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PubMed2002

Inhibitory effect of a novel bradykinin B1 receptor antagonist, R-954, on enhanced vascular permeability in type 1 diabetic mice.

The morbidity and mortality associated with type 1 diabetes are essentially related to the micro- and macrovascular complications that develop over time and lead to several diabetic complications, including hypertension, atherosclerosis, and retinopathy, as well as coronary and renal failure. Normally absent in physiological conditions, the bradykinin B1 receptor (BKB1-R) was recently found to be overexpressed in pathological conditions, including type 1 diabetes. In the present study, we evaluated the effect of the new BKB1-R antagonist, R-954 (Ac-Orn-[Oic2, alpha-MePhe5, D-betaNal7, Ile8]desArg9-bradykinin, on the increase in vascular permeability in streptozotocin (STZ)-diabetic mice. The capillary permeability to albumin was measured by quantifying the extravasation of albumin-bound Evans blue dye in selected target tissues (liver, pancreas, duodenum, ileum, spleen, heart, kidney, stomach, skin, muscle, and thyroid gland). Acute single administration of R-954 (300 microg/kg, i.v.) to type 1 diabetic mice 4 weeks after STZ significantly inhibited the enhanced vascular permeability in most tissues. These data provide further experimental evidence for the implication of BKB1-R in the enhanced vascular permeability associated with type 1 diabetes.

Animals↗
PubMed2004

Possible role of substance P in the ischemia-reperfusion injury in the isolated rabbit lung.

The origin of the endothelial damage leading to the ischemia-reperfusion injury after lung transplantation has not been elucidated. We postulated that neurotransmitters released during the preservation of the donor lung might explain this vascular derangement. Thus, in isolated rabbit lungs preserved over 24 hours, we evaluated the release of acetylcholine (ACh) and substance P (SP), the activity of their major degrading enzymes, acetylcholinesterase (AChE) and neutral endopeptidase (NEP), and changes in the capillary permeability. Both neurotransmitters showed the highest release rate in the first 15 minutes, followed by a sharp exponential decrement at 1, 6, 12 and 24 hours. AChE and NEP activities showed no variation at these time intervals. Basal capillary permeability significantly increased (P<0.01) after 24 hours preservation with saline. This increased permeability was avoided (P<0.01) by the SP fragment 4-11 (an SP receptors antagonist), but not by atropine. These results suggest for the first time a pathogenic role of SP in the ischemia-reperfusion injury, and thus the potential usefulness of SP antagonists as additives in the lung preservation solutions should be explored.

Animals↗
PubMed1986

Ependymal lining of infundibular recess in perinatal rats: relationships with portal capillaries and permeability.

Structure and permeability of the ependymal lining the infundibular recess were studied in perinatal rats with silver impregnation, electron microscopy, radioautography, and tracer techniques. According to our data basal processes of ependymal cells reach the primary portal plexus linking the 3rd ventricle and the hypophysial portal system all through the perinatal period. After birth, some of the processes penetrate into the perivascular space of the primary portal plexus and abut there on the endothelium of capillaries. Ependymal cells of fetuses and neonates are joined by specialized junctions (tight junctions, gap junctions and zonulae adhaerentes). Intraventricularly injected ionic lanthanum crosses the ependymal lining of fetuses both trans- and extra-cellularly everywhere in the infundibular recess. By postnatal day 9 only the rostral portion of the recess remains readily permeable. Caudally, extracellular leakage becomes highly restricted, apparently due to the appearance of circumferential tight junctions. Finally, [3H]dopamine seems to penetrate through the ependymal lining in the same way as ionic lanthanum entering the portal capillaries. These findings suggest that the adenohypophysiotropic neurohormones can penetrate from the cerebrospinal fluid into the portal circulation from the very beginning of the establishment of the hypothalamo-hypophysial functional relationships during ontogenesis.

Animals↗
PubMed1981

Permeability of gastric capillaries to small and large molecules.

The permeability of capillaries in the stomach to small and large solutes was studied with the double-indicator diffusion technique in the dog stomach and by analysis of steady-state lymph and plasma samples in the cat stomach. The effective pore radius in gastric capillaries determined by indicator diffusion was 53 A, whereas steady-state lymph samples predicted a small-pore radius of 47 A. At the highest plasma flow rates studied (achieved by intra-arterial infusion of isoproterenol), indicator diffusion estimates of the permeability-surface area product for raffinose, inulin, and beta-lactoglobulin A were 140, 70, and 8 ml . min-1 . 100 g-1, respectively. The lymph studies indicate that gastric capillaries are more permeable than capillaries in the intestine and colon to albumin and larger molecules. The calculated effective large-pore radius of gastric capillaries was 250 A. The osmotic reflection coefficients (sigma d) ranged from 0.73 +/- 0.03 for albumin to 0.91 +/- 0.02 for beta-lipoprotein (120-A radius). The sigma d for total plasma protein was 0.78 +/- 0.03, indicating a substantial transcapillary oncotic pressure gradient, despite the greater permeability of these capillaries for macromolecules.

Animals↗
PubMed1987

Direct correlation between plasma renin activity and severity of the ovarian hyperstimulation syndrome.

Plasma renin activity (PRA) and aldosterone were measured throughout the luteal phase in 21 anovulatory patients who developed ovarian hyperstimulation syndrome (OHSS) during menotropin induction of ovulation. The pattern of PRA in hyperstimulated cycles is characterized by a midluteal peak, which declines to normal in the late luteal phase in nonconceptual cycles, whereas a sustained elevation of PRA occurs in conceptual cycles. Midluteal PRA is significantly (P less than 0.001) elevated in patients with OHSS compared with controls. In the mild form of the disease, the median of PRA is 7.5 (range 6 to 11) ng angiotensin I (AI)/ml/hr, significantly higher than the median for controls, 3.0 ng AI/ml/hr (range, 1.4 to 5). In moderate OHSS, PRA was 24.5 (range, 10 to 40) ng AI/ml/hr, whereas, in the severe form of OHSS, PRA was 55.0 (range, 29 to 95) ng AI/ml/hr. A significant correlation (P less than 0.05) was demonstrated between PRA and either progesterone or 17 beta estradiol (E2). The renin-angiotensin cascade is implicated in new vessel formation. Angiogenesis itself is associated with a rapid increase in capillary permeability. The recent demonstration of high plasma renin-like activity in human follicular fluid and the present observation of high PRA in patients with OHSS may imply that the locally active renin angiotensin system, through induction of new vessel formation and increase in capillary permeability, may have a casual relationship to the ovarian enlargement and extracellular fluid accumulation that are the hallmarks of OHSS.

Adult↗
PubMedDate not supplied

Pathogenesis of edema formation in burn injuries.

One of the obvious acute features of cutaneous thermal injury is the swelling of the involved tissue. This swelling is caused by a fluid shift from circulating plasma. Along with the evolution of intravenous fluid therapy in trauma and surgery, the implementation of such therapy to burn victims has improved survival. Edema generation aggravated by fluid therapy may, however, represent a source of increased morbidity. This paper presents a review of the literature on postburn edema generation, focusing mainly on fluid physiology. It is well documented that fluid is lost from the circulation into burned tissue because of a moderate increase in capillary permeability to fluid and macromolecules and a modest increase in hydrostatic pressure inside the perfusing microvessels. Recently it was discovered that a very negative interstitial pressure develops in thermally injured skin. This pressure constitutes a strong "suction" adding markedly to the edema generating effect of increased capillary permeability and pressure.

Animals↗
PubMed1993

Liver distribution of 99mTc-DL-homocysteine in experimental hepatitis rats.

Liver accumulation of 99mTc-DL-homocysteine (99mTc-Hcy), which had been found to accumulate in several experimental tumors, was studied using experimental hepatitis models of rats. The distribution of this compound in liver of rats treated with CCl4 (25-100 microL/100 g body weight) was more than five times higher than that of non-treated rats, corresponding to the accumulation of Evans Blue, a marker dye for capillary permeability. Furthermore, in vitro experiments indicated that the liver accumulation of 99mTc-Hcy was due to some changes in the plasma membranes caused by CCl4 administration. These results indicate that lesional accumulation of 99mTc-Hcy is due to, at least in part, an enlarged capillary permeability similar to the case of malignant tissues reported previously.

Animals↗
PubMed2001

[Histopathological changes of lung and right ventricle induced by high concentration of carbon dioxide in rats].

OBJECTIVE: To evaluate if high concentration of carbon dioxide causes any histopathological changes of the lung and right ventricle in rats. METHODS: Wistar rats were divided into control group (Group A, n = 21) and hypercapnic group (Group B, n = 30). Group B received mixed gas exposure (8% CO(2), 21% O(2), 71% N(2)), 7 hours daily for 4 weeks. Arterial blood gas, superoxide dismutase (SOD), lipid peroxide (LPO) in the tissue of the lung and right ventricle were determined. Histopathological changes of the lung and right ventricle were investigated by light microscope, transmission and scanning electron microscope. RESULTS: Decompensated respiratory acidosis [pH 7.21 +/- 0.04, PaCO(2) (56 +/- 3) mm Hg] developed in Group B. SOD in the lung [(463 +/- 174) U/g protein] and ventricle tissue [(235 +/- 94) U/g protein] in Group B were significantly lower than those in Group A (P < 0.01), while LPOs [(8.1 +/- 3.2) nmol/ml and (17 +/- 5) nmol/ml] in group B were significantly higher than those in Group A (P < 0.01). The index of pulmonary capillary permeability in Group B (37 +/- 4) was also higher than that in Group A (28 +/- 4, P < 0.001). Tissue edema in the lung and heart, endothelial cell damage of the small blood vessels and severe myofibril damage of the right ventricle, pulmonary microthrombus formation and increased pulmonary capillary permeability were found in Group B. CONCLUSION: Hypercapnic rat model is successfully reproduced by exposure of 8% CO(2); high concentration of CO(2) causes severe damage of the lung and right ventricle as well as the whole body.

Animals↗
PubMed1984

[Measurement of extravascular lung water by double-indicator dilution method amd its clinical assessment].

In this study, thermal-dye double-indicator dilution method using Lung water computer (Edwards Laboratories) was used to detect the changes of extravascular lung water (EVLW) in 14 patients, including 8 head injuries, one multiple injury, and 5 burns. The coefficient of variation of multiple readings at the same time was 5.04 +/- 3.64% (M +/- SD, n = 180), so reproducibility was excellent. EVLW showed no correlation with cardiac index, Qs/Qt ratio, PAO2/PaO2 ratio, and PaO2/FiO2 ratio, but did show significant correlation with pulmonary capillary wedge pressure (PCWP) (r = 0.50, n = 54, p less than 0.01). In non-septic period of burn patients, EVLW showed good correlation with COP-PCWP gradient (r = -0.75, n = 54, p less than 0.01), better correlation than with PCWP only. In septic period, it had no correlation with the gradient, probably due to the enhanced pulmonary capillary permeability. Although it is very difficult to determine the threshold of EVLW to diagnose pulmonary edema, the elevation of EVLW appeared earlier than the changes of X-ray films. In estimate of EVLW, we must always take into consideration changes in effective vascular bed and pulmonary capillary permeability. The measurement of EVLW was also of much help in the differential diagnosis of pulmonary edema and other lung diseases.

Adolescent↗
PubMed1987

Binding of anti-basement membrane antibody to alveolar basement membrane after intratracheal gasoline instillation in rabbits.

A possible causal relationship has been suggested between hydrocarbon (gasoline, solvents, etc.) exposure and development of anti-basement membrane antibody-associated Goodpasture's syndrome in man. The authors evaluated the effect of hydrocarbons on pulmonary capillary permeability and binding of heterologous anti-basement membrane antibodies in the lungs after intratracheal instillation of minute amounts of unleaded gasoline into rabbits. The anti-glomerular basement membrane (GBM) antibodies used reacted with the alveolar basement membrane (ABM) in vitro by indirect immunofluorescence. The gasoline treatment altered pulmonary capillary permeability, judging from the increased accumulation of systemically administered radioiodinated bovine serum albumin in the alveolar and extravascular spaces of lungs; it also induced focal macroscopic and microscopic pulmonary histologic lesions. The gasoline caused focal in vivo binding of the anti-GBM antibodies to the ABM detectable by immunofluorescence microscopy. No binding was observed in lungs from control rabbits given saline instillations when assayed by immunofluorescence. The paired label radioisotope technique confirmed the increased antibody binding to lungs injured with gasoline (1.08 +/- 0.03 micrograms) versus 0.37 +/- 0.07 microgram after saline (P less than 0.001). These results indicate that gasoline exposure damages a pulmonary barrier that normally prevents binding of anti-GBM/ABM antibody to ABM and suggest that hydrocarbon exposure may be one of perhaps several pneumotoxic events that contribute to the episodic pulmonary hemorrhage in Goodpasture's syndrome by temporarily allowing ABM binding of anti-basement membrane antibodies.

Animals↗
PubMed1991

Morphology and physiology of capillary systems in subregions of the subfornical organ and area postrema.

From recent morphological and physiological studies of capillaries, I shall review four new or revised concepts about blood-tissue communication in the subfornical organ (SFO) and area postrema (AP). First, the capillary systems of SFO and AP exhibit subregional differentiation correlated topographically with cytoarchitecture, densities of immunoreactivity for several peptides and amines, cellular sensitivity to neuroactive substances, afferent neural terminations, and tissue metabolic activity. Thus, contrary to frequent citations, the angioarchitecture and microcirculatory physiology of these small sensory nuclei are not homogeneous. Second, electron microscopic, morphometric, and topographical studies reveal that SFO contains three different types of capillary and AP has two. The differentiated capillary morphology appears to be well organized for specialized functions particularly in SFO subregions. No other body organ or small tissue region is known to have such capillary diversity, further highlighting the complex functions served by SFO. Third, pools of interstitial fluid (Virchow-Robin spaces) surrounding type I and III capillaries in SFO and AP may participate in the receptive properties of these organs as low-resistance pathways for rapid dispersion of blood-borne hormones inside their organ boundaries. The parenchymal walls of Virchow-Robin spaces appear to harbour metabolic mechanisms for hormones such as angiotensin II, and thus could vastly extend the effective blood-brain surface area of permeable capillaries in SFO and AP. Fourth, SFO and AP bear similar physiological characteristics of high blood volume, yet relatively low rates of blood flow. Accordingly, intracapillary blood velocity must be quite slow in these organs, and the duration of transit by blood and circulating messengers rather protracted. This feature of slow blood transit time likely compounds the sensory capability of SFO and AP, rendering increased contact time for blood-borne hormones to penetrate the permeable capillaries of these structures and interact with their known dense populations of receptors for several homeostatic substances involved in regulation of blood pressure and body fluids.

Animals↗
PubMed1994

Cerebral ischemia alters glucose transporter kinetics across rat brain microvascular endothelium. Quantitative analysis by an in situ brain perfusion method.

The purpose of this study was to quantify the changes of blood-brain barrier glucose transporter kinetics following cerebral ischemia using an in situ brain perfusion technique. Sixty-four adult male Sprague-Dawley rats were divided into control and ischemia groups, and a four-vessel occlusion model was used to provide an ischemic insult. To obtain regional capillary permeability area products of glucose and regional perfusion fluid flow rates, the perfusion fluid was dually labeled with 2-deoxy[14C]glucose and [3H]diazepam, and the brain was perfused at a constant rate via the external carotid artery. After sampling tissues from the brain, dual scintillation counting was performed and both regional perfusion fluid flow rates and regional capillary permeability area products were calculated. We determined kinetic parameters, including Vmax, Km and Kd as described in the Michaelis-Menten equation, by the non-linear least squares method. In the ischemia group, a decrease in Vmax and an increase in Km were recognized, which mean decreases in the affinity and the number of functioning glucose transporters. These results suggest that cerebral ischemia downregulates the blood-brain barrier glucose transporters.

Animals↗
PubMed2005

Microcirculation disturbance affects rats with acute severe pancreatitis following lung injury.

AIM: To study the effects of microcirculation disturbance (MD) on rats with acute severe pancreatitis (ASP). METHODS: We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood and did hemorrheologic examination and erythrocyte osmotic fragility test, checked up the water content, capillary permeability, and genetic expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissues, examined the apoptosis degree of blood vessel endothelium while we tested related gene expression of Bax and Bcl-2 in lung tissues. We did the same examination in control group. RESULTS: The viscosity of total blood and plasma, the hematocrit, and the erythrocyte osmotic fragility were all increased. Fibrinogen was decreased. The water content in lung tissues and capillary permeability were increased. Apoptosis degree of blood vessel endothelium was increased too. ICAM-1 genetic expression moved up after 1 h and reached its peak value after 9 h. CONCLUSION: MD plays an important role in ASP following acute lung injury (ALI). The functional damage of blood vessel endothelium, the apoptosis of capillary vessel endothelium, WBC edging-concentration and the increasing of erythrocyte fragility are the main reasons of ALI.

Acute Disease↗
PubMed1990

Pulmonary capillary dynamics and fluid distribution after burn and inhalation injury.

A non-linear macroscopic mathematical model is described for the simulation of the different mechanisms that regulate the pulmonary capillary dynamics in patients with thermal injury. The techniques used in the construction of the model are those of 'system's dynamics'. This model has been incorporated into a patient simulator, which makes it possible to analyse the fluid and protein exchanges in a burn patient. The regulating mechanisms involved are: the pulmonary circulation, the fluid and protein transfer between the plasma and the interstitial space at the pulmonary capillary level, and the pulmonary lymphatic system. As a result of the sensitivity analyses of the model we propose that, for the simulation of the effects of an inhalation injury at the pulmonary capillary level, the parameters to be altered will be the pulmonary capillary permeability coefficient for proteins and the pulmonary capillary surface damaged by the injury. To verify the validity and utility of the model, the clinical progress of a series of burn patients with lung injuries has been compared with the results obtained using simulation.

Burns↗
PubMedDate not supplied

Response of cerebral circulation to topical histamine.

To study the effect of histamine (HA) on brain blood flow and capillary permeability, bilateral parietal craniectomies were made in cats anesthetized with nitrous oxide and ketamine. The dura was removed and solutions of HA in mock cerebrospinal fluid (CSF) in varying concentrations ranging from 10(-5) M to 10(-1) M were irrigated continuously onto the exposed brain while local cerebral blood flow was determined polarographically by hydrogen clearance. Capillary permeability was assessed by determining HA's effect on the 125I-albumin space of the brain. Electrical activity was monitored by electrocorticography. HA consistently dilated pial blood vessels and produced within 15 min a dose-related local hyperemia that subsided 30--60 min after HA was removed. Hyperemia was blocked by cimetidine. HA had no appreciable effect on either the blood-brain barrier to albumin or the electrical activity of the cortex. HA is pharmacologically capable of participating directly in the acute hyperemic response of the brain's microcirculation to physiologic and pathologic stimuli but has little effect on cerebrovascular permeability to protein.

Animals↗