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PubMed1991

Dynamic structure of blood flow in microvessels.

The present article summarizes the author's perennial research on the flow of red blood cells in microvessels, the major determinant of rheological properties of blood in the microcirculation. Two main patterns of blood flow structure in microvessels, in the smallest arteries and veins and in the capillaries are described. The red cell concentration (hematocrit) in the blood flowing in microvessels undergoes regular alterations with changes of blood flow rate and vessel diameter in the microvascular beds. Further, the red blood cell concentration and flow velocity gradients are found in the cross-section of microvessels that should considerably affect the blood rheological properties in the microcirculation. In addition, radial displacements and blood velocity fluctuations of red cells in the flow are discovered in the larger microvessels during ischemic decrease of blood flow rate. The main factor disturbing the normal blood flow structure, and hence the normal rheological properties of blood, is the intravascular aggregation of red blood cells, which is to be diagnosed and eliminated in patients with blood rheological disturbances.

Erythrocyte Aggregation↗

PubMed1991

[Vasoactive intestinal peptide (VIP) concentration in ischemic rat brain microvessels].

UNLABELLED: VIP is extensively localized in the brain, spinal cord and peripheral neurons, and is especially rich in the nerves innervating the cerebral vasculature. VIP is a potent vasodilator of cerebral vessels. The aim of this study was to investigate VIP contents in brain microvessels and their changes during incomplete brain ischemia. METHODS: (1) Bilateral carotid artery ligation was performed in Wistar rats under urethane anesthesia to produce cerebral ischemia, which was further aggravated by bleeding to hypotension with a mean arterial pressure of 50-60 mmHg. At 5, 15 and 30 min after ligation, the rats were decapitated to obtain brain tissue. A sham surgery group served as controls. In some rats cerebral ischemia was confirmed by EEG. (2) Brain microvessels were prepared by brain homogenization in HEPES-Ringer buffer and gradient centrifugation in 30% BSA, followed by filtration through a glass bead column. (3) VIP contents were determined by radioimmunoassay. The results were that VIP contents of 30 min ischemic rats were significantly higher than in the controls (P less than 0.01). VIP contents of cerebral microvessels were also measured in two groups of gerbils. It was found that VIP contents in ischemic gerbils were significantly higher than in the controls (P less than 0.01). These results indicate that: (1) VIP is present in rat and gerbil brain microvessels. (2) During brain injury by ischemia, the increase in VIP content in cerebral microvessels may induce vasodilation and cause an increase in cerebral blood flow. This may well be an autoregulatory response to protect the ischemic brain and may have important pathophysiological implications.

Animals↗

PubMed1989

A new type of amiloride-sensitive cationic channel in endothelial cells of brain microvessels.

Endothelial cells from brain microvessels form the blood-brain barrier. Brain microvessels and endothelial cells isolated from rat brain microvessels express an amiloride-sensitive cationic channel that was characterized using [3H]phenamil binding and patch-clamp experiments. [3H]Phenamil, a labeled amiloride analog, recognizes a single family of binding sites with a dissociation constant of 20-30 nM and a maximum binding capacity of 8-15 pmol/mg protein. The pharmacological profile of the channel (phenamil greater than benzamil greater than amiloride) is very similar to that of the epithelium Na+ channel of mammalian kidney and of frog epithelia. Long-lasting currents were observed in patch-clamp experiments using excised outside-out patches. Application of amiloride or phenamil first produced a rapid flickering of channel activity and then its complete blockade. The mean unit channel conductance at 140 mM Na+ was 23 picosiemens. The selectivity of Na+ over K+ was estimated from reversal potentials to be 1.5:1. Properties of the channel in microvessels are clearly distinct from those of the Na+ channel of the kidney, suggesting the existence of several isoforms of cationic channels that are sensitive to amiloride and its derivatives. The low selectivity cationic channel of endothelial cells in brain microvessels might be important for controlling both Na+ and K+ movements across the blood-brain barrier.

Amiloride↗

PubMed1987

Effects of quantitative undernourishment, ethanol and xylene on coronary microvessels of rats.

The effect of alimentary deficiency, ethanol intake and exposure to xylene on the coronary microvessels and heart weight were investigated in rats. The coronary microvessels of rats, which were undernourished for 5 weeks and which were fed ad libitum were studied with the histomorphometric method of Herrmann et al [19]. In another experiment a group of rats was fed a control liquid diet while another group was fed a liquid diet containing ethanol up to 36% of the total Joule intake. One-half of both groups were placed in an exposure chamber supplied with pure air; the other two half-groups were made to inhale air containing 1000 mg xylene/m3 for 6 h daily, 5 days a week, for a period of 4 weeks. It was found that undernourishment did not cause any morphological reactions in the microvessels and did not affect the relative heart weight. Ethanol increased the contractile activity of the wall cells of coronary microvessels, and also the relative heart weight. The effect of xylene was similar to that of the ethanol. The effect of xylene in combination with ethanol was additive on the one hand (in some parameters), on the other hand there was an inhibition between the effects of the two chemicals (in the case of the number of mv. 10.5 micron less than d less than 21 micron). It is concluded that both ethanol and xylene increase the vascular tone of coronary microvessels and this alteration causes a decrease in the nutritive myocardial blood flow. Undernourishment does not play any role in the increase of vascular tone.

Animals↗

PubMed1979

Lipoprotein lipase and acid lipase activity in rabbit brain microvessels.

A preparation of cerebral microvessels was used to demonstrate the presence of lipoprotein lipase and acid lipase activity in the microvasculature of rabbit brain. Microvessels, consisting predominantly of capillaries, small arterioles, and venules, were islated from rabbit brain. Homogenates were assayed for lipolytic activity using a glycerol-stabilized trioleoylglycerol-phospholipid emulsion as substrate. Lipoprotein lipase activity was characterized with this substrate by previously established criteria including an alkaline pH optimum, increased activity in the presence of heparin and heat-inactivated plasma, and reduced activity in the presence of NaCl and protamine sulfate. A different substrate, containing trioleoylglycerol incorporated into phospholipid vesicles, was used to reveal acid lipase activity that was not affected by heparin, plasma, NaCl, or protamine sulfate. Lipoprotein lipase did not show activity with the vesicle preparation as substrate. Intact microvessels, when incubated in the presence of heparin, release lipoprotein lipase into the incubation solution. In contrast, release of acid lipase activity from intact microvessels was not dependent on heparin. The data show the presence of both lipoprotein lipase and acid lipase in brain microvessels and suggest that lipoproteins are metabolized within the cerebral vasculature.

Animals↗

PubMed1984

Nonenzymatic glycosylation of bovine retinal microvessel basement membranes in vitro. Kinetic analysis and inhibition by aspirin.

Incubation of intact bovine retinal microvessels or isolated retinal microvessel basement membranes (RVBM) with radioactive D-glucose or L-glucose, followed by basement membrane collagenous protein purification, resulted in the isolation of nonenzymatically glycosylated RVBM collagens. Type IV collagen was identified in the RVBM by selective salt fractionation, SDS-polyacrylamide gel electrophoresis, amino acid analysis, and immunoprecipitation with specific antibody. Kinetic analysis of the condensation of glucose with RVBM was carried out by labeling retinal microvessel basement membranes with D-[2-3 H]-glucose and D-[6-14 C]-glucose. The rate constant for aldimine product formation, k1, was 1.95 +/- 0.24 (SD) X 10(-4) mM-1 h-1, and the rate constant for the reversed reaction, k-1, was 5.9 +/- 1.0 X 10(-2) h-1. Based on a rate constant for the Amadori rearrangement, k2, of 8.8 +/- 1.0 X 10(-3) h-1, which was the rate-determining step, the half life of this reaction was 80 +/- 9 h. These data may be useful in estimating the glycosylation of retinal microvessel basement membranes in vivo. The nonenzymatic glycosylation of retinal microvessel basement membrane proteins was progressively inhibited by increasing concentrations (0.1 to 2.0 mM) of aspirin.

Animals↗

PubMed1978

Studies on the monoamine oxidase and catechol-O-methyltransferase of the rat cerebral microvessels.

The rat cerebral microvessels were isolated and assayed both for monoamine oxidase (MAO) and catechol-o-methyltransferase (COMT) activities. Cerebral microvessels and brain filtrate were found to contain both forms (A & B) of MAO. On a per mg protein basis, the cerebral microvessels contained the greatest activity of MAO and COMT than that of brain filtrate and mesenteric artery. Chemical sympathectomy using 6-hydroxydopamine neither decreased total MAO activity, nor the A form of the enzyme, nor did it have any effect on COMT activity in the brain microvessels. These results suggest that COMT and both forms of MAO in the rat brain microvessels are extraneuronal in origin.

Animals↗

PubMed1981

[Measurements of blood flow velocity in pulmonary microvessels with laser-Doppler microscope and investigation of several factors affecting the blood flow velocity (author's transl)].

To examine the blood flow in pulmonary microvessels and its change during positive lung inflation and deflation as well as during regional lung hypoxia or hypercapnia, the blood flow velocity in the microvessels which were observed on the exposed lung surface of anesthetized bullfrogs was measured. This was performed by means of a laser-Doppler microscope and both mean flow velocity (MV) and pulsatile amplitude (PA) were calculated from the obtained flow velocity contour. Hypoxia (pure N2) or hypercapnia (10% CO2) was applied on the regional lung surface of 6 mm in diameter. The blood flow in the pulmonary microvessels was pulsatile and its pulsatility was greatest in arterioles and smallest in capillaries. MV and the ratio of PA to MV in capillaries were 1.46 mm/sec and 0.20, respectively. This ratio was considerably smaller than that in human pulmonary capillaries, which was previously measured by using body plethysmography. The reason for this discrepancy was discussed. During lung inflation and subsequent deflation, the alterations in MV and PA against transpulmonary pressure (TPP) revealed an optimum TPP and an apparent hysteresis. During lung inflation MV was slightly increased until TPP reached about 2.8 cmH2O but was markedly decreased at the larger TPP than the value. During subsequent deflation, MV was slightly lower at any given TPP than during inflation but its change was almost parallel to that in inflation. The change in PA was similar to that in MV. The observed alteration in flow velocity in pulmonary microvessels seemed related to the geometric change in pulmonary vessels. Both lung regional hypoxia and hypercapnia induced the decrements in MV and PA in pulmonary microvessels, which were caused by the vasoconstriction in arterioles and venules. The maximal percentage change in MV and PA in capillaries were -11% and -35% during hypoxia, and -13% and -44% during hypercapnia.

Animals↗

PubMed1982

Lipid metabolism in the aorta and the brain microvessels of rabbits on high cholesterol diet.

The characteristics and properties of lipid metabolism in the aorta and the brain microvessels of rabbits were investigated to clarify the role of lipid metabolism in formation of atherosclerosis. In rabbit aorta, cholesterol esterase and lipase each had an acidic and a neutral optimum pH, whereas acyl-CoA synthetase, acyl-CoA: cholesterol acyltransferase, triglyceride synthesizing activity and choline phosphotransferase each had one neutral optimum pH. These pH optima were similar to those in rats. High cholesterol diet induced atheromatous lesions in the aorta, but not in the brain microvessels. In atheromatous aorta, the acid lipase and acid phosphatase activities were higher than in controls, but not the acid cholesterol esterase activity. Moreover the activities of neutral lipase, acyl-CoA synthetase, acyl-CoA:cholesterol acyltransferase, triglyceride synthesis and choline phosphotransferase were increased, but neutral cholesterol esterase activity was normal. These data suggest that lipis metabolism in the atheromatous aorta is changed in a manner favoring accumulation of lipids, especially cholesterol esters. In controls, most of the above enzyme activities in the brain microvessels were higher than those in the aorta. However, these enzyme activities in the brain microvessels were not changed by cholesterol feeding. Thus it is suggested that the properties of lipid metabolism in the aorta and brain microvessels, including permeability of lipoproteins into the vessel walls, are important in formation of atherosclerosis in addition to the serum factors.

Animals↗

PubMed1995

Cholinergic basal forebrain neurons project to cortical microvessels in the rat: electron microscopic study with anterogradely transported Phaseolus vulgaris leucoagglutinin and choline acetyltransferase immunocytochemistry.

Physiological evidence indicates that central cholinergic pathways are involved in the regulation of cerebral cortical blood flow. We investigated the possible contribution of basal forebrain cholinergic neurons from the substantia innominata (SI) to the innervation of cortical microvessels. Basalo-cortical perivascular nerve terminals were detected by light and electron microscopic immunocytochemistry of anterogradely transported Phaseolus vulgaris leucoagglutinin (PHA-L) following its injection in the SI, and were compared to cortical perivascular cholinergic (immunoreactive for choline acetyltransferase (ChAT)) terminals. The basal forebrain origin of cholinergic terminals was evaluated after unilateral ibotenic acid lesion of the SI. PHA-L varicose fibers reached and surrounded microvessels in all cortical subdivisions examined. When studied at the ultrastructural level in the fronto-parietal and perirhinal cortices, perivascular PHA-L nerve terminals were located significantly closer to microvessels in the fronto-parietal than in the perirhinal cortex (respective average distance of 0.98 +/- 0.09 and 1.34 +/- 0.07 micron; p < 0.01). PHA-L and ChAT terminals in the fronto-parietal cortex compared very well in their perivascular distribution but not in the perirhinal cortex. In both cortices, perivascular PHA-L terminals were similar in size to, but engaged more frequently in synaptic contacts than their ChAT counterparts. Following SI lesion, the density of cortical ChAT terminals including those reaching microvessels decreased significantly (56 and 63%, respectively, p < 0.005) in the fronto-parietal cortex, while the cortical and perivascular denervations were much less pronounced (26%, not significant and 35%, p < 0.05, respectively) in the perirhinal cortex. These results indicate that basal forebrain neurons project preferentially to fronto-parietal cortical microvessels and further show that a significant proportion of these projections are cholinergic. In addition, the difference in distribution and/or synaptic incidence between perivascular PHA-L and ChAT terminals suggested that noncholinergic SI neurons also contribute to these neurovascular associations, and more so in the perirhinal cortex, as further indicated by the lesion studies. Such finding corroborates recent physiological evidence for a functional innervation of the cortical microvascular bed by SI neurons, a role that might be relevant to the overall pathology of Alzheimer's dementia.

Animals↗

PubMed1993

Some remarks on the growth-rate and angiogenesis of microvessels in ischemic stroke. Morphometric and immunocytochemical studies.

Variability in microvessel changes of blood vessel density has prompted us to undertake quantitative morphometric studies of infarcted areas in human brain. In the initial study, brains were obtained at autopsy from 10 patients (ages 45-85). Samples were collected from infarcted hemisphere and controls from the contralateral hemisphere. Formalin fixed, paraffin embedded and thereafter routinely processed sections were stained after Pickworth and with HE. Altogether 6,520 microvessels, representing 10,801 microscopic fields were counted. The Wilcoxon Range test was used for statistical analysis. In 9 of 10 patients in infarcted brain hemispheres, there was a marked increase in microvessel density (p < 0.01), when compared with contralateral brain hemisphere. In addition, a positive correlation was also found between the time of survival and both total density and density of non-perfused blood vessels. To gain a deep insight into the enhanced activity of microvessels, immunocytochemical studies were performed, which have shown, that the vascular endothelial cells in infarcted brain were reactive to two monoclonal antibodies, one, E-9, directed against an activation/proliferation associated endothelial cell specific protein and the other recognizing adhesion molecule VCAM-1. Pan-endothelial Mab PECAM/CD31 was used in those studies for controls and confirmed the obtained results. Our findings strongly support the concept of angiogenesis in the infarcted area. If correlated with morphometric results, it may indicate an important role of microvessels in pathobiology of ischemic stroke.

Aged↗

PubMed1995

Ultrastructural evidence for blood microvessels devoid of an endothelial cell lining in transplanted pancreatic islets.

The aim of the present study was to investigate, at the ultrastructural level, the process of revascularization of freshly isolated islets or cultured islets after transplantation under the kidney capsule of syngeneic mice. Native islets in adult pancreases from mice, pigs, and humans contained only capillaries with fenestrated endothelium. However, the endothelial cell lining was disrupted in both freshly isolated and cultured mouse islets. Shortly after transplantation (6 weeks) approximately 80% of graft microvessels contained no endothelial cell lining. Similar data on microvessel morphology were found when fetal porcine islet-like cell clusters were implanted into athymic nude mice. Re-endothelialization was a slow process, with 25% of the microvessels still lacking endothelium 6 months after transplantation of cultured mouse islets or islet-like cell cluster. However, when freshly isolated mouse islets are used only 25% of microvessels within the islet graft lacked endothelium 6 weeks after implantation. We suggest that capillaries damaged during islet isolation may provide a preformed channel, serving as a scaffold for newly formed islet graft blood vessels. The presence of non-endothelialized microvessels, with an associated lack of barrier function, might make transplanted islets more prone to thrombosis or an attack by the immune system. This provides a tentative explanation for the increased vulnerability of islet grafts when compared with whole pancreas transplants.

Animals↗

PubMedDate not supplied

Prognostic value of tumour microvessel density in cancer of the uterine cervix stage IB to IIB.

High intensity of tumour angiogenesis has been correlated with an increased potential of metastasis and poor prognosis in human malignancies. We investigated 43 patients with cervical cancer stages IB (n = 13), IIA (n = 8) and IIB (n = 22). All patients were treated by radical hysterectomy and lymphadenectomy. In the tumour specimen blood vessels were highlighted by staining endothelial cells for factor VIII. Microvessels were counted on a 200x field (0.74 mm2) in the most active areas of neovascularisation. The mean microvessel counts per field for stage IB, IIA and IIB tumours were 59.6 +/- 28.1, 56.3 +/- 24.3 and 55.7 +/- 55.6, respectively (p-value = n.s.). We found no significant correlation of microvessel density and established prognostic factors like pelvic lymph node involvement, vascular space invasion and stromal reaction. Patients with tumours showing low microvessel density (< 40 microvessels per field) had a significantly poorer recurrence-free interval (log-rank test: p-value = 0.01).

Female↗

PubMed1995

[Clinical significance of argyrophilic nucleolar organizer regions (AgNOR) and microvessel quantitation by staining for factor VIII-related antigen as prognostic indicators in stage I breast cancer].

The clinical significance of AgNOR and microvessel quantitation as prognostic indicators in Stage I breast cancer were examined. This study included 99 patients with Stage I breast cancer, with a median follow-up period of 119 months. AgNOR was stained by Crocker's method and microvessels were identified by immunohistochemical staining for Factor VIII-related antigen in formalin-fixed, paraffin-embedded primary tumors. AgNOR score related with tumor size. Microvessel count was related to estrogen receptor status. When patients were classified into two groups by the mean AgNOR score, higher scores had a tendency to be correlated with shorter overall survival. And when classified by microvessel count, higher counts were significantly associated with shorter overall, survival (p < 0.01). The microvessel count might be a useful predictor and the AgNOR score could be used to corroborate predictions for identifying patients at high risk for relapse and death in Stage I breast cancer.

Breast Neoplasms↗

PubMed1995

Heterogeneity and reproducibility of microvessel counts in breast cancer.

BACKGROUND: Microvessel counting has proven to be of prognostic value in breast cancer, as shown in different retrospective studies. However, methodology has not been studied widely, and this must be done before the method can become clinically applicable. The aim of this study was to determine the degree of heterogeneity and reproducibility of microvessel counts (MC) in breast cancer. EXPERIMENTAL DESIGN: In 10 cases of breast cancer, the available blocks (2-4 blocks) containing invasive tumor parts were selected, and four sections (4 microns) were cut with interdistances of 100 microns. In each section, two or three invasive areas (0.5 x 0.5 cm) were demarcated. Microvessels, visualized by immunohistochemistry (CD31 Ab), were counted by one observer in 10 systematically selected fields of vision (400 x magnification). Furthermore, microvessels were counted in four fields with the highest microvessel density ("hot spots"). Coefficients of variation (CV) were calculated for the different sampling levels. RESULTS: Repeated MC yielded high intra- and interobserver reproducibility (correlation coefficients > 0.92). For the systematic counting method, CV between MC from different areas within one section was on average (17.1% (0.7-52.1). When comparing MC from corresponding areas in different sections from the same black, CV was on average 14.7% (0.5-41.9), and for MC from different blocks of the same tumor, CV was on average 25.8% (9.9-44.6). Nested ANOVA showed an approximately equal contribution to the total variance of the different sampling levels, except for the variation between sections (not significant). For the hot spot MC, CV for different sections from the same block was on average 11.1% (0.7-29.5) and for different blocks from the same tumor, 24.2% (5.7-54.9). Nested ANOVA showed that variation between different blocks from the same tumor contributed most to the total variance. CONCLUSIONS: There is a noteworthy heterogeneity in MC between different areas from the same section, between corresponding areas in different sections from the same block, and between different blocks from the same tumor. Consequently, one must carefully scan all the available tumor material in each case for the best hot spot. The hot spot approach is efficient and reproducible, but only a comparative prognostic evaluation can show whether it is clinically more useful than systematic counts.

Breast Neoplasms↗

PubMed1996

Inhibition of prostaglandin synthesis in newborn pigs increases cerebral microvessel prostaglandin F2 alpha and prostaglandin E2 receptors, their second messengers and vasoconstrictor response to adult levels.

We recently reported that the density of prostaglandin (PG) F2 alpha and E2 receptors (FP and EP) on the cerebral microvasculature of the newborn is less than on that of the adult animal. This study tests the hypothesis that higher levels of PGF2 alpha and PGE2 in the newborn than in the adult brain might down-regulate FP and EP and their functions in the cerebral microvasculature. Newborn pigs (1-2 days old) were treated with ibuprofen (40 mg/kg i.v.) every 6 h for 48 h; and cerebrovascular FP and EP density, receptor-coupled second messenger production and cerebral vasoconstrictor responses to PGF2 alpha and PGE2 were determined. The results showed that ibuprofen treatment in the newborn increased brain microvascular FP and EP densities to levels found in the brains of adult pigs. This up-regulation of prostaglandin receptors was also observed in isolated newborn brain microvessels incubated for 48 h with ibuprofen. PGF 2 alpha, fenprostalene (PGF2 alpha analog), PGE2, 17-phenyl trinor PGE2 (EP1 receptor subtype agonist) and M&B 28,767 (EP3 agonist) caused a significantly greater increase in inositol 1,4,5-triphosphate production in brain microvessels of ibuprofen-treated than in brain microvessels of saline-treated newborn pigs. The cerebral vasoconstrictor effects of PGF2 alpha, 17-phenyl trinor PGE2 and M&B 28,767 were also significantly increased in newborn pigs treated with ibuprofen to levels comparable to those of adults. However, the steady-state level of FP mRNA in cerebral microvasculature did not differ between saline-treated newborn, ibuprofen-treated newborn and adult pigs. It is concluded that the low FP and EP densities in newborn brain microvessels are a result of high levels of brain prostaglandins and that these receptors, receptor-coupled second messengers and cerebral vasoconstrictor responses to FP, EP1 and EP3 stimulation can be up-regulated to adult levels by decreasing endogenous prostaglandin production. The changes in receptor levels were not related to steady-state levels of receptor mRNA in brain microvessels.

Animals↗

PubMed1996

[Corticosteroids limit the decrease in blood flow velocity in the microvessels of the gastric submucosal layer during stress in rats].

To evaluate the influence of stress and corticosteroids on blood flow velocity in gastric submucosal microvessels it was used intravital microfilming by means of a dark-field contact epiobjective. The plasma filled "gap" in the continuous erythrocyte flow were used as the markers to measure linear blood flow velocity. In unstressed rats the linear blood flow velocity was equal to 2.0 +/- 0.08 mm/sec (156 microvessels, 6.4 +/- 0.14 micron in diameter), calculated volume blood flow--(6.9 +/- 0.48) x 10(-5) microliters/sec. Stress (water immersion and restraint) led to a decrease of blood flow velocity in microvessels to more than double. A stress-induced decrease of blood flow velocity was more greater in rats with insufficient corticosteroid production. The linear velocity of blood flow of these rats was lowered to 0.6 +/- 0.06 mm/sec, volume blood flow to (1.6 +/- 0.21) x 10(-5) microliters/sec. Replacement corticosterone therapy increased the blood flow velocity. It was concluded that stress decreases blood flow in microvessels of gastric submucosa. The results revealed that glucocorticoids take part in normalization of blood flow of gastric microvessels during stress and this action can provide antiulcerogenic effect of corticosteroids which was shown by us previously.

Adrenal Cortex Hormones↗

PubMed1997

Associations between neuropeptide Y nerve terminals and intraparenchymal microvessels in rat and human cerebral cortex.

Neuropeptide Y (NPY) can influence local brain perfusion, possibly via direct relationships with the microvascular bed. To evaluate this possibility, the authors quantitatively analyzed by light and electron microscopy the morphological associations between immunostained NPY neuronal elements and intraparenchymal microvessels in the rat and human cerebral cortex. At the light microscopic level in the rat frontoparietal cortex, about 16% of NPY neurons and large proximal processes as well as a subset of nerve terminals not affected by double sympathectomy were associated with penetrating arterioles and local microvessels. In human temporal cortex, a dense network of NPY nerve fibers was observed, many of which approached and/or contacted intracortical vessels. At the ultrastructural level, 14% of NPY axonal varicosities in the rat cerebral cortex were considered perivascular and associated with capillaries (approximately 70%) or microarterioles (approximately 30%). They were particularly enriched in the immediate vicinity (< 0.25 micron) of the microvessels, where the perivascular astrocytic leaflets represented a frequent target. In human cerebral cortex, NPY varicosities were observed in proximity to microvessels corresponding primarily to capillaries. Perivascular NPY varicosities never established synaptic junctions with vascular or astroglial elements. The results show that central NPY nerve terminals associate with microvessels and perivascular astroglial cells in the rat and human cerebral cortex. Thus, NPY released from these nerves could possibly influence (via a parasynaptic mode of action) vascular and/or astrocytic functions depending on the distribution of NPY receptors in these cellular compartments. These results provide morphological support for the effects of NPY on brain perfusion and homeostasis.

Adult↗