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At least 793 records · Page 44Linked to original sources
PubMed1994

Heterogeneity of alpha 1-adrenoceptor subtypes involved in adrenergic contractions of dog blood vessels.

1. We determined the alpha 1-adrenoceptor subtypes involved in adrenergic contractions of eight different blood vessels isolated from the dog. 2. Noradrenaline produced concentration-dependent contractions in all the blood vessels tested, which were competitively inhibited by prazosin, WB4101, HV723 and 5-methylurapidil. However, there was considerable difference between the vessels with regard to the pKB values for all the antagonists. The alpha 1-adrenoceptors of dog vertebral and carotid arteries had high affinity for prazosin (pKB > 9.0) but low affinity for WB4101 (< 8.5), 5-methylurapidil (< 7.5) and HV723 (< or = 8.5). By contrast, HV723 had higher affinity (> 9.0) than prazosin (< 8.3), WB4101 (< 8.7) and 5-methylurapidil (< 8.2) in the portal vein, mesenteric artery and vein, and renal artery. In the femoral artery and vein, however, the four antagonists showed pKB values in the range 8.0-8.7. 3. Chloroethylclonidine (10 microM) produced a remarkable reduction of the contractile responses to noradrenaline in the vertebral and carotid arteries as compared with those in the other vessels. Nifedipine inhibited the responses to noradrenaline in all the tissues tested, and had marked effects in the portal vein. 4. Sympathetic adrenergic contractions induced by transmural electrical stimulation were also inhibited by prazosin and HV723 at different potencies among tissues. The relative potencies of both the antagonists paralleled the relationship in inhibiting the responses to exogenous noradrenaline in each vessel. 5. According to recent alpha l-adrenoceptor subclassification, the present results suggest that the contractions of blood vessels induced by endogenous and exogenous noradrenaline are mediated through different alpha l-adrenoceptor subtypes heterogeneously distributed in each vessel; presumably, the alpha 1 B subtype in the carotid and vertebral arteries, the alpha IN subtype in the visceral region and the alpha IL subtype in the femoral region. Regionally different expression of alpha 1-adrenoceptor subtypes may be in part associated with the regional heterogeneity of sympathetic responses in the blood vessels.

Acetonitriles↗
PubMed1994

Hyperosmolar versus detergent sclerosing agents in sclerotherapy. Effect on distal vessel obliteration.

BACKGROUND: Sclerosing agents produce local endothelial destruction extending to the adventitia of the vessel wall while producing minimal thrombosis formation. They are rapidly inactivated in order to prevent damage far beyond the injection site. It has been stated that detergent sclerosants may have more distal sclerosing capabilities than hyperosmolar sclerosants. OBJECTIVE: The present study compares the in vivo relative potential of polidocanol (POL.), a detergent sclerosing agent, and hypertonic saline (H.S.), a hyperosmolar sclerosant in their effects on distal vessel obliteration. METHOD: Symmetrical Class III reticular vessels of 2-3-mm diameter were injected with equal amounts (0.5 cc) of sclerosing solutions: 0.5% POL. in the left leg and 23.4% H.S. in the right leg. Distance of vessel sclerosing effect was calibrated from the inferior patellar tendon employing a calibrated measuring window. Standard compression (20-30 mm Hg) was employed for 72 hours after each treatment session. Patients were examined at 2-, 4-, 6-, 8-, 10-, and 16-week intervals for vascular sclerosing resolution effect. RESULTS: The mean distance of vessel sclerosis utilizing 23.4% H.S. was 6.24 cm vs 6.34 cm utilizing 0.5% POL. The mean duration of time to clinical disappearance of treated vessels was 6.4 weeks for the H.S.-treated extremity vs 6.2 weeks of the POL.-treated extremity. The difference of both parameters in terms of distance of sclerosing effect and time interval to achieve this effect were not statistically significant for either variable utilizing POL. or H.S. CONCLUSIONS: Hyperosmolar and detergent sclerosants such as POL. and H.S. in comparable concentrations for given vessel diameter may provide equal degrees of vessel obliteration clinically over equivalent periods of time in vivo. Other factors such as minimal sclerosant concentration, hypersensitivity/complication profile, patient discomfort, sclerosant availability, and physician experience are other important factors in choosing a sclerosing agent for a given clinical setting.

Adult↗
PubMedDate not supplied

Surgical approaches to recipient vessels of the fore- and hindlimbs for microvascular free tissue transfer in dogs.

OBJECTIVE: To develop and evaluate surgical approaches to the arteries and veins of the fore- and hindlimbs for use as potential recipient vessels for free tissue transfer. STUDY DESIGN: Experimental anatomic study. SAMPLE POPULATION: Canine cadavers (11): 2 preserved and 9 fresh cadavers. METHODS: Fore- and hindlimbs from 1 preserved cadaver injected with a pigmented silicone/barium mixture, through the common carotid artery and external jugular vein, were cut in 1 cm cross-sections. Tissue sections were used to identify the location of vessels >1 mm that could be used as recipient vessels for free tissue transfer. The other preserved cadaver was used to develop surgical approaches to these vessels. Three surgeons evaluated the written descriptions and illustrations for these approaches using fresh cadavers. Modifications to the surgical approaches were made based on recommendations from these surgeons. RESULTS: Six approaches were developed to isolate forelimb recipient vessels: palmar access, distal medial antebrachial, mid-antebrachial, proximal antebrachial, distal humeral, and mid-humeral vascular access. Twelve approaches were developed to isolate recipient vessels of the hindlimb: plantar access, dorsal tarsal, cranial distal tibial, craniomedial distal tibial, lateral distal tibial, medial distal tibial, medial femorotibial, lateral distal femoral, medial femoral, proximal medial femoral, groin, and proximal lateral femoral vascular access. CONCLUSIONS: Six forelimb and 12 hindlimb sites were identified for surgical access to recipient vessels (>1 mm diameter) suitable for use in free tissue transfer for wound reconstruction. CLINICAL RELEVANCE: For reconstruction of complex wounds of the extremities of dogs, surgeons should consider use of readily accessible recipient vessels that would allow for free tissue transfer to the fore- and hindlimbs.

Anastomosis, Surgical↗
PubMed1999

The role of prostanoids and nitric oxide in endotoxin-induced hyporesponsiveness of equine digital blood vessels.

Endotoxin has been implicated in the pathophysiology of acute laminitis. The aim of this study was to examine the direct effects of endotoxin on isolated equine digital blood vessels. Equine digital veins (EDV), incubated in Krebs-Henseleit solution containing lipopolysaccharide (LPS) (1 microg/ml) became hyporesponsive to 5-HT after 16 h. Cycloheximide and ibuprofen blocked this effect of LPS and increased the maximum response obtained to 5-HT when compared to control vessels. L-nitroarginine methyl ester (L-NAME) reversed the hyporesponsiveness caused by LPS. Vessels maintained in culture medium containing LPS also became hyporesponsive to 5-HT, an effect which was completely prevented by ibuprofen but only partially reversed by L-NAME. Measurements were made of 6-keto PGF1alpha and nitrite production by segments of equine digital artery and vein in culture medium alone or co-cultured with peripheral blood leucocytes. LPS did not stimulate nitrite production from vessel segments but increased nitrite release from leucocytes, an effect which was inhibited by cycloheximide and L-NAME. Lipopolysaccharide increased 6-keto PGF1alpha production by blood vessels, an effect which was inhibited by cycloheximide and ibuprofen but not L-NAME. No synergistic effect on release of nitrite or 6-keto PGF1alpha was noted in co-cultures of blood vessels and leucocytes. These data suggest that induction of cyclo-oxygenase by LPS was a major cause of hyporesponsiveness of digital blood vessels to 5-HT. Release of nitric oxide was not detectable in LPS-stimulated blood vessels maintained in culture even in the presence of activated leucocytes yet L-NAME did protect against LPS-induced hyporesponsiveness indicating nitric oxide synthase induction may play some role in the effect of LPS. These findings are important in furthering our understanding of the pathophysiological mechanisms underlying the vascular changes which occur in acute laminitis.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Endothelium-dependent modulation of pacemaking in lymphatic vessels of the guinea-pig mesentery.

1. Endothelial control of the rate of constrictions and the underlying pacemaker potentials has been studied in vitro in guinea-pig mesenteric lymphatic vessels. 2. ACh stimulated 60% of intraluminally perfused vessels to slow or abolish lymphatic constrictions. This action was inhibited by atropine and was likely to be due to the release of endothelium-derived nitric oxide (EDNO) as the effect was absent after endothelial lysis, mimicked by sodium nitroprusside (SNP), blocked by N omega-nitro L-arginine (NOLA) and partially inhibited by Methylene Blue (MB). 3. The remaining 40% of perfused vessels did not mechanically respond to ACh or SNP. In four of seven such vessels this appeared to be due to excessive perfusion-associated release of EDNO, as incubation with NOLA restored the response to SNP. 4. Application of NOLA or MB in perfused vessels significantly increased constriction frequency, further indicating perfusion-associated release of EDNO. 5. ACh induced a marked increase in endothelial [Ca2+]i of both mechanically responding and non-responding vessels. This ACh-induced increase could be repetitively induced when Ca2+ was present in the perfusate, but rapidly ran down when a Ca(2+)-free EGTA perfusate was used. 6. Intracellular recordings from the smooth muscle of non-perfused vessel segments demonstrated an ACh-induced hyperpolarization and decrease in membrane resistance, changes which were prevented by atropine, NOLA, MB and endothelial lysis and mimicked by SNP. 7. ACh directly reduced the size of the underlying pacemaker potentials termed spontaneous transient depolarizations (STDs). 8. NOLA and MB enhanced STDs in non-perfused vessel segments indicating an endogenous release of EDNO. 9. It is concluded that the lymphatic endothelium produces and releases EDNO endogenously, during perfusion or after stimulation with ACh, to decrease the efficacy of STDs to generate action potentials and resultant constrictions.

Acetylcholine↗
PubMed1994

Shape of the neuroretinal rim and position of the central retinal vessels in glaucoma.

Glaucomatous neuroretinal rim loss can occur in a sequence of sectors with the temporal inferior disc sector as the first and the nasal superior disc sector as the last to be affected. This study evaluated whether the position of the central retinal vessel trunk is correlated with this pattern of glaucomatous rim loss. Morphometrically stereo colour optic disc photographs of 157 glaucomatous eyes and 67 normal eyes were checked. In the normal and glaucomatous eyes, the central retinal vessel trunk was located eccentrically in the upper nasal quadrant of the optic disc. Taking into account the vertically oval disc shape, the distance to the central vessel trunk was largest for the temporal inferior disc region and shortest for the nasal superior disc area. An abnormal form of the glaucomatous neuroretinal rim was found in eyes with an atypical location of the retinal vessel trunk. Also in these glaucomatous eyes, the rim loss was usually most and least marked in that sector with the longest and shortest distance, respectively, to the central retinal vessel trunk. One could infer that the sequence of rim loss in glaucoma is dependent upon the distance of the region to the central retinal vessel trunk; the further away the region from the retinal vessel trunk, the more likely it is to be affected by rim loss. This suggest that the distance from the central retinal vessels is one factor among others that is correlated with the regional vulnerability of the neuroretinal rim to the glaucomatous process.

Adult↗
PubMed1987

Have "formal investigations" into fishing vessel losses ceased?

Systematic studies of 618 fishing vessel losses between January 1961 and December 1982 have shown a significantly increased incidence of total losses from 1972 onwards. Comparison of mean pre- and post-1972 rates indicated an increase of 120% from 2.54 to 5.58 losses per 1000 vessels at risk. Parallel examination of the mortality of fishermen from all occupational accidents showed no improvement. For deaths arising from vessel losses alone, the mean crude death rate, for the same periods, increased by 13%. Despite these findings, formal investigations (courts of inquiry) into fishing losses, ordered by the Department of Transport according to specified criteria, decreased in number from about 1975 onwards. The mean number fell by 61% from 3.1 (1961-71) to 1.2 a year (1972-82). Furthermore, the reduction in the rate of formal investigations into fishing vessel losses (-84%; p less than 0.0001) was greater than the corresponding reduction (-61%; p less than 0.001) in United Kingdom merchant vessel investigations and this difference was statistically significant (p less than 0.01). During 1972-82 there were 61 fewer fishing investigations than predicted from the rate at which these were ordered during 1961-71. The last took place in 1979. None of the 141 fishing vessel losses between January 1980 and December 1982 proceeded to formal investigation. The possibility that the criteria for ordering formal investigations have not been fulfilled by the circumstances of fishing vessel losses from 1975 onwards is assessed as one explanation for this paradoxical finding of an inverse relation between losses and investigations. The accident investigation and public reporting procedures for aviation accidents should be adobted for marine accidents in general and fishing vessel losses in particular.

Accidents, Occupational↗
PubMed2006

Effect of blood vessels on measurement of nodule volume in a chest phantom.

PURPOSE: To identify, by using a chest phantom, whether vessels that contact lung nodules measuring less than 5 mm in diameter will affect nodule volume assessment. MATERIALS AND METHODS: Forty synthetic nodules (20 with ground-glass attenuation and 20 with solid attenuation) that measured less than 5 mm in diameter were placed into a chest phantom either adjacent to (n = 30) or isolated from (n = 10) synthetic vessels. Nodules were imaged by using low-dose (20 mAs) and diagnostic (120 mAs) multi-detector row computed tomography (CT). Nodules that were known to lie in direct contact with vessels were confirmed by visual inspection. Nontargeted 1.25 x 1.00-mm sections were analyzed with a three-dimensional computer-assisted method for measuring nodule volume. A mixed-model analysis of variance was used to examine the influence of several factors (eg, the presence of adjacent vessels; tube current-time product; and nodule attenuation, diameter, and location) on measurement error. RESULTS: The mean absolute error (MAE) for all nodules adjacent to vessels was 2.3 mm(3), which was higher than the MAE for isolated nodules (1.9 mm(3)) (P < .001). This difference proved significant only for diagnostic CT (2.2 mm(3) for nodules adjacent to vessels vs 1.3 mm(3) for nodules isolated from vessels) (P < .05). A larger MAE was noted for nodules with ground-glass attenuation (2.3 mm(3)) versus those with solid attenuation (2.0 mm(3)), for increasing nodule volume (1.66 mm(3) for nodules smaller than 20 mm(3) vs 2.83 mm(3) for nodules larger than 40 mm(3)), and for posterior nodule location (P < .05). CONCLUSION: The presence of a vessel led to a small yet significant increase in volume error on diagnostic-quality images. This represents less than one-third of the overall error, even for nodules larger than 40 mm(3) or approximately 4 mm in diameter. This increase, however, may be more important for smaller nodules with errors of less than 3 mm(3).

Diagnostic Errors↗
PubMed1997

The dissected aorta: part III. Anatomy and radiologic diagnosis of branch-vessel compromise.

PURPOSE: To determine the anatomic, hemodynamic, and radiologic characteristics of branch-vessel compromise in patients with aortic dissection. MATERIALS AND METHODS: Sixty-two patients with aortic dissection were evaluated with aortography (n = 62), intravascular ultrasound (US) (n = 35), and manometry (n = 56). Branch-vessel compromise with ischemia was suspected in 40 of these patients. Radiologic and manometric findings were correlated with clinical findings of ischemia. Femoral artery pulse strength was correlated with access from the respective femoral artery to the true and false lumina of the dissected aorta. RESULTS: Twenty-six of 40 patients suspected of having ischemia had angiographic evidence of branch-vessel compromise, and intravascular US helped identify two types of branch-vessel compromise in them: static (dissection intersected and narrowed the vessel origin) and dynamic (dissection spared the vessel origin, but the dissection flap appeared to compress the true lumen at or above the origin and covered the origin). False-lumen pressure in classic dissections exceeded (n = 16) or equaled (n = 30) true-lumen pressure. Branch vessels that arose exclusively from the false lumen were well perfused. Findings of a dissection flap oriented concave toward the false lumen were 91% sensitive and 72% specific for a true-lumen pressure deficit. CONCLUSION: Intravascular US and manometric findings clarify the mechanisms of branch-vessel compromise after aortic dissection and provide a rational guide for percutaneous treatment.

Adolescent↗
PubMed2005

Recognizing extrahepatic collateral vessels that supply hepatocellular carcinoma to avoid complications of transcatheter arterial chemoembolization.

Extrahepatic collateral arteries commonly supply hepatocellular carcinomas if the tumors are large or peripherally located. Because development of these vessels interferes with effective control of the tumor with transcatheter arterial chemoembolization (TACE), radiologists should become familiar with the imaging findings of extrahepatic collateral vessels to detect them at an early stage. The authors observed 2104 such vessels in 860 patients over 5.5 years. The extrahepatic collateral vessels observed originated from the inferior phrenic artery, omental branch, adrenal artery, intercostal artery, cystic artery, internal mammary artery, renal or renal capsular artery, branch of the superior mesenteric artery, gastric artery, and lumbar artery. The authors suspected extrahepatic collateral vessels when (a) a tumor grew exophytically or invaded adjacent organs, (b) a tumor was in contact with the ligaments and bare area of the liver, (c) a hypertrophied extrahepatic collateral vessel was observed on a computed tomographic (CT) scan, (d) a peripheral defect of iodized oil retention within a tumor was seen during chemoembolization or on a follow-up CT scan, (e) a local recurrence developed at the peripheral portion of the treated tumor during follow-up, or (f) a sustained elevation in serum alpha-fetoprotein level was noted despite adequate embolization of the hepatic artery. When both the hepatic artery and extrahepatic collateral vessels supply a tumor, additional extrahepatic collateral vessel chemoembolization should be attempted to increase the therapeutic efficacy of TACE for hepatocellular carcinoma.

Adult↗
PubMed1986

Effects of vasodilator stimuli on resistance of large and small cerebral vessels.

We have examined effects of vasodilator stimuli on segmental resistance in the cerebral circulation. Our hypothesis was that resistance of large arteries, as well as small vessels, contributes to cerebral vascular responses to vasodilator stimuli. We measured cerebral blood flow with microspheres in anesthetized rabbits and measured pressure in pial arteries approximately 100 microns diameter using a servo-null method. These values were used to calculate resistance of large arteries (greater than 100 microns diameter) and small vessels (less than 100 microns diameter). Under control conditions, resistance of large arteries accounted for one-third to one-half of total cerebral vascular resistance. Intracarotid infusion of acetylcholine (1 microgram/min) reduced large arterial resistance by 69% and small vessel resistance by 58%. Adenosine also produced marked reductions in resistance of both large and small cerebral vessels. In contrast, seizures reduced large arterial resistance by 50% and small vessel resistance by 85%. Pial arterial pressure, which depends on the ratio of large and small vessel resistance, increased during infusion of acetylcholine and adenosine, but decreased during seizures. We conclude that both large and small cerebral vessels are responsive to acetylcholine and adenosine, and seizures produce preferential reduction in resistance of small vessels.

Acetylcholine↗
PubMed2000

Amelioration with vessel dilator of acute tubular necrosis and renal failure established for 2 days.

Seventeen Sprague-Dawley rats had ischemic nonoliguric acute renal failure (ARF) induced by vascular clamping resulting in their preischemic blood urea nitrogen (BUN) and creatinine levels of 16 +/- 1 and 0.56 +/- 0.05 mg/dl to increase to 162 +/- 4 and 8.17 +/- 0.5 mg/dl, P < 0.001, respectively, at day 4 of postischemia. Vessel dilator, a 37-amino-acid cardiac peptide hormone (0.3 microg x kg(-1) x min(-1) ip), decreased the BUN and creatinine levels to 53 +/- 17 mg/dl and 0.98 +/- 0.12 mg/dl (P < 0.001) in another seven animals where ARF had been established for 2 days. Water excretion doubled with ARF and was further augmented by vessel dilator. Transthoracic echocardiography revealed left ventricular dilation as a probable cause of the increase in vessel dilator in the circulation with ARF, and vessel dilator infusion reversed this dilation. At day 6 of ARF, mortality decreased to 14% with vessel dilator from 88% without vessel dilator. Acute tubular necrosis was <5% in the vessel dilator-treated rats compared with 25% to >75% in the placebo-treated ARF animals. We conclude that vessel dilator improves acute tubular necrosis and renal function in established ARF.

Acute Kidney Injury↗
PubMed2002

"Sausage-string" appearance of arteries and arterioles can be caused by an instability of the blood vessel wall.

Vascular damage induced by acute hypertension is preceded by a peculiar pattern where blood vessels show alternating regions of constrictions and dilations ("sausages on a string"). The pattern occurs in the smaller blood vessels, and it plays a central role in causing the vascular damage. A related vascular pattern has been observed in larger vessels from several organs during angiography. In the larger vessels the occurrence of the pattern does not appear to be related to acute hypertension. A unifying feature between the phenomenon in large and small vessels seems to be an increase in vascular wall tension. Despite much research, the mechanisms underlying the sausage pattern have remained unknown. Here we present an anisotropic model of the vessel wall and show that the sausage pattern can arise because of an instability of the vessel wall. The model reproduces many of the key features observed experimentally. Most importantly, it suggests that the "sausaging" phenomenon is neither caused by a mechanical failure of the vessel wall due to a high blood pressure nor is it due to standing pressure waves caused by the beating of the heart. Rather, it is the expression of a general instability phenomenon. Experimental data suggest that the structural changes induced by the instability may cause secondary damage to the wall of small arteries and arterioles in the form of endothelial hyperpermeability followed by local fibrinoid necrosis of the vascular wall.

Algorithms↗
PubMed1978

Fluid leaks from extra-alveolar vessels in living dog lungs.

Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.

Animals↗
PubMed2005

Anatomically based finite element models of the human pulmonary arterial and venous trees including supernumerary vessels.

Studies of the origin of pulmonary blood flow heterogeneity have highlighted the significant role of vessel branching structure on flow distribution. To enable more detailed investigation of structure-function relationships in the pulmonary circulation, an anatomically based finite element model of the arterial and venous networks has been developed to more accurately reflect the geometry found in vivo. Geometric models of the arterial and venous tree structures are created using a combination of multidetector row X-ray computed tomography imaging to define around 2,500 vessels from each tree, a volume-filling branching algorithm to generate the remaining accompanying conducting vessels, and an empirically based algorithm to generate the supernumerary vessel geometry. The explicit generation of supernumerary vessels is a unique feature of the computational model. Analysis of branching properties and geometric parameters demonstrates close correlation between the model geometry and anatomical measures of human pulmonary blood vessels. A total of 12 Strahler orders for the arterial system and 10 Strahler orders for the venous system are generated, down to the equivalent level of the terminal bronchioles in the bronchial tree. A simple Poiseuille flow solution, assuming rigid vessels, is obtained within the arterial geometry of the left lung, demonstrating a large amount of heterogeneity in the flow distribution, especially with inclusion of supernumerary vessels. This model has been constructed to accurately represent available morphometric data derived from the complex asymmetric branching structure of the human pulmonary vasculature in a form that will be suitable for application in functional simulations.

Adult↗
PubMed1991

Lymphatic vessels in the developing diaphragm of the rat.

Diaphragms of fetal, neonatal and young albino rats have been observed both under light and electron microscopes to examine the presence and distribution of lymphatic vessels and their morphological features. In fetal diaphragms of between 18 and 22 days of gestation, no normal lymphatic vessels can be seen; only after birth, specifically in neonatal and 2-day-old rats, small lymphatic vessels appear; they are in close proximity to the blood vessels in the inner areas of the muscle. As the rats get older, lymphatic vessels are also observed in the subserosa where an abundant connective tissue is present. The fine structure of diaphragmatic lymphatic vessels is different at different ages. In neonatal rats of up to 2 days, the endothelial wall is very thin and often holed. The relationships between contiguous endothelial cells are characterized by simple end-to-end or overlapping structures. The basement membrane is virtually absent. Within the first week of life, the endothelial wall becomes more complex; along the wall, complex interdigitations between two contiguous endothelial cells often touch. A discontinuous basement membrane and collagen and elastic fibers surround the vessels. In the older rats (from 14 to 25 to 140 days), next to the complex interdigitations which characterize the junction between two contiguous endothelial cells, cellular flaps interdigitate forming a channel which opens out either to the exterior or the interior of the vessel. Dense bundles of elastic and collagen fibers are closely apposed to the endothelial wall.

Animals↗
PubMed1992

Delivery of passivating proteins to sutures during passage through the vessel wall reduces subsequent platelet deposition by blocking fibrinogen adsorption.

Intraluminal vascular suture material, which attracts fewer than the expected number of platelets compared with the same biomaterial exposed to blood in vitro, differs from the untreated biomaterial in that it has been passed once through the vessel wall. The mechanism by which this apparently trivial maneuver reduces platelet deposition was investigated. Polypropylene suture (7-0 Prolene) was passed through human arteries (fetal and adult), and platelet deposition to the suture was measured in a standardized perfusion chamber. Single vessel passage of the sutures reduced platelet deposition by 68 +/- 23%, which contrasts sharply with the power of prostaglandin E1 (1 microM PGE1 is sufficient to abolish platelet shape change and aggregation), which inhibited only 11% of platelet deposition to the sutures. Aspirin treatment of the vessel (to prevent PGI2 formation) or endothelial stripping (to remove the ability to produce nitric oxide) had no effect on the degree of inhibition. Passage of the suture through a vessel analogue (expanded polytetrafluoroethylene) did not inhibit platelet deposition. 125I-fibrinogen adsorption to the suture after vessel passage was reduced to a degree similar to that of platelet deposition. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of proteins eluted from vessel-passed sutures revealed bands at 66, 47, and 16 kd. Western blotting indicated the presence of large amounts of albumin and hemoglobin, a moderate amount of haptoglobin, and only trace amounts of fibrinogen. When sutures were exposed to each of these proteins in vitro before perfusion, albumin and hemoglobin were found to reproduce the effect of vessel passage alone on platelet deposition. We conclude that albumin and hemoglobin adsorb to sutures during their passage through the vessel subendothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adsorption↗
PubMed1992

Endothelium-derived relaxing factor in brain blood vessels is not nitric oxide.

BACKGROUND: The endothelium-derived relaxing factor that mediates the actions of acetylcholine is now most frequently identified as nitric oxide. Nitric oxide is believed to have numerous important regulating actions in neurons, blood vessels, and several other biological systems. SUMMARY OF REVIEW: The literature concerning tissue other than cerebral blood vessels supports the conclusion that the endothelium-derived relaxing factor for acetylcholine is either nitric oxide or a compound formed from and containing nitric oxide (for example, a nitrosothiol). However, papers can be found indicating that this endothelium-derived mediator is not nitric oxide. In brain blood vessels the evidence is strongly against the conclusion that nitric oxide is the endothelium-derived mediator for acetylcholine. If this mediator is formed from nitric oxide, either in brain vessels or in other vessels, no data are available delineating how this synthesis is regulated or whether and where nitric oxide leaves the nitroso compound to initiate dilation. Indeed, cerebrovascular data now cast doubt on the commonly held belief that nitrosovasodilators regulate vascular tone by giving off nitric oxide to vascular smooth muscle. CONCLUSIONS: In brain blood vessels the chemical identity of the endothelium-derived relaxing factor mediating the action of acetylcholine is unknown, but this relaxing factor does not appear to be nitric oxide. If the mediator contains nitric oxide, as is probably the case, the means by which it activates vascular guanylate cyclase and/or produces dilation is unknown. Since this relaxing factor inhibits platelet adhesion/aggregation in cerebral vessels as well as relaxing these vessels, the chemical identification of this relaxing factor and the elucidation of its mode of action are extremely important to our understanding and control of cerebrovascular phenomena in health and disease.

Acetylcholine↗