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PubMed1997

Isolation of villous microvessels from the human placenta.

A method for isolating the microvessels of the human placental villi has been developed in order to culture perivascular cells. It consists of an initial selection of the villi by serial sieving. The villi retained by the 75 microns sieve were digested by collagenase-dispase. A Percoll gradient permitted the isolation of microvessels still surrounded by stromal fibres and cells. Another digestion by collagenase-dispase eliminated the contaminant elements and allowed, after a new Percoll gradient, microvessels with endothelium, basement membrane and a few perivascular cells to be obtained. Each step of the isolation of microvessels was monitored by light or electron microscopy. Our study confirms the isolation of microvessels embedded in their basement membrane and the preservation of endothelial and perivascular cells after digestion. This method, which has permitted the culture of placental endothelial cells and pericytes, appears of interest for studying microvascular angiogenesis and permeability.

Blood Vessels↗

PubMed1995

Microvessel quantification in primary colorectal carcinoma: an immunohistochemical study.

The vascularisation of human primary colorectal carcinomas was studied immunohistochemically using the endothelial cell markers CD31 and factor VIII-related antigen. Tumour sections were systematically scanned at a magnification of x 100 to find areas of intense neovascularisation. Microvessel counts within these vascular 'hotspots' were performed at magnification x 250. Regions in which tumour cords were surrounded by a collagen IV-positive basement membrane were compared with those in which this was absent and with normal mucosa. CD31 appeared to be a more sensitive marker for endothelial cells than factor VIII-related antigen (mean 185 +/- 59 and 120 +/- 38 microvessels mm-2). Within individual tumour sections microvessel counts in vascular hotspots with highest vessel density correlated significantly with microvessel counts in vascular hotspots with second highest vessel density (P < 0.01). Microvessel counts in tumour areas where collagen IV-positive basement membrane were absent exceeded those in areas where it was present (factor of 1.7) and those in normal mucosa (factor of 1.6). The differences in vessel density between individual tumours and the low variability in vessel density within individual tumours using this quantification technique allow us to investigate the prognostic value of vessel density in areas of intense neovascularisation in human primary colorectal carcinomas.

Adult↗

PubMed1994

Cytokine-mediated activation of cultured CNS microvessels: a system for examining antigenic modulation of CNS endothelial cells, and evidence for long-term expression of the adhesion protein E-selectin.

Much of what is known of endothelial responses to cytokines has been derived from in vitro studies using cultured human umbilical vein endothelial cells (EC). Less is known of CNS EC responses and whether intact endothelium responds similarly to cultured cells. We have used techniques by which rat CNS microvessels can be isolated, then cultured in vitro, to study the response of intact endothelium to activation with cytokines. These microvessels are composed of viable EC and perivascular cells, predominantly pericytes. Expression of EC activation antigens in multicellular systems such as cultured microvessels can be assessed quantitatively using immunofluorescence laser cytometry. Interferon gamma increased immunologically reactive major histocompatibility complex class II antigens (< 300 to 2,398 +/- 225 average fluorescence intensity), while tumor necrosis factor alpha induced an increase in vascular cell adhesion molecule-1 (2,167 +/- 171) and E-selectin (1,628 +/- 315). CNS EC appeared to respond similarly to cultured EC with the exception that E-selectin expression was not transiently expressed but was maintained by microvessel EC for 24 and 48 h. Cultured CNS microvessels provide a good system for studying EC activation.

Animals↗

PubMed2002

Tumour microvessel density as predictor of chemotherapy response in breast cancer patients.

The aim of this study was to evaluate the predictive value of intratumoural microvessel density in breast cancer. We studied immunohistochemically primary tumours of 104 patients with metastasised breast cancer who took part in a randomised multicentre trial comparing docetaxel to sequential methotrexate and 5-fluorouracil. Vessels were highlighted with factor VIII staining and counted microscopically. Microvessel density was compared with clinical response to chemotherapy and patient survival. The microvessel density of the primary tumour was not significantly associated with patient's response to chemotherapy, time to progression or overall survival in the whole patient population or in the docetaxel or methotrexate and 5-fluorouracil groups. However, disease-free survival was longer in patients with low microvessel density (P=0.01). These findings suggest that microvessel density of the primary tumour cannot be used as a predictive marker for chemotherapy response in advanced breast cancer.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2002

Flow cytometric quantification of tumour endothelial cells; an objective alternative for microvessel density assessment.

Assessment of microvessel density by immunohistochemical staining is subject to a considerable inter-observer variation, and this has led to variability in correlation between microvessel density and clinical outcome in different studies. In order to improve the method of microvessel density measurement in tumour biopsies, we have developed a rapid, objective and quantitative method using flow cytometry on frozen tissues. Frozen tissue sections of archival tumour material were enzymatically digested. The single-cell suspension was stained for CD31 and CD34 for flow cytometry. The number of endothelial cells was quantified using light scatter- and fluorescence-characteristics. Tumour endothelial cells were detectable in a single cell suspension, and the percentage of endothelial cells detected in 32 colon carcinomas correlated highly (r=0.84, P<0.001) with the immunohistochemical assessment of microvessel density. Flow cytometric endothelial cells quantification was found to be more sensitive especially at lower levels of immunohistochemical microvessel density measurement. The current method was found to be applicable for various tumour types and has the major advantage that it provides a retrospective and quantitative approach to the angiogenic potential of tumours.

Cell Count↗

PubMed2000

Sphingosine-1-phosphate and sphingosylphosphorylcholine constrict renal and mesenteric microvessels in vitro.

Sphingolipids such as sphingosine-1-phosphate (SPP) and sphingosylphosphorylcholine (SPPC) can act both intracellularly and at G-protein-coupled receptors, some of which were cloned and designated as Edg-receptors. Sphingolipid-induced vascular effects were determined in isolated rat mesenteric and intrarenal microvessels. Additionally, sphingolipid-induced elevations in intracellular Ca(2+) concentration were measured in cultured rat aortic smooth muscle cells. SPPC and SPP (0.1-100 micromol l(-1)) caused concentration-dependent contraction of mesenteric and intrarenal microvessels (e.g. SPPC in mesenteric microvessels pEC(50) 5.63+/-0.17 and E(max) 49+/-3% of noradrenaline), with other sphingolipids being less active. The vasoconstrictor effect of SPPC in mesenteric microvessels was stereospecific (pEC(50) D-erythro-SPPC 5.69+/-0.08, L-threo-SPPC 5.31+/-0.06) and inhibited by pretreatment with pertussis toxin (E(max) from 44+/-5 to 19+/-4%), by chelation of extracellular Ca(2+) with EGTA and by nitrendipine (E(max) from 40+/-6 to 6+/-1 and 29+/-6%, respectively). Mechanical endothelial denudation or NO synthase inhibition did not alter the SPPC effects, while indomethacin reduced them (E(max) from 87+/-3 to 70+/-4%). SPP and SPPC caused transient increases in intracellular Ca(2+) concentrations in rat aortic smooth muscle cells in a pertussis toxin-sensitive manner. Our data demonstrate that SPP and SPPC cause vasoconstriction of isolated rat microvessels and increase intracellular Ca(2+) concentrations in cultured rat aortic smooth muscle cells. These effects appear to occur via receptors coupled to pertussis toxin-sensitive G-proteins. This is the first demonstration of effects of SPP and SPPC on vascular tone and suggests that sphingolipids may be an hitherto unrecognized class of endogenous regulators of vascular tone.

Animals↗

PubMed2002

Mechanisms of heterogeneous endothelial cytoplasmic calcium increases in venular microvessels.

OBJECTIVE: Localized inflammatory leaky sites form at regions of the microvessel wall with the largest increase in endothelial cell cytoplasmic calcium concentration, [Ca(2+)](i). We investigated the mechanisms that modulate localized increases in [Ca(2+)](i) in individual endothelial cells of microvessels after exposure to ATP. METHODS: [Ca(2+)](i) was measured by using digital fluorescence microscopy and fura-2 in the endothelial cells forming the walls of individually perfused frog mesenteric microvessels. The spread of [Ca(2+)](i) from a localized mechanical stimulus was also measured. RESULTS: The peak [Ca(2+)](i) after ATP showed marked heterogeneity, ranging from 227 to 1469 nM from resting values of 69 +/- 5 nM. After depolarization with high-potassium solutions, the endothelial cells with the largest peak increase in [Ca(2+)](i) had the largest fractional reduction. Localized increases in [Ca(2+)](i) due to mechanical stimulus did not spread. CONCLUSION: The key mechanism regulating the heterogeneity in initial peak increase in [Ca(2+)](i) is a calcium-dependent process regulated by the calcium influx itself. One such mechanism, the calcium-dependent opening of additional potassium channels leading to membrane hyperpolarization and increased driving force for calcium entry through passive conductance pathways, accounts for a significant amount of the heterogeneity of [Ca(2+)](i) in our experiments. Further investigations of both localized calcium influx and membrane potentials in the endothelial cells of intact microvessels in both frog and mammals using the imaging methods developed for these investigations are needed to understand the formation of localized leaky sites in inflamed microvessels.

Adenosine Triphosphate↗

PubMed2002

Microvessel density in prostate carcinoma.

The objective of this work was to assess the correlation between microvessel density (MVD), pathological stage and disease recurrence in a series of patients who underwent radical prostatectomy for prostate cancer. Pathological material from 75 consecutive radical prostatectomies performed before 1994 without neo-adjuvant treatment, in which sufficient follow-up data were available, was re-examined. Paraffin embedded material was re-cut and hematoxylin and eosin (H&E) stained. Areas of maximal angiogenesis within tumor were identified. Expression of CD34 was investigated by using the monoclonal antibody MY 10. Within the areas of maximal angiogenesis, microvessels expressing CD34 were counted and specimens were divided into two groups, one showing a count of less than 90 microvessels per microscopic field at 200 x magnification (MVD<90), the second more than 90 microvessels (MVD>90). The MVD was then related to pathological stage, Gleason score (GS) and outcome of the disease. Mean follow-up was 84 months. Clinical or biochemical progression was observed in 38.6% of patients. In low GS cases, MVD was always <90, whereas in GS 5-6, half had MVD <90 and half were >90. In high GS MVD was always >90. MVD was positively associated with a higher pathological stage. Progression of the disease was observed in 20% of MVD <90 and in 51% in MVD >90 (P=0.006). Mantel-Haensz test showed a correlation between MVD and time to progression (P<0.05). Although problems exist in methods of counting and in the cut-off number of vessels, which can discriminate the risk categories, it may be concluded that microvessel counts, using CD34 monoclonal antibody, can accurately predict the outcome of radical prostatectomy.

Antibodies, Monoclonal↗

PubMed2000

Hot spot microvessel density and the mitotic activity index are strong additional prognostic indicators in invasive breast cancer.

AIMS: Recent studies have drawn attention to intratumoral microvessel density (MVD) as a prognostic factor in invasive breast cancer. Various methods have been applied to assess MVD and the prognostic value of MVD in different studies varies considerably. Counting of microvessels in the most highly vascularized area (hot spot) of a tumour is the method most widely used. In this study we compared three counting methods. METHODS AND RESULTS: To assess MVD in 112 cases of invasive breast cancer with long-term follow-up we performed microvessel counting in the hot spot of the tumour in four and 10 fields of vision (HS-MVD4 and HS-MVD10) and microvessel counting in 10 fields of vision distributed systematically over the whole tumour area (global MVD). The HS-MVD4, HS-MVD10 and global MVD showed good correlations with each other. HS-MVD4 provided the highest number of microvessels (median value 71) followed by HS-MVD10 and global MVD, with median values of 58 and 39, respectively. HS-MVD4 showed the best prognostic value for overall survival (P = 0.0001) whereas HS-MVD10 showed less (P = 0.01) and the global MVD showed no (P = 0.75) prognostic value. In univariate analysis, the HS-MVD4 was the second strongest prognostic factor after tumour size. In multivariate survival analysis, the HS-MVD4, mitotic activity index (MAI), lymph node status and tumour size were found to be independent prognostic factors. When combining MVD4 and MAI in lymph node negative patients, none of the patients with low MVD (< 71/mm2) and a low MAI (< 10 per 10 HPF) died, in contrast to patients with a high MVD or high MAI who have a 10-year survival of 57%. CONCLUSIONS: These data suggest that the hot spot MVD in four fields of vision is a major independent prognostic factor for overall survival in invasive breast cancer. For the first time, it is shown that hot spot MVD provides additional prognostic information to well established factors like lymph node status and the MAI, and may therefore be useful for designing treatment strategies in invasive breast cancer.

Breast Neoplasms↗

PubMed1997

Expression of thymidine phosphorylase in uterine sarcoma and uterine leiomyoma: association with microvessel density and Doppler blood flow analysis.

The aim of this study was to determine whether the expression of thymidine phosphorylase (TP) by uterine sarcoma and leiomyoma cells is associated with the density of microvessels within the tumor, and with Doppler ultrasound-derived peak systolic velocity (PSV) of blood flow. Sections of tissue from four uterine sarcomas and 41 uterine leiomyomas which had been used in a previous study to determine intratumoral peak systolic velocity were analyzed for the cellular expression of TP and the intratumoral density of microvessels by immunohistochemistry, using monoclonal antibody to TP and factor VIII-related antigen, respectively. The main outcome measures were whether or not the tumor cells were TP-positive or TP-negative, and the microvessel count within each tumor type. Uterine sarcomata were classified as TP-positive and uterine leiomyomata as TP-negative. The microvessel count in uterine sarcomas was significantly higher than that in uterine leiomyomas (p = 0.002, Mann-Whitney U test). We concluded that the expression of TP by uterine sarcoma cells is associated with an increase in microvessel density and with a higher peak systolic velocity.

Antibodies, Monoclonal↗

PubMed1998

Multidrug resistance-related transport proteins in isolated human brain microvessels and in cells cultured from these isolates.

The multidrug transporter, P-glycoprotein (Pgp), at the blood-brain barrier is thought to be important for limiting access of toxic agents to the brain, but controversy surrounds its cellular location, whether on endothelium or on adjacent astrocyte foot processes. In the present study, the distribution of protein and mRNA for Pgp and for another transporter, multidrug resistance-associated protein (MRP), is compared with that for the endothelial marker, platelet-endothelial cell adhesion molecule-1 (PECAM-1) and for the astrocyte-derived glial fibrillary acidic protein (GFAP) in microvessels isolated from human brain and in cells grown from these microvessels. Activities of the multidrug transporters are assessed in the cultured cells from the effects of transport inhibitors on intracellular [3H]vincristine accumulation. The isolated microvessels show strong immunocytochemical staining for Pgp and PECAM-1 and little or no staining for GFAP and MRP, and they contain mRNAs detectable by RT-PCR encoding only Pgp and PECAM-1, but not GFAP or MRP. Thus, Pgp may well be synthesised and expressed on cells within the microvessels rather than on adherent astrocyte foot processes. In cells grown from the microvessels, although PECAM-1 remains, Pgp expression decreases and MRP appears. Evidence suggests these multidrug transporters are functionally active in the cultured cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMedDate not supplied

The inverse relationship between microvessel counts and tumor volume in breast cancer.

Angiogenesis has emerged as an indicator of metastatic potential in invasive breast cancer. Exponential tumor growth and the appearance of metastasis are observed as new microvessels form. We postulated that the relevance of angiogenesis would be enhanced if analyzed as a function of tumor volume rather than greatest diameter alone and that microvessel counts would proportionately increase as does volume. Since tumors are three-dimensional solids, volume was calculated using the formula for an ellipsoid, V = pi/6 (a x b x c). Sixty-four tumors < or = 2.5 cm were studied and analyzed in 5 mm incremental ranges. Mean microvessel counts did not vary significantly among these tumor size groups. However, analysis of microvessel counts as a function of tumor volume decreased from 947.1/cm3 (0-0.5 cm) to 18.1/cm3 (2.1-2.5 cm), a greater than 50-fold difference. High microvessel density in small cancers supports the notion of metastasis as an early event, making these small tumors perhaps ideal targets for antiangiogenic agents.

Breast Neoplasms↗

PubMed2000

In vivo formation of complex microvessels lined by human endothelial cells in an immunodeficient mouse.

We have identified conditions for forming cultured human umbilical vein endothelial cells (HUVEC) into tubes within a three-dimensional gel that on implantation into immunoincompetent mice undergo remodeling into complex microvessels lined by human endothelium. HUVEC suspended in mixed collagen/fibronectin gels organize into cords with early lumena by 24 h and then apoptose. Twenty-hour constructs, s.c. implanted in immunodeficient mice, display HUVEC-lined thin-walled microvessels within the gel 31 days after implantation. Retroviral-mediated overexpression of a caspase-resistant Bcl-2 protein delays HUVEC apoptosis in vitro for over 7 days. Bcl-2-transduced HUVEC produce an increased density of HUVEC-lined perfused microvessels in vivo compared with untransduced or control-transduced HUVEC. Remarkably, Bcl-2- but not control-transduced HUVEC recruit an ingrowth of perivascular smooth-muscle alpha-actin-expressing mouse cells at 31 days, which organize by 60 days into HUVEC-lined multilayered structures resembling true microvessels. This system provides an in vivo model for dissecting mechanisms of microvascular remodeling by using genetically modified endothelium. Incorporation of such human endothelial-lined microvessels into engineered synthetic skin may improve graft viability, especially in recipients with impaired angiogenesis.

Animals↗

PubMed2006

The correlation of angiogenesis with metastasis in primary cutaneous melanoma: a comparative analysis of microvessel density, expression of vascular endothelial growth factor and basic fibroblastic growth factor.

AIM: To establish whether there is a correlation between angiogenesis and metastasis in primary cutaneous melanoma (PCMM). METHODS: We studied the microvessel density and the expression of vascular endothelial growth factor (VEGF) and basic fibroblastic growth factor (bFGF) in 22 cases of PCMM with metastasis at presentation (metastatic group) and 28 cases of PCMM without metastasis for 24 months or more (non-metastatic group). Microvessels were stained with CD31/PECAM-1 antibody and counted. We assessed the proportion of VEGF expression in tumour cells, lymphocytes infiltrating the tumour (TIL) and lymphocytes at the periphery of the tumour, as well as the proportion of bFGF expression in tumour cell cytoplasms, nuclei and intra- and peritumoral vessels. RESULTS: An increased microvessel density was detected in the metastatic group (15-33 [24.09 +/- 5.55] versus 2-24 [12.96 +/- 6.02]). Moreover, enhanced expression of VEGF in tumour cells and peritumoral lymphocytes (Chi-square p = 0.038 and p = 0.018) and bFGF in peritumoral vessels (chi(2) p = 0.013) correlated with the simultaneous presence of melanoma metastasis in PCMM. Furthermore, microvessel density was correlated with the expression of bFGF in peritumoral vessels (rs = 0.53, p = 0.049) and VEGF in tumour cells (rs = 0.37, p = 0.019). CONCLUSION: Microvessel density as well as the expression of both VEGF and bFGF might be informative concerning the progression of melanoma.

Adult↗

PubMed2004

Microvessels promote motor nerve survival and regeneration through local VEGF release following ectopic reattachment.

OBJECTIVES: Nerves and blood vessels form a close association during embryogenesis. Growth and guidance factors initially attributed to either nerves or vessels are now known to affect both tissues; prominent among these is vascular endothelial growth factor (VEGF). The authors investigated whether axons would associate with blood vessels in a regenerating system and questioned whether VEGF is integral to neurotization following axotomy. METHODS: In hamsters 8-12 weeks of age, the accessory nerve (CN XI) to the retractor muscle of the cheek pouch was cut and the proximal stump was reattached ectopically onto the muscle. Vascular casting and immunolabeling were used to quantify the extent of neurovascular association during regeneration. A role for VEGF was investigated using immunolocalization of VEGF and its receptor (sVEGFR2) as well as local sequestration of VEGF with soluble receptor (sVEGFR1). RESULTS: Regenerating axons aligned with microvessels of the vasa nervorum along a "chaperone" region during outgrowth from the reattachment site and while entering the muscle. In this approximately 1-mm region, VEGF protein was expressed by growing microvessels despite a approximately 50% reduction (p < .05) in total muscle VEGF concentration. VEGFR2 was expressed by regenerating axons and growth cones. Sequestration of VEGF by sVEGFR1 impaired neurotization by approximately 40% (p < .05). The chaperone region ended where regenerating microvessels anastomosed with the native microcirculation and their expression of VEGF protein diminished. CONCLUSIONS: Regenerating axons and blood vessels align during outgrowth from ectopic reattachment. This interaction dissipates as vascular anastomoses form with established microvessels and axons target muscle fibers. Local production of VEGF by growing microvessels supports motor nerve survival and regeneration.

Animals↗

PubMed1997

Correlation of vascular endothelial growth factor expression and microvessel density in cervical intraepithelial neoplasia.

BACKGROUND: Angiogenesis (the formation of new blood vessels) appears to be required for the growth of invasive tumors, but little information exists about its role in the development of preinvasive lesions. We examined microvessel density and expression of vascular endothelial growth factor in specimens of cervical intraepithelial neoplasia (CIN), a preinvasive lesion of the uterine cervix, to determine whether a connection could be established between these parameters of angiogenesis and the grade of dysplasia (i.e., tissue abnormality). METHODS: Sections of biopsy specimens from 83 patients with grades I-III CIN were examined retrospectively. Microvessels were localized by use of a polyclonal antibody directed against factor VIII-related antigen; vascular endothelial growth factor was detected by means of a monoclonal antibody. Reported P values are two-sided. RESULTS: Highest microvessel densities and highest expression of vascular endothelial growth factor were found in a narrow border region between CIN lesions and the underlying stroma. A significant correlation was observed between high vascular endothelial growth factor expression and high microvessel density (Kendall's tau = 0.27; 95% confidence interval [CI] = 0.03-0.50; P = .018). Mean microvessel density values +/- standard deviations for CIN I, CIN II, and CIN III lesions were 19.4 +/- 5.8, 21.9 +/- 7.0, and 34.1 +/- 14.8, respectively (Kendall's tau = 0.46; 95% CI = 0.30-0.61; P<.0001). Corresponding values for vascular endothelial growth factor expression were 8.3 +/- 3.5, 8.4 +/- 2.0, and 12.2 +/- 3.6, respectively (Kendall's tau = 0.41; 95% CI = 0.20-0.60; P<.0001). CONCLUSIONS: Our results are consistent with the idea that progression of cervical dysplasia is dependent on angiogenesis.

Endothelial Growth Factors↗

PubMed2006

Microarray analysis of blood microvessels from PDGF-B and PDGF-Rbeta mutant mice identifies novel markers for brain pericytes.

Normal blood microvessels are lined by pericytes, which contribute to microvessel development and stability through mechanisms that are poorly understood. Pericyte deficiency has been implicated in the pathogenesis of microvascular abnormalities associated with diabetes and tumors. However, the unambiguous identification of pericytes is still a problem because of cellular heterogeneity and few available molecular markers. Here we describe an approach to identify pericyte markers based on transcription profiling of pericyte-deficient brain microvessels isolated from platelet-derived growth factor (PDGF-B)-/- and PDGF beta receptor (PDGFRbeta)-/- mouse mutants. The approach was validated by the identification of known pericyte markers among the most down-regulated genes in PDGF-B-/- and PDGFRbeta-/- microvessels. Of candidates for novel pericyte markers, we selected ATP-sensitive potassium-channel Kir6.1 (also known as Kcnj8) and sulfonylurea receptor 2, (SUR2, also known as Abcc9), both part of the same channel complex, as well as delta homologue 1 (DLK1) for in situ hybridization, which demonstrated their specific expression in brain pericytes of mouse embryos. We also show that Kir6.1 is highly expressed in pericytes in brain but undetectable in pericytes in skin and heart. The three new brain pericyte markers are signaling molecules implicated in ion transport and intercellular signaling, potentially opening new windows on pericyte function in brain microvessels.

ATP-Binding Cassette Transporters↗

PubMed1997

Region-specific and agent-specific dilation of intracerebral microvessels by volatile anesthetics in rat brain slices.

BACKGROUND: Volatile anesthetics are potent cerebral vasodilators. Although the predominant site of cerebrovascular resistance is attributed to intracerebral arterioles, no studies have compared the actions of volatile anesthetics on intraparenchymal microvessels. The authors compared the effects of halothane and isoflurane on intracerebral arteriolar responsiveness in hippocampal and neocortical microvessels using a brain slice preparation. METHOD: After Institutional Review Board approval, hippocampal or neocortical brain slices were prepared from anesthetized Sprague-Dawley rats and placed in a perfusion-recording chamber, superfused with artificial cerebrospinal fluid. Arteriolar diameters were monitored with videomicroscopy before, during, and after halothane or isoflurane were equilibrated in the perfusate. PGF2alpha preconstricted vessels before anesthetic administration. A blinded observer using a computerized videomicrometer analyzed diameter changes. RESULTS: Baseline microvessel diameter and the degree of preconstriction were not different between groups. In the hippocampus, the volatile agents produced similar, concentration-dependent dilation (expressed as percent of preconstricted control +/- SEM) of 68 +/- 6% and 79 +/- 9% (1 MAC) and 120 +/- 3% and 109 +/- 5% (2 MAC) (P < 0.05) during halothane and isoflurane, respectively. In the cerebral cortex, isoflurane caused significantly less vasodilation than did similar MAC levels of halothane (84 +/- 9% vs. 42 +/- 5% dilation at 1 MAC; 121 +/- 4% vs. 83 +/- 5% dilation at 2 MAC halothane vs. isoflurane, respectively). CONCLUSION: Halothane and isoflurane differentially produce dose-dependent dilation of intraparenchymal cerebral microvessels. These findings suggest that local effects of the volatile anesthetics on intracerebral microvessel diameter contribute significantly to alterations in cerebrovascular resistance and support previously described heterogeneous actions on cerebral blood flow produced by these agents.

Anesthetics, Inhalation↗