132 vessels, 12 animals). The coefficient of variation (CV = SD/Mean) was close to 0.1 for vessels larger than 15 microns and up to 0.4 for smaller vessels. In individual isolated vessels, the ratio of calculated pressure drop using the actual diameter measurements (delta P) to pressure drop assuming an average diameter (delta Po) was between 1.05 and 3.0 (at constant volume flow rate); this ratio correlated significantly with the CV for that vessel. Using an iterative mathematical model of network blood flow in a mesenteric network, we investigated the effects on single-vessel delta P/delta P0 of using a single average estimate of diameter for each microvessel segment, compared to the inclusion of variations in each vessel diameter expected from the single-vessel data. The results from the model indicated that single vessel delta P/delta Po values obtained with expected diameter variations in each vessel varied between 0.01 and 100. This implies that the axial variations in vessel diameter that exist in vivo may affect the calculations of vessel pressure drop both in single vessels and in microvascular networks.

Animals↗
PubMed1982

Muscarinic cholinergic receptor sites in cerebral blood vessels.

Muscarinic cholinergic receptor sites in cerebral blood vessels were analyzed directly by using radioligand binding techniques with the specific muscarinic antagonist [3H]quinuclidinyl benzilate (QNB) as ligand. Specific binding of [3H]QNB to membrane preparations from isolated bovine pia-arachnoid vessels was found to be saturable, of high affinity (Kd = 5.4 X 10(-10) M) and selectively inhibited by muscarinic antagonists (atropine) and agonists (acetylcholine, carbachol and methacholine). Scatchard and Hill plot analyses of the data indicated one class of sites for the antagonists, but two independent classes of sites were revealed with the agonists. Interestingly, the high and low affinities of the agonist sites correlated with the concentrations of agonist which have been reported to produce dilation and contraction, respectively, of isolated pial artery segments. A substantial number of specific [3H]QNB binding sites also were measured in isolated bovine cerebral microvessels providing direct evidence for muscarinic receptors in intracerebral vessels. In contrast, specific [3H]QNB binding was barely detectable in mesenteric blood vessels. Choline acetyltransferase (ChAT) activity was measured in parallel with [3H]QNB binding. The relative distribution of choline acetyltransferase was correlated with that for the binding, with the highest values observed in the intracerebral microvessels. This suggests a functional innervation of the cerebrovascular muscarinic receptors.

Animals↗
PubMed2004

Mechanisms underlying the effect of E. coli endotoxin on contractile function of lymphatic vessels.

E. coli endotoxin decreased the amplitude and frequency of spontaneous phasic contractions in isolated bovine mesenteric lymphatic vessels. This substance in a concentration of 5 mg/liter blocked spontaneous contractions and reduced tonic tension of smooth muscle cells. The dilatory effect of endotoxin on lymphatic vessels was primarily realized via stimulation of synthesis of NO and prostacyclin by endotheliocytes.

Animals↗