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At least 559 records · Page 31Linked to original sources
PubMed1998

Early flow surface endothelialization before microvessel ingrowth in accelerated graft healing, with BrdU identification of cellular proliferation.

The purpose of this report was to determine if flow surface endothelialization could precede microvessel ingrowth from the perigraft area in porous Dacron grafts, by using an accelerated graft healing model with short implant periods. Dacron grafts were implanted in the abdominal aorta of 22 dogs and wrapped in autogenous inferior vena cava (IVC), which provided excellent conditions for extramural angiogenesis, microvessel development, and ingrowth toward the graft. Retrieval times were 7 days (n = 4), 8 days (n = 5), 9 days (n = 4), 10 days (n = 3), 11 days (n = 4) and 12 days (n = 3) postoperatively. Graft surfaces were evaluated for thrombus coverage, cell coverage, and the number of micro-ostia. Components and cellular types in the graft wall and on the surface were studied and characterized with H&E, histochemical, and immunocytochemical staining. BrdU labeling was also used, to identify the areas where cells were actively proliferating. All grafts were patent. Although the degree of IVC/graft attachment varied, isolated islands of endothelial-like cells were found at the midgraft areas at each time period, and immunocytochemically confirmed as endothelial cells. There were two healing patterns: (1) surface endothelialization before microvessel/tissue ingrowth from the perigraft areas, and (2) surface endothelialization with full wall microvessel and tissue presence. Surface endothelialization was observed before perigraft tissue ingrowth, indicating that fallout healing is an independent source of endothelialization for porous grafts.

Animals↗
PubMed1982

Effect of age on beta-adrenergic receptors on cerebral microvessels.

The responsiveness of beta-adrenergic receptors in cerebral microvessels was studied in aged rats by measuring cAMP formation induced by norepinephrine and [125I]iodohydroxybenzylpindolol binding. The density of beta-receptor sites is reduced by aging in the rat cerebral microvessels. These results suggest that the changes in brain circulation during aging may be at least partially due to a reduction of the beta-adrenergic control of cerebral microvessels.

Aging↗
PubMed1982

Ultrastructure of frog cerebral and pial microvessels and their impermeability to lanthanum ions.

Permeabilities of single pial microvessels in the frog are now being estimated. Fine structural information on these vessels will therefore be needed in attempts to correlate structure and permeability. Microvessels from the dorsal part of the telencephalon and from the overlying pial layer in the common frog (Rana temporaria) and their permeability to lanthanum ions were studied in the electron microscope. Extensive structural similarities between the endothelial lining of cerebral and pial microvessels were demonstrated, indicating similarity in functional characteristics. Adjacent endothelial cells in both categories of vessels were joined by elaborate tight junctions. Lanthanum ions did not permeate the endothelium. Diffusion of the ion in the interendothelial clefts was stopped by the junctions. It is concluded that the frog has an endothelial blood-brain barrier which is tight to lanthanum ions.

Animals↗
PubMed1986

Vasopressin binds to microvessels from rat hippocampus.

Recent evidence suggests that vasopressin may influence the permeability of the endothelium of brain capillaries. We measured the binding of [125I]arginine-8-vasopressin ([125I]AVP) to microvessels isolated from different regions of the rat brain. The study revealed saturable and specific binding of [125I]AVP to microvessels isolated from hippocampus. Scatchard analysis confirmed a single class of high affinity sites with an equilibrium dissociation constant, Kd, of 3.2 nM and an apparent maximal binding capacity of 205 fmol/mg protein. No binding was observed to microvessels from neocortex and striatum.

Animals↗
PubMed1993

ATP-sensitive potassium channels are not expressed in brain microvessels.

We used [3H]glibenclamide binding to assess ATP-sensitive K+ channels in isolated cerebral microvessels and in the cerebral cortex of the rat. We found no measurable specific glibenclamide binding in cerebral microvessels despite its abundance in cerebral cortical membranes, implying that ATP-sensitive K+ channels are not present in cerebral microvessels.

Adenosine Triphosphate↗
PubMed1982

Functional identification of adenylate cyclase-coupled adenosine receptors in rat brain microvessels.

It was investigated whether adenosine affects the adenylate cyclase system of microvessels, isolated from the rat cerebral cortex, via an external receptor recently classified as R-site receptor. Several adenosine analogs caused GTP-dependent stimulation of adenylate cyclase. The rank order of potency: NECA (5'-(N-ethylcarboxamido)-adenosine, EC50 0.2 microM) greater than adenosine (0.71 microM) = 2-chloroadenosine (0.72 microM) greater than L-PIA (N6-(L-phenylisopropyl)-adenosine, 1.03 microM) greater than D-PIA (N6-(D-phenylisopropyl)-adenosine, 5.27 microM) is consistent with that for agonism at activatory (Ra-site) adenosine receptors in other tissues. Adenylate cyclase stimulation by PIA displayed stereoselectivity. The action of NECA was competitively antagonized by 8-phenyltheophylline. These findings provide functional evidence for Ra-site adenosine receptors in rat brain microvessels. However, direct identification of these receptors by binding studies was not possible. Binding of [3H]NECA to rat brain microvessels displayed rapid on-off kinetics and saturability, but equivocal specificity.

Adenosine↗
PubMed1989

Renal vasodilatation and microvessel adenylate cyclase stimulation by synthetic parathyroid hormone-like protein fragments.

The hypercalcemia caused by malignancy factor, also called parathyroid hormone-related protein (PTHrP), exhibits most of the biological activities of parathyroid hormone (PTH) in kidney and bone. On the basis of the well-documented vascular action of PTH, we characterized the vasodilator action of human (h) PTHrP-(1-34) on a preparation of the isolated rat kidney, and its activity to stimulate adenylate cyclase in microvessels isolated from rabbit kidney cortex. Injection of sequential cumulative doses of hPTHrP-(1-34) into the isolated kidney preparation produced increasing vasodilatation up to 10(-8) M (EC50 of 3 x 10(-9) M) and decreasing responses thereafter. The maximal effect represented 26% of the reference relaxation induced by papaverine. Single injections of hPTHrP-(1-34) resulted in a greater (over 60%) vasodilatation. These results were reminiscent of the tachyphylaxis that occurs after repeated exposure to the peptide. The (3-34) PTH antagonist inhibited the hPTHrP-induced vasodilatation. Human PTHrP-(1-34) was equipotent with hPTH-(1-34) (EC50 values of 3 x 10(-9) M) but 5-fold less potent than rat (r) PTH-(1-34) in stimulating microvessel adenylate cyclase. GTP enhanced the enzyme responses to the peptides but reduced their potency. Both (3-34) and (7-34) PTH antagonists were inhibitors of hPTHrP- or PTH-stimulated microvascular adenylate cyclase. Synthetic hPTHrP-(1-16) had neither vasodilator nor adenylate cyclase-stimulating activity. This hPTHrP fragment exhibited some inhibitory effect on the hPTHrP-(1-34)-induced stimulation of microvessel adenylate cyclase. These results indicate that hPTHrP possesses PTH-like activity to cause vasorelaxation and to stimulate microvascular adenylate cyclase in the kidney.

Adenylyl Cyclases↗
PubMed1988

Lysosomal enzyme activities in the cerebral microvessels in spontaneously and renal hypertensive rats.

In an attempt to clarify the role of lysosomal enzymes in the developmental mechanisms of the changes of cerebral microvessels under hypertensive conditions, the activities of acid phosphatase, N-acetyl-beta-glucosaminidase, and beta-glucuronidase in the isolated microvessels from the cerebral cortex of spontaneously and renal hypertensive rats were biochemically studied. The activities of all the enzymes were higher than those in normotensive control animals, although there was a variation in intensity according to the age and kind of enzymes. The enzyme activities in spontaneously hypertensive rats showed a tendency to increase with advancing age. Hypertension seems to increase activities of lysosomal enzymes in cerebral microvessels, and this activation may in turn play a role in the development of further hypertensive cerebrovascular and cerebral changes.

Acetylglucosaminidase↗
PubMed1984

Distribution of parathyroid hormone-sensitive adenylate cyclase in isolated rabbit renal cortex microvessels and glomeruli.

The effect of the synthetic amino-terminal fragment of bovine parathyroid hormone, bPTH-(1-34), on the adenylate cyclase of microvessels and glomeruli isolated from rabbit kidney cortex was studied in the presence and absence of guanosine triphosphate (GTP). bPTH-(1-34) stimulated the vascular and glomerular adenylate cyclase in a dose-dependent manner with apparent ED50 values of 11.5 nM and 64 nM respectively, in the absence of GTP. 10(-4)M GTP greatly amplified the vascular response to bPTH-(1-34) while, in the glomeruli, both GTP and bPTH-(1-34) had only additive effects. In the presence of GTP, vascular and glomerular apparent ED50 were 190 nM and 64 nM respectively. [Nle8, Nle18, Tyr34] -bPTH-(3-34) amide, described as a PTH antagonist, inhibited the action of bPTH-(1-34) in the microvessels and to a lesser extent in the glomeruli. PTH is therefore a potent stimulator of adenylate cyclase in rabbit renal microvessels and glomeruli, and may play a role in the regulation of renal blood flow and glomerulo-tubular feedback control.

Adenylyl Cyclases↗
PubMed1985

Adrenergic receptors on cerebral microvessels in control and parkinsonian subjects.

The binding of adrenergic ligands (3H-prazosin, 3H-clonidine, 3H-dihydroalprenolol) was studied on a preparation of cerebral microvessels in the prefrontal cortex and putamen of control and Parkinsonian subjects. The adrenergic receptor density in microvessels of control patients was less than 0.5% and 3.3% respectively of the total binding. A significant decrease in the number of alpha-1 binding sites was observed on microvessels in the putamen of patients with Parkinson's disease.

Aged↗
PubMed1983

Adrenergic neurons: are they present on microvessels in cheek pouches of hamsters?

Catecholaminergic innervation was investigated in the cheek pouch, mesentery, and cremaster muscle of the hamster. These tissues were removed from normal hamsters after anesthetization with sodium pentobarbital. They were prepared immediately for visualization of catecholamines by using a glyoxylic acid fluorescent technique. Visualization was accomplished via a Zeiss fluorescent microscope with a 470-nm barrier and a 420-nm excitation filter. No fluorescence was observed in or around the microvessels of the cheek pouch; however, intense fluorescence was demonstrated around and along microvessels in the mesentery and cremaster muscle. Thus, within the limitations of this technique, this study demonstrates that local catecholamines, either as a component of adrenergic neurons or a part of the local tissue milieu, are nondetectable in the microvessels within the cheek pouch as compared to mesenteric and muscle tissue of the hamster.

Adrenergic Fibers↗
PubMed1992

Regulation of amino acid uptake into cerebral microvessels.

The carrier-mediated transport systems, found in cerebral endothelium, are responsible for maintaining the nutrient milieu of the CNS. The objective of this study was to identify what factors might regulate the sodium-dependent A-system of neutral amino acid transport in isolated cerebral microvessels. The uptake of amino acids into isolated microvessels was measured using methylaminoisobutyric acid (MeAIB) a nonhydrolyzable A-analog of the A-system carrier. The results indicated that stimulation of adrenergic (both alpha and beta) receptors significantly (P less than 0.05-0.02) increased the uptake of MeAIB. While the muscarinic agonist carbachol alone did not alter the uptake of MeAIB, it blocked the stimulation evoked by adrenergic agonists. Furthermore, addition of the metal ion, aluminum also significantly (P less than 0.05) increased specific uptake of MeAIB by 95%, when compared to untreated controls. These results indicate that the uptake of neutral amino acids, through the A-system, into cerebral microvessels, can be modulated by adrenergic and cholinergic receptors, as well as the metal ion aluminum. Since the A-system of amino acid transport may control appropriate levels of amino acids in brain, modulation of the uptake of amino acids by adrenergic and cholinergic receptors and by aluminum, may be associated with an imbalance of amino acids and possible neurotransmitter defects in the CNS.

Aluminum↗
PubMed1992

In vivo microscopic studies of age-related changes in the structure and the reactivity of cerebral microvessels.

To determine if hemodynamic changes in cerebral microvessels could contribute to the age-related changes in the blood-brain barrier (BBB) function, the cerebral microvessels of male Fischer 344 rats at different ages were studied using intravital fluorescence microscopy. Aging in rats was associated with significant arteriovenous shunting in the cerebral microvessels without alterations in blood flow characteristics or changes in vascular permeability to FITC dextran (150 kDa). The basal diameter of terminal arterioles examined in 24- to 27-month-old (aged) rats (28.6 +/- 2.8 microns) was not different from that in 12- to 15-month-old (intermediate age) rats (32.5 +/- 2.5 microns) or in 3- to 6-month-old (young) rats (28.6 +/- 3.0 microns). At 3 s following addition of 5% BaCl2 there was 23.3 +/- 3.47% constriction of arterioles in young rats and 14.8 +/- 5.16% constriction in intermediate age rats, but only a 3.43 +/- 5.69% change in aged rats (P less than 0.03). This initial brief constriction phase was followed by a dilatory response which was similar in all age groups. One minute following suffusion with artificial cerebrospinal fluid, the arteriolar diameter essentially returned to baseline in all rats examined. It is concluded that aging in rats is associated with alterations in cerebral microvascular reactivity in vivo along with arteriovenous shunting. These changes may contribute to age-related alterations in the BBB function.

Aging↗
PubMed1980

The synthesis of prostaglandins by bovine cerebral microvessels.

Bovine cerebral microvessels (arterioles and capillaries) synthesize prostacyclin (PGI2, measured as 6-keto PGF1 alpha), PGF2 alpha, PGE2 and thromboxane A2 (measured as TXB2) when incubated in glucose-bicarbonate buffer for 30 minutes. Rapid freezing and thawing decreased the subsequent synthesis of 6-keto PGF1 alpha by cerebral microvessels and raised the basal levels of this metabolite within the incubation medium. At low concentrations, the addition of arachidonic acid (0.16 microM) did not stimulate prostacyclin or prostaglandin production; at higher concentrations (16 microM), the synthesis of PGI2 and PGF2 alpha was inhibited. Activation of lipase by the peptide melittin stimulated the synthesis of all arachidonic acid metabolites to the same extent. Thus cerebral microvessels deacylate cellular lipids and metabolize endogenous arachidonic acid to form prostaglandins, prostacyclin and related compounds as previously demonstrated in larger blood vessels. The synthesis and release of these molecules may be important for modulating the tone and reactivity of small blood vessels within the brain.

Animals↗
PubMed1995

Involvement of nitric oxide in IFN-gamma-mediated reduction of microvessel smooth muscle cell proliferation.

Previous studies in our laboratory demonstrated that murine cerebral microvessel smooth muscle cells (SMC) activate syngeneic CD4+ T-cells in vitro. These T-cells, or their culture supernatants, in turn, strongly inhibit proliferation of the SMC. The present study focuses on IFN-gamma as a mediator of inhibition of SMC proliferation, and addresses the molecular mechanism of this inhibition. IFN-gamma profoundly reduced the proliferation of murine brain microvessel smooth muscle cells in vitro. Three lines of evidence indicate that nitric oxide contributed to this effect: (1) IFN-gamma-mediated inhibition of proliferation correlated with the quantity of nitrite, a stable breakdown product of nitric oxide, in culture supernatants; (2) the addition of N(g)- monomethyl-l-arginine, and inhibitor of nitric oxide synthesis, restored proliferation to control or near control levels; and (3) the addition of hemoglobin, which has a high affinity for, and thus sequesters nitric oxide, also resulted in significant restoration of the proliferative response. However, the nitric oxide donating chemical sodium nitro-prusside, at concentrations up to 100 microM, had no direct cytostatic effect. These results suggest that nitric oxide is a necessary but insufficient component in IFN-gamma-mediated inhibition of microvessel smooth muscle cell proliferation. TNF-alpha also stimulated nitric oxide production by the smooth muscle cells, but was not as potent as IFN-gamma at inhibiting proliferation. Knowledge of the physiological effects of lymphokines on cells of the brain microvasculature will contribute towards a better understanding of inflammatory processes in diseases such as multiple sclerosis and infectious encephalitis.

Animals↗
PubMed1981

Regional distribution of neurohumoral responsive adenylate cyclase in rabbit brain microvessels.

Neurohumoral activation of adenylate cyclase was evaluated in microvessel fractions isolated from different regions of the rabbit brain. The greatest degree of enzyme by norepinephrine, dopamine and histamine was observed in microvessels from the brain stem, hippocampus and hypothalamus. The least degree of enzyme stimulation occurred in the thalamic preparation while the cerebellar microvessels were sensitive to norepinephrine alone.

Adenylyl Cyclases↗
PubMed1984

Immunoelectronhistochemical evidence for innervation of brain microvessels by vasopressin-immunoreactive neurons in the rat.

Peroxidase-antiperoxidase (PAP) immunocytochemistry at the electron microscopic level was used to describe the fine structural characteristics of vascular connections between vasopressin (VP)-immunoreactive neuronal elements and cerebral microvessels in the rat. In the majority of connections, somata or neural processes (mainly dendrites) showing VP-like immunoreactivity were separated from the vessel wall by thin glial processes. In addition, some VP-positive elements could establish direct contacts with the basal lamina of the endothelium or of a pericyte associated with the capillary bed. The findings provide immunocytochemical evidence that the vasopressinergic neuronal elements can directly innervate microvessels in the brain and thereby participate in regulating the local permeability of and the flow through the cerebral microvessels.

Animals↗