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PubMed2003

Microcirculation in insulin resistance and diabetes: more than just a complication.

The microvascular bed is an anatomical entity which is governed by specific, highly regulated mechanisms which are closely adapted to the specific function of each vascular segment. Among those, small arteriolar vasomotion and capacity of small vessels to constrict in response to physical and humoral stimuli play a major role. Other processes of importance for the adequacy of nutritive perfusion are haemorheological properties of whole blood and red cells, adhesiveness of leukocytes and capillary permeability. This review provides some description of these phenomena, how they impact on organ function and how they appear in diabetes. Metformin, as a unique example among the drug arsenal, exerts various effects preferentially at the level of smallest vessels (arterioles, capillaries, venules). This review summarises our actual knowledge and includes several new data showing its high potential for reducing microvascular dysfunction. Most of these unique properties have also been demonstrated in non-diabetic animals or humans, suggesting they are intrinsic to the drug and not secondary to diabetic metabolic improvement. A particular focus is put on the relevance of metformin's capacity to stimulate slow wave arteriolar vasomotion and improve functional capillary density, whereby nutritive flow can be re-established. Finally, the implication of microcirculation in other aspects of insulin resistance and diabetes, such as macroangiopathy and metabolic control, is discussed and strengthens the concept of a broad involvement of microvascular dysfunction in these diseases as well as the potential interest of introducing adapted treatment early in the history of a patient's diabetes.

Arterioles↗
PubMed1981

[Scanning electron microscopic study on corrosion casts for rabbit ovarian follicle microvasculature during the ovulatory and luteinizing process (author's transl)].

The microvasculature of rabbit ovarian follicles were investigated three-dimensionally with resin casting/SEM technique during ovulation and corpus luteum formation. The basic vascular pattern around Graafian follicles remains essentially unchanged, except for expansion of the blood vessels to keep pace with follicle growth, until ovulation occurs. The resin leaked out from the inner capillary wreath and could not get into the apical vessels just prior to ovulation. These findings indicate the increased capillary permeability and congestion of blood stream at the apical region shortly before ovulation. At 3-5 hours after ovulation, the unusually dilated vessels were developed into the follicular cavity, and then the fine vessels in radiating arrangement sprouted from the theca capillary wreath in one or two days. There seems to be regulatory roles of vascular systems in ovulatory and luteinizing process.

Animals↗
PubMed1992

The effect of prednisolone on substance P-induced vascular permeability in mice.

The effect of prednisolone on the substance P (SP)-induced vascular permeability increase in male ddY, WBB6 F1(-)+/+ (control) and WBB6 F1-W/WV (no mast cell in skin or internal organs) mice was investigated. 1) SP (1-10,000 pg/site) increased vascular permeability in ddY, WBB6 F1(-)+/+ and WBB6 F1-W/WV mice ears. 2) SP (100 pg/site)-induced vascular permeability was inhibited by prednisolone (10 mg/kg) administered intraperitoneally 3 to 12 hours prior to the elicitation of the reaction in ddY mice. When dexamethasone at a dose of 1 mg/kg was administered intraperitoneally 2 to 24 hours prior to the elicitation of the reaction, significant inhibition was observed. When prednisolone was administered intraperitoneally 8 hours prior to the elicitation of the reaction, the SP-induced capillary permeability increase in both ddY and WBB6 F1-W/WV mice was clearly inhibited by the drug at doses of 5 and 10 mg/kg. 3) Diphenhydramine (1 and 10 mg/kg) inhibited SP-induced vascular reaction in ddY mice but not in WBB6 F1-W/WV mice. 4) Atropine (10 mg/kg) inhibited SP-induced vascular reaction in both ddY and WBB6 F1-W/WV mice. But acetylcholine did not cause an increase of vascular permeability in ddY and WBB6 F1-W/WV mice ears. 5) Prednisolone (5 mg/kg) inhibited histamine- and serotonin-induced vascular permeability in ddY and WBB6 F1-W/WV mice ears. 6) Prednisolone (5 and 10 mg/kg) inhibited the SP-induced histamine release from ddY mice peritoneal mast cells. These results suggest that the vascular effect of SP is mediated by both mast cell dependent (release of histamine from mast cells) and mast cell independent mechanisms. Prednisolone inhibits the SP-induced vascular permeability mediated by both mechanisms in mice.

Animals↗
PubMed2003

A new bioactive steroidal saponin from Sansevieria cylindrica.

A new steroidal saponin was isolated from the leaves of Sansevieria cylindrica. Its structure was established as (3beta,12beta,15alpha,25S)-26-(beta-D-glucopyranosyloxy)-22-hydroxyfurost-5-en-3-yl 12-O- (6-deoxy-alpha-L-mannopyranosyl)-15-O-(6-deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranoside. The structural identification was performed using detailed analyses of (1)H and (13)C NMR spectra including 2D NMR spectroscopic techniques (COSY, HETCOR, HMBC and HMQC) and chemical conversions. The steroidal saponin showed no haemolytic effects in the in vitro assays and demonstrated inhibition of the capillary permeability activity.

Acetic Acid↗
PubMed1976

Aspiration pneumonia: experimental evaluation of albumin and steroid therapy.

An experimental model using an ex vivo perfused ventilated canine pulmonary lobe was used to study aspiration pneumonia. After intrabronchial acid instillation, the lobe weight tripled, air way pressure and pulmonary artery pressure doubled, and intrapulmonary shunting increased from 5.5% to 53.4%. If large quantities of albumin were added to the lobe perfusate 5 minutes after intrabronchial acid instillation, weight gain, air way and pulmonary artery pressure, and intrapulmonary shunting were unchanged from control levels. If large quantities of steroid were added to the lobe perfusate 5 minutes after intrabronchial acid instillation, the lobe weight doubled but air way pressure and pulmonary artery pressure, and intrapulmonary shunting were not significantly different from control values. It is surmised that intrapulmonary acid aspiration causes an immediate and marked changed in pulmonary capillary permeability. Albumin administration by counteracting this permeability change, and steroid administration by modifying the permeability change, are both beneficial following acid aspiration.

Albumins↗
PubMed1987

Treatment of porcine Pseudomonas ARDS with combination drug therapy.

A combination drug therapy (Poly-5: ibuprofen 12.5 mg/kg, methylprednisolone 30 mg/kg, cimetidine 150 mg, diphenhydramine 10 mg/kg, and ketanserin 0.2 mg/kg) given at 20 and 120 minutes after starting continuous intravenous Pseudomonas (Ps, 5 X 10(8) CFU/20 kg/min) was studied in three groups of swine: saline control (C, n = 9), Ps alone (Ps, n = 8), and Ps plus Poly-5 (n = 5). PaO2, systemic (SAP) and pulmonary arterial (PAP) pressures, cardiac index (CI), thermal-cardiogreen extravascular lung water (EVLW), pulmonary albumin flux (slope index, SI), and arterial blood serotonin levels (5-HT) were measured. Ps produced significant (p less than 0.05) increases in PAP, EVLW, and SI with decreases in PaO2, CI, and SAP. 5-HT fell significantly compared to baseline. Poly-5 prevented (p less than 0.05) the rise in EVLW and SI and the fall in PaO2 and CI compared to Ps. PAP and SI were maintained at C until 90 and 150 minutes, respectively. SAP fell significantly from C at 30, 60, and 180 minutes. 5-HT was significantly lower than Ps throughout, and significantly lower than baseline at 180 minutes. Combined blockade of arachidonic acid metabolites, histamine, and serotonin receptors prevented hypoxemia, increased pulmonary capillary permeability, and cardiovascular deterioration in this porcine septic ARDS model.

Animals↗
PubMed2001

Keratinocyte growth factor attenuates hydrostatic pulmonary edema in an isolated, perfused rat lung model.

Hydrostatic pulmonary edema is a common complication of congestive heart failure, resulting in substantial morbidity and mortality. Keratinocyte growth factor (KGF) is a mitogen for type II alveolar epithelial and microvascular cells. We utilized the isolated perfused rat lung model to produce hydrostatic pulmonary edema by varying the left atrial and pulmonary capillary pressure. Pretreatment with KGF attenuated hydrostatic edema formation. This was demonstrated by lower wet-to-dry lung weight ratios, histological evidence of less alveolar edema formation, and reduced alveolar accumulation of intravascularly administered FITC-labeled large-molecular-weight dextran in rats pretreated with KGF. Thus KGF attenuates injury in this ex vivo model of hydrostatic pulmonary edema via mechanisms that prevent increases in alveolar-capillary permeability.

Animals↗
PubMed2000

Lung overexpression of the vascular endothelial growth factor gene induces pulmonary edema.

We hypothesized that the angiogenic mediator, vascular endothelial growth factor (VEGF), known to be expressed in the lung and to be capable of inducing local edema in skin, might evoke the development of lung edema if expressed in excess amounts. To test this hypothesis, we developed an in vivo model of VEGF overexpression in the lung on the basis of delivery to the respiratory epithelium of the VEGF165 complementary DNA by an E1(-) adenovirus vector (AdVEGF165). Administration of AdVEGF165 by the intratracheal route (10(9) plaque-forming units [pfu]) to C57Bl/6 mice showed increased expression of VEGF messenger RNA in lung tissue by Northern analysis. Overexpression of VEGF protein in the lung at Days 1 to 10 was confirmed by enzyme-linked immunosorbent assay. Intratracheal administration of AdVEGF165 resulted in a dose-dependent increase in lung wet/dry weight ratios over time, lung histology showed widespread intra- alveolar edema, and pulmonary capillary permeability was significantly increased as quantified by the Evans blue dye assay and [(131)I]albumin permeability. To confirm the specificity of these observations, mice were pretreated with intranasal administration of an adenovirus vector expressing a truncated soluble form of the VEGF receptor flt-1 (Adsflt). Adsflt (10(9) pfu) pretreatment completely abrogated the increased lung wet/dry weight ratio caused by AdVEGF165 administration, whereas an identical adenovirus vector with an irrelevant transgene had no effect upon subsequent AdVEGF165-induced pulmonary edema. Together, these data suggest that overexpression of VEGF in the lung may be one mechanism of increased pulmonary vascular permeability in the early stages of acute lung injury.

Administration, Inhalation↗
PubMed1989

[Ozone-induced airway hyperresponsiveness in guinea pigs].

We studied the time related changes of airway hyperresponsiveness induced by ozone inhalation (2.9 ppm, 30 min) in guinea pigs. In unanesthetized and spontaneously breathing guinea pigs, the respiratory resistance was measured by a forced oscillation technique. The respiratory resistance and respiratory frequency were unchanged until 24 hours after ozone inhalation. In mechanically ventilated guinea pigs, airway responsiveness to inhaled methacholine was determined using a modification of the Konzett-Rössler technique, and after methacholine challenge bronchoalveolar lavage (BAL) was performed for cell yield. At 1 hour and 3 hours after ozone inhalation, airway responsiveness was increased significantly, but returned to the control level at 6 hours. In the BAL fluid, there was a significant increase in neutrophils at 3 hours after ozone inhalation and thereafter. In the separated groups, before air or ozone inhalation, human serum albumin (HSA) was administered intravenously, and BAL was performed 1 hour after inhalation. In the ozone inhalation group, the concentration of HSA in BALF was increased significantly compared to the air inhalation group. These results suggest that airway hyperresponsiveness induced by ozone inhalation may occur before the influx of neutrophils into the airways and may depend on some structural changes such as submucosal and mucosal edema induced by the enhancement of capillary permeability.

Air Pollutants↗
PubMed1979

Protection by plasma proteins of the isolated lamb heart perfused with stroma-free hemoglobin at 38 degrees.

Isolated lamb hearts were perfused for eight hours at 38 degrees with stroma-free hemoglobin solution (SFHS). The preservation of cardiac structure and function was studied. Control hearts perfused with blood (N = 6) developed no ventricular failure or significant weight gain (13% +/- 5), showed no alteration of cellular ultrastructure, and little interstitial edema. Hearts perfused with 7% (N = 7) or 11% (N = 5) SFHS contracted less well, became edematous (22% and 44% weight gain) and showed altered mitochondria, capillary endothelial swelling and hemoglobin extravasation into the interstitial space. The addition of 5-7% albumin to SFHS (N = 9) markedly reduced interstitial edema (weight gain 11% +/- 13), preserved mitochondria, prevented endothelial swelling, and limited transcapillary escape of hemoglobin. Thus isolated hearts perfused with SFHS develop vascular endothelial damage and an increase in capillary permeability. The addition of plasma proteins to the perfusate protects against this injury.

Animals↗
PubMed1998

Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects.

Mast cells are involved in atopic disorders, often exacerbated by stress, and are located perivascularly close to sympathetic and sensory nerve endings. Mast cells are activated by electrical nerve stimulation and millimolar concentrations of neuropeptides, such as substance P (SP). Moreover, acute psychological stress induces CRH-dependent mast cell degranulation. Intradermal administration of rat/human CRH (0.1-10 microM) in the rat induced mast cell degranulation and increased capillary permeability in a dose-dependent fashion. The effect of CRH on Evans blue extravasation was stronger than equimolar concentrations of the mast cell secretagogue compound 48/80 or SP. The free acid analog of CRH, which does not interact with its receptors (CRHR), had no biological activity. Moreover, systemic administration of antalarmin, a nonpeptide CRHR1 antagonist, prevented vascular permeability only by CRH and not by compound 48/80 or SP. CRHR1 was also identified in cultured leukemic human mast cells using RT-PCR. The stimulatory effect of CRH, like that of compound 48/80 on skin vasodilation, could not be elicited in the mast cell deficient W/Wv mice but was present in their +/+ controls, as well as in C57BL/6J mice; histamine could still induce vasodilation in the W/Wv mice. Treatment of rats neonatally with capsaicin had no effect on either Evans blue extravasation or mast cell degranulation, indicating that the effect of exogenous CRH in the skin was not secondary to or dependent on the release of neuropeptides from sensory nerve endings. The effect of CRH on Evans blue extravasation and mast cell degranulation was inhibited by the mast cell stabilizer disodium cromoglycate (cromolyn), but not by the antisecretory molecule somatostatin. To investigate which vasodilatory molecules might be involved in the increase in vascular permeability, the CRH injection site was pretreated with the H1-receptor antagonist diphenhydramine, which largely inhibited the CRH effect, suggesting that histamine was involved in the CRH-induced vasodilation. The possibility that nitric oxide might also be involved was tested using pretreatment with a nitric oxide synthase inhibitor that, however, increased the effect of CRH. These findings indicate that CRH activates skin mast cells at least via a CRHR1-dependent mechanism leading to vasodilation and increased vascular permeability. The present results have implications for the pathophysiology and possible therapy of skin disorders, such as atopic dermatitis, eczema, psoriasis, and urticaria, which are exacerbated or precipitated by stress.

Animals↗
PubMed2000

Urinary albumin excretion and transcapillary escape rate of albumin in malignancies.

Transcapillary escape rate of albumin was determined in 22 patients with different malignancies. In addition, urinary albumin excretion rate was measured in 24-h urine samples using a sensitive immunoassay. Increased urinary albumin excretion was defined as >/=20 microg/min according to conventional standards. Renal glomerular filtration and tubular function was estimated by 51Cr-EDTA plasma clearance and urinary beta 2-microglobulin, respectively. Median urinary albumin excretion rate was 15.0 microg/min (range 6-510 microg/min) and the frequency of increased urinary albumin excretion was 41%. This agrees with other studies showing increased albuminuria in several types of malignant diseases. Patients with advanced disease (tumour, node, metastasis (TNM) stage II-IV) had a significantly higher urinary albumin excretion rate than patients with localized disease (TNM stage I). Serum creatinine, glomerular filtration rate and urinary beta 2-microglobulin were all within normal limits. Median transcapillary escape rate of albumin was 5.5 %/h (range 2-8 %/h) and this level is comparable with values in healthy subjects. There was no significant difference in transcapillary escape rate between patients with elevated urinary albumin excretion and the normoalbuminuric group. Median value of the absolut outflux of albumin was 10.6 g/h with similar levels in patients with increased urinary albumin excretion and patients with normoalbuminuria. Our results indicate a high prevalence of minor glomerular dysfunction with a slightly elevated urinary albumin excretion in patients with malignancies. The normal endothelial function, as estimated by the transcapillary escape rate of albumin, suggests an overall unaffected capillary permeability and increased urinary albumin loss appears to be an isolated renal phenomenon in cancer patients.

Adult↗
PubMed1981

[Mechanisms of acute pulmonary edema during meningococcal shock in children (author;s transl)].

Meningococcic shocks may induce fatal acute pulmonary edemas. Ten children, who died in this condition, have been compared to 19 others, who during the treatment of the shock, developed right heart failure, without acute pulmonary edema (8 deaths, 11 survivals). The three groups of children could not be differentiated regarding their clinical status on admission, during the shock phase, or the treatments administered. Composition, volume and speed of administration of fluids were similar in the three groups. An increase in pulmonary capillary permeability could have occurred, and lead to the development of acute pulmonary failure, as presented by the children of the first group.

Acute Disease↗
PubMed1984

Aphakic cystoid macular edema. The pharmacology of ocular trauma.

Ocular tissues, like those of other organs, exhibit limited morphologic reactions to trauma, i.e., hyperemia, abrupt vasodilation, increased blood flow; increased permeability of blood vessels, edema and increased tissue pressure (disrupted blood-ocular barrier); and later, a cellular inflammatory response. The cystoid macular edema (CME) that occurs after surgery for cataract has a considerably higher incidence in more severely traumatized eyes. It is characterized by increased perifoveal capillary permeability that may be related either to prior vasoconstriction or to vasodilation, and it may be accompanied by a cellular inflammatory response either in the (uvea) ciliary body, vitreous, or retina, or in combination thereof. Virtually all the physiologic, metabolic, and morphologic responses to trauma can be assigned to liberation of endogenous mediators. The lesions that occur after ocular trauma may be related to the synthesis and release of prostaglandins. There is moderate support for this hypothesis, but other or additional endogenous mediators must also be considered as contributing to the production of retinal edema as a nociceptive response to trauma. The various factors that may contribute to development of CME, and their mechanisms of action, are discussed. The speculations and hypotheses contained in this review need to be confirmed or denied by applications to the eye of techniques that have been used successfully in other organ systems. Adequate prophylaxis may be provided by cyclooxygenase inhibitors, but it is more likely accomplished with corticosteroids. However, definitive clinical tests have not been done, and it should be noted that excellent surgery with minimal disruption of the blood-ocular barrier is the best prophylaxis for this iatrogenic disease. When the lesion is established and does not respond to large doses of corticosteroids, a careful study is needed to decide whether vitreous inflammation and/or strand formation accounts for the irreversibility.

Animals↗
PubMed1984

The three-dimensional organization of tight junctions in a capillary endothelium revealed by serial-section electron microscopy.

Estimates of capillary permeability for hydrophilic solutes are generally interpreted in terms of Pappenheimer's pore theory. The intercellular clefts of the capillary endothelium are considered a likely structural equivalent to the postulated system of small hydrophilic pores. However, correlation of permeabilities and cleft structure requires more knowledge of the detailed structure of the tight junctions which appear to obliterate the clefts. In this study the organization of tight junctions in endothelium of rat heart capillaries has been investigated by serial-section electron microscopy. Cross-sectioned intercellular clefts were photographed in a series of 190 consecutive sections (average thickness approximately equal to 40 nm) and in a series of 16 consecutive sections (average thickness approximately equal to 12.5 nm). Seventy-one junctional segments, each extending over 5-32 consecutive sections, were reconstructed. The endothelial junctions were organized as irregular networks of lines of contact between neighboring cells. Six pathways circumventing the lines of contact were followed through the entire junctional region of the clefts providing a tortuous pathway connecting the luminal and abluminal aspects of the clefts. Moreover, the individual lines of contact were provided with discrete discontinuities, apparently 4 nm wide. The observations support the notion that the paracellular pathway in capillary endothelium is permeable not only to small solutes but also to certain macromolecules.

Animals↗
PubMed1984

Murine sarcoma virus-induced brain tumors. Concurrent measurements of blood flow and transcapillary transport.

Intracerebral inoculation of Murine Sarcoma Virus (MSV) into rats induces highly vascular brain tumors. Blood flow, F, and a unidirectional blood-to-tissue transfer constant, K, were measured concurrently in 16 separate brain tumors in 13 rats. Regional measurements of F and K were obtained using double-label quantitative autoradiography with 131I-iodoantipyrine, 14C-alpha aminoisobutyric acid, and computerized microdensitometry with image analysis. Regional tissue extraction fractions (E) were calculated for different brain and tumor regions. The following observations were made: intracerebral inoculation of MSV in rats of different ages produced a single histologic tumor type (angiosarcoma), although tumor yield decreased and latency increased when older rats were inoculated; whole tumor blood flow values averaged 63.9 +/- 20.9 (SD) ml hg-1 min-1, less than F of tumor-free gray matter; the mean value of the transfer constant was 1.19 +/- 0.84 ml hg-1 min-1, 5 times the value in contralateral tumor-free brain; moderate regional variation of F and K values were observed within each tumor, with increased K values extending into the regions of brain around tumor; mean extraction fractions (E) of AIB for whole tumor were low (range = 0.0021 to 0.08), with a distinct and decreasing gradient from tumor center to BAT; there was poor correlation between F, K and E values, and tumor histology, including regions that microscopically appeared highly vascular; in most regions of the MSV-induced brain tumors, capillary permeability and/or surface area seem to be determinant in blood-to-tissue transport processes.

Aminoisobutyric Acids↗
PubMed1982

Effects of captopril on renal function in hypertensive patients.

The effects of captopril (SQ 14225) on renal function were studied in 10 hypertensive patients. After 7 weeks of treatment (75 to 500 mg/day) renal plasma flow was practically unchanged and glomerular filtration rate was only slightly decreased despite a significant decrease in blood pressure. All indexes of glomerular capillary permeability and of tubular anatomic integrity remained normal during the treatment period.

Adult↗