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PubMed2006

The role of vessel maturation and vessel functionality in spontaneous fluctuations of T2*-weighted GRE signal within tumors.

Acute hypoxia (transient cycles of hypoxia-reoxygenation) is known to occur in solid tumors and is generally believed to be caused by tumor blood flow instabilities. It was recently demonstrated that T2*-weighted (T2*w) gradient echo (GRE) MRI is a powerful non-invasive method for investigating periodic changes in tumor pO2 and blood flow associated with acute hypoxia. Here, the possible correlation between tumor vessel immaturity, vessel functionality and T2*w GRE signal fluctuations was investigated. Intramuscularly implanted FSa II fibrosarcoma-bearing mice were imaged at 4.7 T. Maps of spontaneous fluctuations of MR signal intensity in tumor tissue during air breathing were obtained using a T2*w GRE sequence. This same sequence was also employed during air-5% CO2 breathing (hypercapnia) and carbogen breathing (hypercapnic hyperoxia) to obtain parametric maps representing vessel maturation and vessel function, respectively. Vascular density, vessel maturation and vessel perfusion were also assessed histologically by using CD31 labeling, alpha-smooth muscle actin immunoreactivity and Hoechst 33242 labeling, respectively. About 50% of the tumor fluctuations occurred in functional tumor regions (responsive to carbogen) and 80% occurred in tumor regions with immature vessels (lack of response to hypercapnia). The proportion of hypercapnia-responsive voxels were found to be twice as great in fluctuating than in non-fluctuating tumor areas (P: 0.22 vs 0.13). Similarly, the proportion of functional voxels was somewhat greater in fluctuating tumor areas (P: 0.54 vs 0.43). The mean values of MR signal changes during hypercapnia (VD) and during carbogen breathing (VF) (significant voxels only) were also larger in fluctuating than in non-fluctuating tumor areas (P < 0.05). This study demonstrated that adequate vessel functionality and advanced vessel maturation could explain at least in part the occurrence of spontaneous T2*w GRE signal fluctuations. Functionality and maturation are not required for signal fluctuations, however, because a large fraction of fluctuations could still occur in non-perfused and/or immature vessels.

Animals↗

PubMed1996

Photothermally induced vessel-wall necrosis after pulsed dye laser treatment: lack of response in port-wine stains with small sized or deeply located vessels.

The optimal treatment of port-wine stains is laser-induced selective photothermolysis. Lesion color and location and the age of the patient are reported to influence the therapeutic outcome. This study was initiated to analyze the outcome not only by the clinical response of lightening, but also in terms of photothermally induced necrosis to the vessel wall. Punch biopsy specimens were taken from 51 patients before treatment. Post-treatment biopsies were taken after exposure to a pulsed dye laser (585-nm wavelength, 0.45-ms pulse length) with an irradiant fluence of 6.5 J/cm2. Vessel diameter, depth, and wall thickness were measured in all histologic slides. The viability of the vessel walls was evaluated using an enzyme histochemical method. Port-wine stains with good blanching had significantly more superficially located vessels than the moderate and poor responders (p < 0.000). The moderate and good responding lesions consisted of moderate-sized vessels with diameters of 38 +/- 17 micrometers and 38 +/- 19 micrometers (mean +/- SD), respectively. The lesions showing poor blanching had significantly smaller vessels, with a diameter of 19 +/- 6.5 micrometers < 0.000). Analyses of the post-treatment specimens showed that coagulated vessels were superficially located and of moderate size, whereas the viable vessels were small with a median diameter of 14 micrometers. The probability of coagulation correlated with the thickness of the vessel wall. These data indicate that the therapeutic outcome of port-wine stains can be improved by using the lesional vessel parameters to select the optimal laser wavelength, pulse duration, and dose.

Humans↗

PubMedDate not supplied

A histochemical study of cerebral cortical vessels and ganglionic vessels of the caudatoputamen in aging normotensive rats.

The goal was to describe the metabolic profile of ganglionic and cortical arteries and arterioles in aging normotensive male rats. Five enzymes indicative of key metabolic pathways in the vessel walls were semiquantitatively evaluated using bright-field histochemical microscopy. Lactate dehydrogenase showed significant reactivity which increased with vessel diameter in cortical and ganglionic vessels in all age groups tested. Succinate dehydrogenase and cytochrome oxidase showed little reactivity in both cortical and ganglionic vessels, suggesting a reduced role for aerobic metabolic pathways. Myosin ATPase reactivity was high in cortical and ganglionic vessels. Only this enzyme showed an increased reactivity that was correlated with the age and diameter of the vessel. Glucose-6-phosphate dehydrogenase reactivity was more pronounced in cortical than ganglionic vessels, suggesting that the hexose-monophosphate-shunt may be more active in the cortical vessels. There were no regional differences in enzyme reactivity throughout the caudatoputamen. In conclusion, both the cortical and ganglionic vessels are metabolically active, with significant anaerobic glycolysis, and reduced, but observable capacity for aerobic metabolism. The decreased myosin ATPase reactivity and the low level of glucose-6-phosphate dehydrogenase reactivity in the ganglionic arterioles of senescent rats may contribute to the susceptibility of these vessels to cerebrovascular accidents.

Adenosine Triphosphatases↗

PubMedDate not supplied

Differentiating the infarct-related artery on initial electrocardiogram in single or multi-vessel disease in acute inferior myocardial infarction and evaluating involvement of vessels using correspondence analysis.

Initial electrocardiography changes were compared prospectively with the findings of coronary angiography to predict the infarct-related artery (IRA) in cases of single- and multi-vessel disease and to demonstrate the relationship between other coexisting coronary involvements and IRA in patients who presented with acute inferior myocardial infarction (AMI). ST elevations or depressions of at least 1 mm (0.1 mV) were evaluated in the leads I, aVL, and V1-V6. Of the 160 patients hospitalized due to inferior AMI, 153 (96%) underwent coronary angiography using standard methods. The angiograms were screened for stenotic lesions using quantitative coronary angiography to confirm significance, which was considered >50% vessel lumen diameter reduction. Among single-vessel involvements, the IRA was either the circumflex artery (Cx) or right coronary artery (RCA). In conditions in which IRA was detected as either Cx or RCA, 1-, 2-, and 3-vessel involvements were also detected. Correspondence analysis was performed to show the vessel involvements accompanying IRA. Compared with patients with IRA as RCA, the presence of ST depressions in the leads V1 or V2 and aVL were more frequently seen in patients with IRA as Cx (p=0.000, p=0.015, respectively). Among all vessel involvements in which IRA was either Cx or RCA, a ST-segment depression in leads V1 or V2 (p=0.000) and aVL (p=0.000) and a ST-segment elevation in lead I (p=0.005) were considered to be significant for Cx, and a ST-segment depression in lead I for RCA involvement (p=0.010). According to correspondence analysis, the most frequent single-vessel involvement seen in inferior AMI was RCA; when IRA was RCA, a multi-vessel involvement included RCA and Cx; and when IRA was Cx, a single-vessel involvement included the left anterior descending (LAD) artery most frequently, and RCA+LAD less frequently (p=0.000). In inferior AMI, RCA was the most common IRA; however, the possibility of multi-vessel disease is increased when Cx is found to be the IRA. In patients presenting with inferior AMI, the presence of ST-depression in the leads aVL and V1-2 is a sensitive finding that indicates Cx stenosis rather than RCA stenosis and is not affected by coexisting other coronary artery involvements.

Electrocardiography↗

PubMed1988

Exercise-induced precordial ST-segment depression in prior inferior myocardial infarction with single-vessel disease; with special reference to its mechanisms and distinction from multi-vessel disease.

We investigated the mechanisms of exercise-induced precordial ST-segment depression on the electrocardiogram in prior inferior myocardial infarction with single-vessel disease and attempted to differentiate the ST-segment depression between single- and multi-vessel disease. Subjects included three groups: group Ia (n = 11), inferior myocardial infarction with single-vessel disease that showed no precordial ST-segment depression; group Ib (n = 7), inferior myocardial infarction with single-vessel disease accompanied by precordial ST-segment depression; and group II (n = 10), inferior myocardial infarction with multi-vessel disease. The subjects underwent 12-lead exercise electrocardiography, stress Tl-201 myocardial imaging and stress radionuclide ventriculography. Exercise-induced precordial ST-segment depression observed in group Ib was associated with large infarction and infarction extending into the inferoseptal wall of the left ventricle on myocardial image. On stress ventriculography, worsening of the septal wall motion was more frequently observed in group Ib than in group Ia. Coronary arteriography revealed a higher rate of rich collateral vessels to the infarcted zone in group Ib than in group Ia. When we compared the diagnostic ability for detecting multi-vessel disease in prior inferior myocardial infarction, although sensitivity was not different among three tests, both exercise electrocardiography and radionuclide ventriculography had poor specificity and predictive value compared to stress Tl-201 myocardial imaging. Thus we concluded that exercise-induced precordial ST-segment depression observed in prior inferior myocardial infarction with single-vessel disease should reflect a peri-infarctional ischemia located in the inferoseptal wall of the left ventricle, and that stress Tl-201 myocardial imaging is the most accurate method for diagnosing multi-vessel disease in prior inferior myocardial infarction.

Cardiac Output↗

PubMed1988

Acute myocardial infarction associated with single vessel coronary artery disease: an analysis of clinical outcome and the prognostic importance of vessel patency and residual ischemic myocardium.

The long-term outcome and the significance of residual ischemic myocardium, as assessed by predischarge exercise thallium scintigraphy and vessel patency, were studied in 97 patients with single vessel coronary artery disease by angiography 12 +/- 4 days after uncomplicated myocardial infarction. During a mean follow-up period of 39 +/- 17 months, no patients died, 6 (6%) had a recurrent nonfatal infarction and 25 (26%) experienced rapidly progressive angina requiring hospitalization. Although neither exercise-induced angina nor ST segment depression was predictive of a recurrent cardiac event, the mean number of infarct zone scan segments showing thallium redistribution (1.0 +/- 1.0 versus 0.5 +/- 0.8, p = 0.01) and the percent of patients with infarct zone redistribution (61 versus 39%, p = 0.05) were greater in those patients who experienced a late ischemic event. Kaplan-Meier analysis demonstrated a lower event-free survival rate in patients with redistribution (n = 45) than in those without redistribution (n = 52) (p = 0.019). Although no patient received immediate thrombolytic therapy, the infarct-related vessel was angiographically patent in 40 patients (41%). Vessel patency did not influence event-free survival, although a patent vessel, as compared with an occluded vessel, was associated with a greater prevalence of non-Q wave infarction (58 versus 21%, p less than 0.001), fewer persistent infarct zone thallium defects (1.2 +/- 1.1 versus 2.0 +/- 1.2, p = 0.001), more reversible infarct zone thallium defects (1.0 +/- 1.0 versus 0.5 +/- 0.9, p = 0.02) and a trend toward a higher left ventricular ejection fraction (53 +/- 10% versus 49 +/- 12%, p = 0.07). In summary, uncomplicated myocardial infarction in patients with single vessel coronary artery disease is associated with a very low incidence of subsequent death and reinfarction. The presence of infarct zone thallium redistribution, compared with its absence, is predictive of a higher cardiac event rate. These data should be considered when recommending prophylactic percutaneous transluminal angioplasty after uncomplicated myocardial infarction in asymptomatic patients with single vessel coronary disease. On the basis of these results, future randomized trials designed to evaluate the therapeutic efficacy of revascularization in asymptomatic postinfarction patients with single vessel disease should limit enrollment to those patients with residual ischemia located within the infarct zone.

Adult↗

PubMed2000

[Retinal vessel reaction to 100% O2-breathing--functional imaging using the retinal vessel analyzer with 10 volunteers].

BACKGROUND: Retinal vessel diameter assessment is complicated by various components among them dynamic changes due to vasomotoric effects. Measurement of these diameters was usually obtained from fundus photographs. Functional diameter changes induced by external stimuli were difficult to evaluate because of their dynamic nature. The Retinal Vessel Analyzer (RVA) allows continuous on-line measurement of those dynamic changes. Whether functional changes due to 100% O2 breathing can be assessed by RVA is investigated in this study. MATERIALS AND METHODS: Continuous on-line registration of retinal arterial and venous branch vessels was obtained in 10 healthy volunteers. A baseline was taken during the first minute. Then for 5 minutes 100% O2 was delivered by mask. Further recording ensued for 4 minutes, while breathing room air. Vessel diameter change in percent to baseline was calculated for each individual and for a mean of the group. RESULTS: Each individual demonstrated vasoconstriction. The mean diameter reduction for the group was 6.5% for arteries and 15% for veins. CONCLUSIONS: RVA allows assessment of functional retinal branch vessel reactions. Retinal branch vessels diameters are denominators for capillary perfusion. RVA might be able to demonstrate an individual vessel's regulation potential by purposeful stimulation to constrict and dilate. This property could be helpful in understanding pathophysiologic processes as well as improving diagnosis and therapeutic effects in diseases influencing ocular perfusion such as diabetes, retinal vessel occlusion or even glaucoma. Further evaluation of effects of systemic diseases might be an additional application of functional retinal vessel diameter assessment by RVA.

Adult↗

PubMed2002

Impact of deep vessel wall injury and vessel stretching on subsequent arterial remodeling after balloon angioplasty: a serial intravascular ultrasound study.

BACKGROUND: Arterial remodeling has been shown to be responsible for lumen narrowing after nonstent interventions. METHODS: To examine the impact of deep vessel wall injury (DI) after balloon angioplasty on the subsequent vessel remodeling process, we performed serial intravascular ultrasound (IVUS) analysis in 47 native coronary artery lesions that underwent balloon angioplasty. An IVUS study was performed before and after balloon angioplasty and repeated at follow-up. Vessel and lumen area were measured at the narrowest site before intervention. Plaque area was calculated as vessel area minus lumen area. DI was defined as the presence of plaque/vessel wall fracture deep in the medial layer (sonolucent zone by IVUS) after angioplasty. RESULTS: After angioplasty, DI was present in 18 (38%, DI group) and absent in 29 (62%, non-DI group) of lesions. During follow-up, changes in vessel area in the DI group were significantly larger than in the non-DI group (P =.007). There were no significant differences in changes in plaque area. A trend toward greater late lumen loss was observed in the non-DI group (P =.05). In the DI group, changes in lumen area correlated better with changes in vessel area (r = 0.81, P <.0001) than with changes in plaque area (r = 0.32, P =.20). However, in the non-DI group, changes in lumen area correlated with changes in plaque area (r = -0.55, P =.002), but not with changes in vessel area (r = 0.30, P =.11). CONCLUSIONS: Deep vessel wall injury after balloon angioplasty is associated with the magnitude of the subsequent vessel remodeling process. The differences in the remodeling process may have implications regarding adjunctive therapies to prevent restenosis after balloon angioplasty.

Aged↗

PubMed2000

How to apply a discrete vessel model in thermal simulations when only incomplete vessel data are available.

For accurate predictions of the temperature distribution during hyperthermia treatment a thermal model should incorporate the individual impact of discrete vessels. In clinical practice not all vessels can be reconstructed individually. This paper investigates five possible strategies to model the thermal impact of these missing vessels. A tissue volume with a detailed, realistic, counter-current discrete vasculature is heated and the steady-state temperature distribution is calculated using our Discrete Vasculature (DIVA) thermal model. To mimic incomplete discrete vasculatures the full tree is gradually stripped, that is, the number of discretely described vessels is reduced in four steps until no discrete vessels are left. At each strip level the steady state temperature distribution is calculated for five different strategies to model the missing vessels. The strategies all use a local or global heat sink model in addition to the discrete vasculature. The resulting temperature distributions are compared with the full tree simulation. With increasing strip level the correspondence with the full tree simulation deteriorated for all strategies. An optimal strategy was found to model the missing vessels depending on the available angiographic data. It was also found that simulations with a decreased number of discrete vessels, or no vessels at all, yield temperatures which are too high. Theoretically this can be compensated by increasing the thermal conductivity; finding the optimal value is done empirically.

Blood↗

PubMed2005

Retinal vessel diameters and cerebral small vessel disease: the Rotterdam Scan Study.

The direct visualization of retinal vessels provides a unique opportunity to study cerebral small vessel disease, because these vessels share many features. It was reported that persons with smaller retinal arteriolar-to-venular ratio tended to have more white matter lesions on MRI. It is unclear whether this is due to arteriolar narrowing or venular dilatation. We investigated whether smaller arteriolar or larger venular diameters or both were related to severity and progression of cerebral small vessel disease. We studied 490 persons (60-90 years) without dementia from a population-based cohort study. At baseline (1990-1993), retinal arteriolar and venular diameters were measured on digitized images of one eye of each participant. In 1995-1996, participants underwent cerebral MRI scanning. We rated the severity of periventricular white matter lesions on a 9-point scale, approximated a total subcortical white matter lesion volume (range: 0-29.5 ml) and rated the presence of lacunar infarcts. On average 3.3 years later, 279 persons had a second MRI. Changes in periventricular and subcortical white matter lesions were rated with a semi-quantitative scale, and progression was classified as no, minor and marked. An incident infarct was a new infarct on the follow-up MRI. Neither venular nor arteriolar diameters were related to the severity of cerebral small vessel disease. Larger venular diameters were, however, associated with a marked progression of cerebral small vessel disease. Age and gender adjusted odds ratios (ORs) per standard deviation increase were 1.71 [95% confidence interval (CI): 1.11-2.61] for periventricular, 1.72 (95% CI: 1.09-2.71) for subcortical white matter lesion progression and 1.59 (95% CI: 1.06-2.39) for incident lacunar infarcts. These associations were independent of other cardiovascular risk factors. Only the OR for incident lacunar infarcts was attenuated (1.24; 95% CI: 0.72-2.12). No association was observed between arteriolar diameters and progression of cerebral small vessel disease. In conclusion, retinal venular dilatation was related to progression of cerebral small vessel disease. The mechanisms underlying venular dilatation deserve more attention, as they may provide new clues into the pathophysiology of cerebral small vessel disease.

Age Factors↗

PubMed2005

Influence of lumen shape and vessel geometry on plaque stresses: possible role in the increased vulnerability of a remodelled vessel and the "shoulder" of a plaque.

OBJECTIVE: To use finite element modelling to look at the impact of lumen shape and vessel geometry on stress distribution in a vessel. METHODS: A finite element model of an atherosclerotic plaque in a coronary artery was created and a non-linear analysis with Ogden strain energy function was done. The three most common shapes seen in an artery with an eccentric plaque--namely an elliptical lumen inside a circular vessel (A), a circular lumen inside an elliptical vessel, typical of a vessel with positive remodelling (B), and a circular lumen inside a circular vessel (C)--were modelled with and without lipid. Stress was analysed in the region of the fibrous cap separating the lumen from the plaque and the region of maximum stress along the circumference of the lumen was noted. RESULTS: In a normal circular shaped coronary artery, the haemodynamic stresses were uniformly distributed all around the circle. However, if the circle was changed to an ellipse, the stresses were redistributed along the major axis and dropped substantially along the minor axis. The stresses in a positively remodelled vessel (B) were significantly greater than in A and C, by almost 100%. Moreover, the haemodynamic stresses increased significantly towards the major axis or the shoulder in A and B, due to lumen shape and vessel geometry alone, even in the absence of lipid in the model. The stresses also had a direct relation with the thickness of the lipid pool and an inverse relation with cap thickness and lumen stenosis. CONCLUSIONS: The increased vulnerability of the shoulder region of a plaque and a remodelled coronary artery are due, apart from other factors, to increased biomechanical stresses as a result of lumen shape and vessel geometry.

Coronary Artery Disease↗

PubMed2000

Histomorphometric analysis of irradiated recipient vessels and transplant vessels of free flaps in patients undergoing reconstruction after ablative surgery.

The aim of the study was to investigate, histomorphometrically, quantitative and qualitative changes in irradiated neck recipient vessels and transplant vessels used for microsurgical anastomoses in free flaps in patients undergoing preoperative radiotherapy and chemotherapy. In 55 patients receiving 42 radial forearm flaps, 6 latissimus dorsi flaps, 6 osteomyocutaneous fibula grafts and 1 lateral arm flap, a total of 220 vessels were obtained from neck recipient vessels and transplant vessels during anastomosis. Three groups were formed: Group 1 (16 patients) treated with no radiotherapy or chemotherapy; Group 2 (20 patients) treated with preoperative irradiation (40-50 Gy) and chemotherapy (800 mg/m2 5-FU and 20 mg/m2 cisplatin) 1.5 months prior to surgery; Group 3 (19 patients) treated with radiotherapy (60-70 Gy) (median interval 78.7 months; IQR 31.3 months) prior to surgery. From each of the 220 vessel specimens, 3 sections each were histomorphometrically investigated, both qualitatively and quantitatively. To evaluate these changes as a function of age, radiation dose and chemotherapy, a statistical analysis was performed using analysis of covariance and chi-square tests. In Group 3, qualitative changes (intima dehiscence, hyalinosis) were found in recipient arteries significantly more frequently (25%, P=0.009) than in Groups 1 and 2. For Group 3 recipient arteries, histomorphometry revealed a significant decrease in the ratio of media area/total vessel area (median 0.53, IQR 0.10) in comparison with Group 1 (P= 0.02) (median 0.60, IQR 0.29) and Group 2 (P=0.046) (median 0.59, IQR 0.10). No significant differences were found between the vessels of Groups 1 and 2 (P= 0.48). Age and chemotherapy did not appear to have a significant influence on vessel changes in this study.

Adult↗

PubMed1990

Relationship between vessel wall 13-HODE synthesis and vessel wall thrombogenicity following injury: influence of salicylate and dipyridamole treatment.

We performed studies to determine the relationship between injured vessel wall thrombogenicity, vessel wall 13-hydroxyoctadecadienoic acid (13-HODE) synthesis and cAMP levels in rabbit treated with salicylate or dipyridamole. Injured vessel wall thrombogenicity was measured as the number of 3H-adenine labelled platelets adhered to the subendothelial basement membrane exposed by air injury in carotid arteries of rabbits treated orally with salicylate or dipyridamole. Vessel wall 13-HODE was measured by HPLC and vessel wall cAMP was measured by RIA. Vessel wall thrombogenicity was increased two-fold in rabbits treated with salicylate and decreased by half in rabbits treated with dipyridamole. The levels of vessel wall cAMP levels were correlated both with the plasma dipyridamole levels and increases in 13-HODE synthesis. cAMP levels were unaffected by salicylate treatment, but 13-HODE synthesis was decreased. We conclude that there is a significant relationship between vessel wall cAMP levels and 13-HODE synthesis, which in turn, influences subsequent vessel wall thrombogenicity.

Animals↗

PubMed1989

Peripheral arterial disease in large vessels is epidemiologically distinct from small vessel disease. An analysis of risk factors.

The authors used noninvasive techniques, including flow velocity by Doppler ultrasound, to accurately assess and distinguish between large and small vessel peripheral arterial disease in a population study in southern California, 1978-1981. In 565 men and women aged 38-82 years, there were 69 cases of large vessel peripheral arterial disease, 19 of which were severe, and 90 cases of isolated small vessel peripheral arterial disease. In cross-sectional multivariate analysis in men, large vessel peripheral arterial disease was significantly associated with age, pack-years of cigarettes smoked, systolic blood pressure, fasting plasma glucose, and marginally with obesity. Similar analysis in women revealed significant associations only for age and systolic blood pressure, although the associations for pack-years of cigarettes, obesity, and low density lipoprotein cholesterol were suggestive. By contrast, isolated small vessel peripheral arterial disease was not significantly associated with any of the major cardiovascular disease risk factors, including two measures of carbohydrate metabolism, fasting plasma glucose and glycosylated hemoglobin. These findings, coupled with our earlier report that large vessel peripheral arterial disease but not isolated small vessel peripheral arterial disease was independently predictive of subsequent mortality, suggest that large vessel peripheral arterial disease and isolated small vessel peripheral arterial disease are epidemiologically, as well as pathophysiologically, distinct entities.

Adult↗

PubMed2005

The transverse cervical vessels as recipient vessels for previously treated head and neck cancer patients.

BACKGROUND: A major challenge in head and neck reconstruction in patients with a "frozen neck" is the limited availability of recipient vessels including the carotid artery system. The aim of the present study was to investigate the suitability of the transverse cervical vessels as recipient vessels for free flap reconstruction in head and neck cancer patients. METHODS: Thirty-three sides of necks in 26 patients requiring free flap reconstruction were explored. The presence, location, and size of the transverse cervical vessels were documented. RESULTS: Two arteries (6 percent) and four veins (12 percent) were unavailable. Eight arteries (24 percent) and two veins (6 percent) had a diameter of less than 2 mm, 23 arteries (70 percent) and 18 veins (55 percent) had a diameter of 2 to 3 mm, and nine veins (27 percent) were larger than 3 mm. The contralateral neck was explored because of the lack of suitable ipsilateral vessels in six patients (23 percent). The transverse cervical vessels were unsuitable on both sides in two patients (8 percent). All the available transverse cervical vessels were found to be free of disease. Moderate scarring in the supraclavicular region was present in two cases. All flaps survived without vascular events. CONCLUSIONS: The transverse cervical vessels were thus suitable as recipient vessels in 92 percent of patients and should be the first choice in difficult head and neck reconstructions.

Adult↗

PubMed2005

NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels.

NO has been shown to mediate angiogenesis; however, its role in vessel morphogenesis and maturation is not known. Using intravital microscopy, histological analysis, alpha-smooth muscle actin and chondroitin sulfate proteoglycan 4 staining, microsensor NO measurements, and an NO synthase (NOS) inhibitor, we found that NO mediates mural cell coverage as well as vessel branching and longitudinal extension but not the circumferential growth of blood vessels in B16 murine melanomas. NO-sensitive fluorescent probe 4,5-diaminofluorescein imaging, NOS immunostaining, and the use of NOS-deficient mice revealed that eNOS in vascular endothelial cells is the predominant source of NO and induces these effects. To further dissect the role of NO in mural cell recruitment and vascular morphogenesis, we performed a series of independent analyses. Transwell and under-agarose migration assays demonstrated that endothelial cell-derived NO induces directional migration of mural cell precursors toward endothelial cells. An in vivo tissue-engineered blood vessel model revealed that NO mediates endothelial-mural cell interaction prior to vessel perfusion and also induces recruitment of mural cells to angiogenic vessels, vessel branching, and longitudinal extension and subsequent stabilization of the vessels. These data indicate that endothelial cell-derived NO induces mural cell recruitment as well as subsequent morphogenesis and stabilization of angiogenic vessels.

Animals↗

PubMed1987

Quantitative analysis of cerebral vessels in the newborn puppy: the structure of germinal matrix vessels may predispose to hemorrhage.

Intracerebral hemorrhage in premature infants commonly originates in the germinal matrix (GM). We performed a quantitative analysis of cerebral microvasculature from newborn puppies, a model for neonatal periventricular and intraventricular hemorrhage, at the light and electron microscopic level. GM vessels were compared with those of other brain regions in an effort to delineate pathogenetically significant structural features that might predispose to hemorrhage. Light microscopic examination revealed that GM vessel density (103.0 vessels/mm2) was similar to that in white matter (98.3 vessels/mm2), but lower than that of cortex (155.6 vessels/mm2) or caudate (259.9 vessels/mm2). Mean blood vessel diameter was slightly larger in GM (9.0 mu) than cortex (6.9 mu), caudate (7.9 mu), and white matter (8.9 mu). Ultrastructurally, GM vessels were thinner along greater portions of their circumferences than vessels from other brain regions, as shown by their smaller ratio of vessel wall area/vessel lumen area and their greater fraction of vessel wall with thickness less than 0.25 mu. In addition, a significantly larger fraction of GM capillary wall lacked direct contact with perivascular structures. We postulate that the larger size, thinner walls, and diminished support from surrounding neuropil, which characterize GM vessels, may render them more susceptible to both physical (e.g. hypertension) and metabolic (e.g. hypoxia) insults than vessels from other brain regions.

Animals↗

PubMed1999

Lymphatic vessels of the human heart: precollectors and collecting vessels. A morpho-structural study.

Only topographic and distributional data are available on the lymphatic outflow vessels of the human heart. Here we describe their structural and ultrastructural features. Fragments of the atria, ventricles and fat surrounding the major coronary branches were obtained from hearts of dilated cardiomyopathy patients. Serial semithin sections were observed under light microscopy and used for tridimensional reconstructions. Ultrathin sections were observed by transmission electron microscopy. Precollectors, the initial lymphatic outflow routes of the heart, are small valved vessels with irregular, discontinuous musculature. They originate in the subepicardial region from a network of epicardial, and from scattered myocardial absorbing lymphatic vessels and drain into the collecting vessels accompanying the major coronary branches. Collecting vessels are larger but structurally similar to precollectors. Wall musculature is independent of the size of the vessel. Their ultrastructure is the same as that of precollectors. Endothelial cells have many Weibel-Palade bodies, cytoplasmic filaments and focal adhesions. The basement membrane is discontinuous and anchoring filaments are frequent and conspicuous. The subendothelial layer contains much elastin. Human heart collecting vessels and precollectors may only be distinguished by their size. The scarcity of musculature suggests that lymph progression in this district is mainly ensured by cardiac revolutions. Their ultrastructural features are determined by adaptation to dynamic forces. The architecture of these vessels (random, disorderly, discontinuous, lacking any exact plan) and their large variations in caliber are in line with the ontogenetic hypothesis that peripheral lymphatic vessels originate from the coalescence of mesenchymal lacunae.

Cardiomyopathy, Dilated↗