Changes In Capillary Permeability Research Articles

Mechanisms of Myocardial Edema Development in CVD Pathophysiology.

Myocardial edema is the excess accumulation of fluid in the myocardial interstitium or cardiac cells that develops due to changes in capillary permeability, loss of glycocalyx charge, imbalance in lymphatic drainage, or a combination of these factors. Today it is believed that this condition is not only a complication of cardiovascular diseases, but in itself causes aggravation of the disease and increases the risks of adverse outcomes. The study of molecular, genetic, and mechanical changes in the myocardium during edema may contribute to the development of new approaches to the diagnosis and treatment of this condition. This review was conducted to describe the main mechanisms of myocardial edema development at the molecular and cellular levels and to identify promising targets for the regulation of this condition based on articles cited in Pubmed up to January 2024.

Acute brain injury increases pulmonary capillary permeability via sympathetic activation-mediated high fluid shear stress and destruction of the endothelial glycocalyx layer

Neurogenic pulmonary edema secondary to acute brain injury (ABI) is a common and fatal disease condition. However, the pathophysiology of brain-lung interactions is incompletely understood. This study aims to investigate whether sympathetic activation-mediated high fluid shear stress after ABI would damage pulmonary endothelial glycocalyx thus leading to increased pulmonary capillary permeability. The tricuspid annular plane systolic excursion (TAPSE) was detected in a rat model of controlled cortical impact (CCI) and CCI + transection of the cervical sympathetic trunk (TCST). Changes in pulmonary capillary permeability were assessed by analyzing the Evans blue, measuring the dry/wet weight ratio of the lungs and altering protein levels in the bronchoalveolar lavage fluid (BALF). The parallel-plate flow chamber system was used to simulate the fluid shear stress in vitro. Western blotting and immunofluorescence staining were used to determine the expression levels of hyaluronan-binding protein (CEMIP), syndecan-1 and tight junction proteins (TJPs, including claudin-5 and occludin). TCST could restrain cardiac overdrive and sympathetic activation in a rat model of CCI. Compared to the CCI group, the CCI + TCST group showed a reduction of CEMPI (which degrades hyaluronic acid), along with an increase of syndecan-1 and TJPs. CCI + TCST group presented decreasing pulmonary capillary permeability. In vitro, high shear stress (HSS) increased the expression of CEMIP and reduced syndecan-1 and TJPs, which was coordinated with the results in vivo. Our findings show that sympathetic activation-mediated high fluid shear stress after ABI would damage pulmonary endothelial glycocalyx thus leading to increased pulmonary capillary permeability.

Cardiovascular Insights for the Appropriate Management of Chronic Venous Disease: A Narrative Review of Implications for the Use of Venoactive Drugs.

Evidence suggests that chronic venous disease (CVD) may be a cardiovascular disorder, as patients with CVD are prone to developing arterial (atherosclerosis) and venous (thromboembolism) diseases. This may be partly explained by shared risk factors. Thus, patients with CVD or cardiovascular disease require careful history-taking and physical assessment to identify coexisting pathologies and risk factors. This article summarises a symposium at the XIX World Congress of the International Union of Phlebology held in Istanbul, Turkey, in September 2022. Common pathophysiological features of CVD and cardiovascular disease are endothelial injury, hypercoagulability and systemic inflammation. In CVD, inflammation primarily affects the microcirculation, with changes in capillary permeability, vein wall and valve remodelling and increase in oxidative stress. Once patients develop symptoms/signs of CVD, they tend to reduce their physical activity, which may contribute to increased risk of cardiovascular disease. Data show that the presence of CVD is associated with an increased risk of cardiovascular disease, including peripheral arterial disease and heart failure (HF), and the risk of adverse cardiovascular events increases with CVD severity. In addition, patients with cardiovascular disease, particularly those with HF, are at increased risk of venous thromboembolism (VTE) and should be assessed for VTE risk if they are hospitalised with cardiovascular disease. Therefore, CVD management must include a multi-specialty approach to assess risk factors associated with both the venous and arterial systems. Ideally, treatment should focus on the resolution of endothelial inflammation to control both CVD and cardiovascular disease. International guidelines recommend various conservative treatments, including venoactive drugs (VADs), to improve the symptoms/signs of CVD. Micronized purified flavonoid fraction (MPFF) is a VAD, with high-quality evidence supporting its use in relieving symptoms/signs of CVD and improving quality of life. Moreover, in large-scale observational studies, MPFF has shown superior effectiveness in real-world populations compared with other VADs. Video Abstract. (MP4 97173 kb).

Mechanical Ventilation Exacerbates Poly (I:C) Induced Acute Lung Injury: Central Role for Caspase-11 and Gut-Lung Axis.

BackgroundThe mechanisms by which moderate tidal volume ventilation (MTV) exacerbates preexisting lung injury are unclear. We hypothesized that systemic endotoxemia via the gut-lung axis would lead to non-canonical and canonical inflammasome activation and pyroptosis in a two-hit model involving polyinosinic-polycytidylic acid (Poly(I:C)), a synthetic analog of dsRNA and MTV and that this would associate with acute lung injury (ALI).MethodsAnesthetized mice were administered Poly(I:C) intratracheally and then 6 h later, they were mechanically ventilated for 4 h with otherwise non-injurious MTV (10ml/kg). Changes in intestinal and alveolar capillary permeability were measured. Further documentation of ALI was assessed by evans blue albumin permeability, protein and IL-1 family concentration in bronchoalveolar lavage fluid (BALF) or plasma, and histopathology in cohorts of wildtype (WT), whole body genetically ablated caspase-11 (caspase-11-/-), caspase-1/caspase-11 double knockout (caspase-1/11-/-), gasdermin D (GSDMD)-/-, nucleotide-binding domain leucine-rich repeat-containing protein 3 (NLRP3)-/- and advanced glycosylation end product-specific receptor (RAGE) -/- mice.ResultsNon-injurious MTV exacerbated the mild lung injury associated with Poly(I:C) administration. This included the disruption of alveolar-capillary barrier and increased levels of interleukin (IL)-6, high mobility group proteins 1 (HMGB-1), IL-1β in BALF and IL-18 in plasma. Combined (Poly(I:C)-MTV) injury was associated with increase in gastrointestinal permeability and endotoxin in plasma and BALF. Poly(I:C)-MTV injury was sensitive to caspase-11 deletion with no further contribution of caspase-1 except for maturation and release of IL-18 (that itself was sensitive to deletion of NLRP3). Combined injury led to large increases in caspase-1 and caspase-11. Genetic ablation of GSDMD attenuated alveolar-capillary disruption and release of cytokines in combined injury model.ConclusionsThe previously noted exacerbation of mild Poly(I:C)-induced ALI by otherwise non-injurious MTV is associated with an increase in gut permeability resulting in systemic endotoxemia. The gut-lung axis resulted in activation of pulmonary non-canonical (cytosolic mediated caspase-11 activation) and canonical (caspase-1) inflammasome (NLRP3) mediated ALI in this two-hit model resulting in GSDMD sensitive alveolar capillary barrier disruption, pyroptosis (alveolar macrophages) and cytokine maturation and release (IL-1β; IL-18). Pharmacologic strategies aimed at disrupting communication between gut and lung, inhibition of inflammasomes or GSDMD in pyroptosis may be useful in ALI.

Chronic Consumption of Bovine Dairy Milk Attenuates Dietary Saturated Fatty Acid-Induced Blood-Brain Barrier Dysfunction.

Ingestion of Western-diets enriched in long chain saturated fatty acids (LCSFA) are associated with increased risk of blood-brain barrier (BBB) dysfunction and neurovascular inflammation. Potential mechanisms include vascular insult as a consequence of metabolic aberrations, or changes in capillary permeability resulting in brain parenchymal extravasation of pro-inflammatory molecules. Bovine dairy milk (BDM) is potentially a significant source of dietary LCSFA, however, BDM contains an array of bioactive molecules purported to have vascular anti-inflammatory properties. This study investigated the effects of full cream (4% total fat) and delipidated (skim) BDM on BBB integrity and neuroinflammation in wild-type mice. Mice consuming substantial amounts of full cream or skim BDM with LCSFA-enriched chow were dyslipidemic compared to control mice provided with standard chow and water. However, there was no evidence of BBB dysfunction or neuroinflammation indicated by parenchymal abundance of immunoglobulin G and microglial recruitment, respectively. Positive control mice maintained on an LCSFA-enriched diet derived from cocoa-butter and water, had marked BBB dysfunction, however, co-provision of both full cream and skim milk solutions effectively attenuated LCSFA-induced BBB dysfunction. In mice provided with low-fat chow and full cream BDM drinking solutions, there were substantial favorable changes in the concentration of plasma anti-inflammatory cytokines. This study suggests that consumption of BDM may confer potent vascular benefits through the neuroprotective properties exuded by the milk-fat globule membrane moiety of BDM.

Altered pulmonary capillary permeability in immunosuppressed guinea pigs infected with Legionella pneumophila serogroup 1.

In immunosuppressed hosts, Legionella pneumophila (Lp) infection usually develops into severe pneumonia, which is pathologically characterized by increased vascular permeability and pulmonary edema. At present, mechanisms associated with changes in pulmonary capillary permeability (PCP) and the pathogenesis of pulmonary edema in immunosuppressed hosts with Lp infection are unclear. Therefore, in the present study an animal model of normal and immunosuppressed guinea pigs infected with Lp was established. An isolated perfused lung system was used to investigate the extent of changes in PCP. Pathological and immunofluorescence examinations were performed to explore the mechanism underlying these changes. The results indicated that PCP increased with the highest magnitude in immunosuppressed guinea pigs infected with Lp, with repeated ANOVA indicating synergism between infection and immunosuppression (P=0.0444). Hematoxylin and eosin staining and electron microscopy revealed more severe morphological damages in the lung tissues and pulmonary capillaries of the immunosuppressed animals infected with Lp compared with normal animals infected with Lp. Immunofluorescence analysis showed that immunosuppression reduced the expression of the vascular endothelial cell junction protein VE-cadherin (P=0.027). Following Lp infection, VE-cadherin expression was significantly lower in the immunosuppressed guinea pigs compared with their immunocompetent counterparts (P=0.001). These results suggest that immunosuppression combined with Lp infection induces more significant damage to pulmonary capillaries compared with Lp infection alone, resulting in a significantly increased PCP.

Neuro-Immune Hemostasis: Homeostasis and Diseases in the Central Nervous System.

Coagulation and the immune system interact in several physiological and pathological conditions, including tissue repair, host defense, and homeostatic maintenance. This network plays a key role in diseases of the central nervous system (CNS) by involving several cells (CNS resident cells, platelets, endothelium, and leukocytes) and molecular pathways (protease activity, complement factors, platelet granule content). Endothelial damage prompts platelet activation and the coagulation cascade as the first physiological step to support the rescue of damaged tissues, a flawed rescuing system ultimately producing neuroinflammation. Leukocytes, platelets, and endothelial cells are sensitive to the damage and indeed can release or respond to chemokines and cytokines (platelet factor 4, CXCL4, TNF, interleukins), and growth factors (including platelet-derived growth factor, vascular endothelial growth factor, and brain-derived neurotrophic factor) with platelet activation, change in capillary permeability, migration or differentiation of leukocytes. Thrombin, plasmin, activated complement factors and matrix metalloproteinase-1 (MMP-1), furthermore, activate intracellular transduction through complement or protease-activated receptors. Impairment of the neuro-immune hemostasis network induces acute or chronic CNS pathologies related to the neurovascular unit, either directly or by the systemic activation of its main steps. Neurons, glial cells (astrocytes and microglia) and the extracellular matrix play a crucial function in a “tetrapartite” synaptic model. Taking into account the neurovascular unit, in this review we thoroughly analyzed the influence of neuro-immune hemostasis on these five elements acting as a functional unit (“pentapartite” synapse) in the adaptive and maladaptive plasticity and discuss the relevance of these events in inflammatory, cerebrovascular, Alzheimer, neoplastic and psychiatric diseases. Finally, based on the solid reviewed data, we hypothesize a model of neuro-immune hemostatic network based on protein–protein interactions. In addition, we propose that, to better understand and favor the maintenance of adaptive plasticity, it would be useful to construct predictive molecular models, able to enlighten the regulating logic of the complex molecular network, which belongs to different cellular domains. A modeling approach would help to define how nodes of the network interact with basic cellular functions, such as mitochondrial metabolism, autophagy or apoptosis. It is expected that dynamic systems biology models might help to elucidate the fine structure of molecular events generated by blood coagulation and neuro-immune responses in several CNS diseases, thereby opening the way to more effective treatments.

Typhae pollen polysaccharides ameliorate diabetic retinal injury in a streptozotocin-induced diabetic rat model

Ethnopharmacological relevanceAccording to ancient traditional Chinese medicine, Typhae Pollen (TP) is commonly used to treat fundus haemorrhage because it improves blood circulation. Aims of the studyThis study evaluated the role of the main TP component, polysaccharides (TPP), on diabetic retinopathy (DR) and its possible mechanisms of inhibiting inflammation and improving blood circulation. Materials and methodsAfter successful establishment of a diabetic rat model, TPP was administered to diabetic rats for treatment, and the rats were sacrificed at 12 weeks. Retinal electrophysiology and ultrastructures were observed, and serum interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) levels were also measured. Changes in the retinal expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were examined by immunofluorescence. A mouse model of acute blood stasis was then established, and the effects of TPP on haemorheology were observed. The anti-inflammatory effect of TPP was analysed based on the changes in abdominal capillary permeability and the degree of auricle swelling in the mice. ResultsIn streptozotocin (STZ)-induced DR rats, TPP (0.4 g/kg) treatment restored electrophysiology indexes and retinal ultrastructures, reduced serum IL-6 and TNF-α levels, decreased VEGF and bFGF expression in retinal tissues, and improved haemorheology indexes. Moreover, TPP reduced abdominal capillary permeability and relieved auricle swelling in a dose-dependent manner. ConclusionsTPP treatment ameliorated DR by inhibiting inflammation and improving blood circulation.

Alterations of the Blood-Brain Barrier and Regional Perfusion in Tumor Development: MRI Insights from a Rat C6 Glioma Model.

ObjectivesAngiogenesis and anti-angiogenetic medications play an important role in progression and therapy of glioblastoma. In this context, in vivo characterization of the blood-brain-barrier and tumor vascularization may be important for individual prognosis and therapy optimization.MethodsWe analyzed perfusion and capillary permeability of C6-gliomas in rats at different stages of tumor-growth by contrast enhanced MRI and dynamic susceptibility contrast (DSC) MRI at 7 Tesla. The analyses included maps of relative cerebral blood volume (CBV) and signal recovery derived from DSC data over a time period of up to 35 days after tumor cell injections.ResultsIn all rats tumor progression was accompanied by temporal and spatial changes in CBV and capillary permeability. A leakage of the blood-brain barrier (slow contrast enhancement) was observed as soon as the tumor became detectable on T2-weighted images. Interestingly, areas of strong capillary permeability (fast signal enhancement) were predominantly localized in the center of the tumor. In contrast, the tumor rim was dominated by an increased CBV and showed the highest vessel density compared to the tumor center and the contralateral hemisphere as confirmed by histology.ConclusionSubstantial regional differences in the tumor highlight the importance of parameter maps in contrast or in addition to region-of-interest analyses. The data vividly illustrate how MRI including contrast-enhanced and DSC-MRI may contribute to a better understanding of tumor development.

Oxidative Stress and Nuclear Factor κB (NF-κB) Increase Peritoneal Filtration and Contribute to Ascites Formation in Nephrotic Syndrome

Water accumulation in the interstitium (edema) and the peritoneum (ascites) of nephrotic patients is classically thought to stem from the prevailing low plasma albumin concentration and the decreased transcapillary oncotic pressure gradient. However, several clinical and experimental observations suggest that it might also stem from changes in capillary permeability. We addressed this hypothesis by studying the peritoneum permeability of rats with puromycin aminonucleoside-induced nephrotic syndrome. The peritoneum of puromycin aminonucleoside rats displayed an increase in the water filtration coefficient of paracellular and transcellular pathways, and a decrease in the reflection coefficient to proteins. It also displayed oxidative stress and subsequent activation of NF-κB. Scavenging of reactive oxygen species and inhibition of NF-κB prevented the changes in the water permeability and reflection coefficient to proteins and reduced the volume of ascites by over 50%. Changes in water permeability were associated with the overexpression of the water channel aquaporin 1, which was prevented by reactive oxygen species scavenging and inhibition of NF-κB. In conclusion, nephrotic syndrome is associated with an increased filtration coefficient of the peritoneum and a decreased reflection coefficient to proteins. These changes, which account for over half of ascite volume, are triggered by oxidative stress and subsequent activation of NF-κB.

MRI measurement of blood–brain barrier transport with a rapid acquisition refocused echo (RARE) method

Dynamic Contrast Enhanced (DCE) MRI is increasingly being used to assess changes in capillary permeability. Most quantitative techniques used to measure capillary permeability are based on the Fick equation that requires measurement of signal reflecting both plasma and tissue concentrations of the solute being tested. To date, most Magnetic Resonance Imaging (MRI) methods for acquiring appropriate data quickly rely on gradient recalled echo (GRE) type acquisitions, which work well in clinical low field settings. However, acquiring this type of data on high field small animal preclinical MRIs is problematic due to geometrical distortions from susceptibility mismatch. This problem can be exacerbated when using small animal models to measure blood brain barrier (BBB) permeability, where precise sampling from the superior sagittal sinus (SSS) is commonly used to determine the plasma concentration of the contrast agent. Here we present results demonstrating that a standard saturation recovery rapid acquisition refocused echo (RARE) method is capable of acquiring T1 maps with good spatial and temporal resolution for Patlak analysis (Patlak, 1983) to assess changes in BBB Gd-DTPA permeability following middle cerebral artery occlusion with reperfusion in the rat. This method limits known problems with magnetic susceptibility mismatch and may thus allow greater accuracy in BBB permeability measurement in small animals.

Chemotherapy-induced changes in cardiac capillary permeability measured by fluorescent multiple indicator dilution.

Anthracyclines cause severe irreversible cardiac toxicity. The study of changes in cardiac permeability with chemotherapy could enhance the understanding of mechanisms behind cardiac damage, and provide useful information to evaluate anthracycline cardiotoxicity. Thirty-six rats (12 Sprague-Dawley, 12 Wistar, 12 Fischer-344) were randomly assigned to control (n=21) or doxorubicin (n=15), and injected i.p. with a cumulative dose of 18mg/kg doxorubicin in saline (vehicle) or vehicle aloneover 12days. Echocardiography was performed at baseline and on day 11. An isolated heart experiment was done on day 12 to obtain perfused heart pressure values, and to measure cardiac capillary permeability using a Texas Red/sodium fluorescein multiple indicator dilution method. Control animals had significantly lower average permeability-surface-area-products (0.035±0.013cm(3)/s) than doxorubicin animals (0.066±0.023cm(3)/s), PSP±SD, p<0.001. These permeability changes correlated with significant functional changes. There was a significant decline in cardiac function with a deleterious effect of chemotherapy on fractional shortening (p<0.001), left ventricular developed pressure (p<0.001), contractility (p<0.001), and relaxation (p=0.02). Based on our results, cardiac capillary permeability changes can be detected after in vivo chemotherapy treatment using our fluorescent multiple indicator dilution technique, and may provide valuable information in evaluating cardiotoxicity of novel drugs.

The dynamic changes of capillary permeability and upregulation of VEGF in rats following radiation-induced brain injury.

To explore the dynamic changes of capillary permeability and the expression of VEGF in cerebral cortex after RIBI. Male SD rats were randomly divided into the RIBI group and control group, and the RIBI group was randomly subdivided into five groups for analysis on day 1, 3, 7, 14, and 28, respectively. We established an RIBI model, and then evaluated BBB permeability by EB. We also measured the expression of VEGF with IHC stain and western blot. EB extravasation in injured cortex of RIBI group was increased at five time points compared with the control group. The western blot results and IHC revealed that the levels of VEGF expression in the RIBI groups was significantly increased at day 1 compared with the control group, then rose to a maximum at day 7, and subsequently the levels of expression recovered from day 14 to 28. The increases in both BBB permeability and VEGF expression in the brain cortex of RIBI groups at same time period confirmed the possibility of brain injury following irradiation of 6Gy.

Measurement of choroid plexus perfusion using dynamic susceptibility MR imaging: capillary permeability and age-related changes

The cerebrospinal fluid (CSF) plays a major role in the physiology of the central nervous system. The continuous turnover of CSF is mainly attributed to the highly vascularized choroid plexus (CP) located in the cerebral ventricles which represent a complex interface between blood and CSF. We propose a method for evaluating CP functionality in vivo using perfusion MR imaging and establish the age-related changes of associated parameters. Fifteen patients with small intracranial tumors were retrospectively studied. MR Imaging was performed on a 3T MR Scanner. Gradient-echo echo planar images were acquired after bolus injection of gadolinium-based contrast agent (CA). The software developed used the combined T1- and T2-effects. The decomposition of the relaxivity signals enables the calculation of the CP capillary permeability (K2). The relative cerebral blood volume (rCBV), mean transit time (MTT), and signal slope decrease (SSD) were also calculated. The mean permeability K2 of the extracted CP was 0.033+/-0.18 s(-1). K2 and SSD significantly decreased with subject's age whereas MTT significantly increased with subject's age. No significant correlation was found for age-related changes in rCBV and rCBF. The decrease in CP permeability is in line with the age-related changes in CSF secretion observed in animals. The MTT increase indicates significant structural changes corroborated by microscopy studies in animals or humans. Overall, DSC MR-perfusion enables an in vivo evaluation of the hemodynamic state of CP. Clinical applications such as neurodegenerative diseases could be considered thanks to specific functional studies of CP.

Angiotensin II Contributes to Diabetic Renal Dysfunction in Rodents and Humans via Notch1/Snail Pathway

In nondiabetic rat models of renal disease, angiotensin II (Ang II) perpetuates podocyte injury and promotes progression to end-stage kidney disease. Herein, we wanted to explore the role of Ang II in diabetic nephropathy by a translational approach spanning from in vitro to in vivo rat and human studies, and to dissect the intracellular pathways involved. In isolated perfused rat kidneys and in cultured human podocytes, Ang II down-regulated nephrin expression via Notch1 activation and nuclear translocation of Snail. Hairy enhancer of split-1 was a Notch1-downstream gene effector that activated Snail in cultured podocytes. In vitro changes of the Snail/nephrin axis were similar to those in renal biopsy specimens of Zucker diabetic fatty rats and patients with advanced diabetic nephropathy, and were normalized by pharmacological inhibition of the renin-angiotensin system. Collectively, the present studies provide evidence that Ang II plays a relevant role in perpetuating glomerular injury in experimental and human diabetic nephropathy via persistent activation of Notch1 and Snail signaling in podocytes, eventually resulting in down-regulation of nephrin expression, the integrity of which is crucial for the glomerular filtration barrier.

Investigation Into the Impact of Diagnostic Ultrasound with Microbubbles on the Capillary Permeability of Rat Hepatomas

Ultrasound-targeted microbubble destruction (UTMD) takes advantage of transiently increased capillary permeability to enhance the release of tumor-specific drugs from blood vessels into sonicated tumor tissues. However, the application of focused ultrasound is limited because of the lack of an appropriate image-monitoring system. In this study, hepatoma-bearing Sprague-Dawley rats were insonicated with low-frequency diagnostic ultrasound and injected with Evans Blue (EB) dye and microbubbles through their tail veins to test changes in capillary permeability. We studied how the mechanical index, sonication duration and the injected microbubble (MB) concentration affect the hepatoma vascular permeability by quantitatively evaluating the EB delivery efficiency. Confocal laser scanning microscopy was used to observe the deposition of red fluorescence–dyed EB in tumor tissues. In addition, P-selectin, a type of biochemical marker that reflects vascular endothelial cell activation, was identified using an immunoblotting analysis. The experimental results reveal that EB delivery efficiency in tumor tissues was greater in groups with the diagnostic ultrasound–mediated UTMD (8.40 ± 0.71 %ID/g) than in groups without UTMD (1.73 ± 0.19 %ID/g) and EB delivery efficiency could be affected by MI, sonication duration and MB dose. The immunoblotting analysis indicates that diagnostic ultrasound–induced UTMD results in the vascular endothelial cell activation to increase capillary permeability, justifying the high quantity of EB deposited in tumor tissues.

Tracing the changes in capillary permeability during rat anaphylaxis.

Tracing the changes in capillary permeability during rat anaphylaxis.

EVALUATION OF CHANGES OF CAPILLARY PERMEABILITY.

EVALUATION OF CHANGES OF CAPILLARY PERMEABILITY.

Effect of hydrocortisone on capillary permeability changes induced by Echis carinatus (saw-scaled viper) venom in the rat.

Effect of hydrocortisone on capillary permeability changes induced by Echis carinatus (saw-scaled viper) venom in the rat.

Treatment of Recurrent Focal Segmental Glomerular Sclerosis Posttransplant With a Multimodal Approach Including High-Galactose Diet and Oral Galactose Supplementation

Treatment of Recurrent Focal Segmental Glomerular Sclerosis Posttransplant With a Multimodal Approach Including High-Galactose Diet and Oral Galactose Supplementation