Control Of Fluid Volume Research Articles

What a Neurosurgeon Should Know about the Endolymphatic Sac: Part 1–Anatomy and Physiology

Abstract Objective To describe the microsurgical anatomy and the physiology of the endolymphatic sac (ES) that a neurosurgeon should know. Methods Review of previous studies from 1927 to 2021, from basic and translational research using human and animal ES tissue or cells, as well as previous reviews about the subject. The present article is divided into three parts. In this first part, we review the microsurgical anatomy and physiology of the ES. Results The ES is a structure situated in the inner ear, together with the cochlea, the vestibular system, and other structures. Differently from its adjacent structures, the ES does not have a specialized epithelium; instead, it has mitochondria-rich cells and ribosomal-rich cells, which are responsible for ionic transportation and secretory activity. Apart from these functions, the ES is also responsible for homeostasis regulation of the inner ear, endolymphatic fluid volume control, immune response, elimination of inner ear cellular debris and floating otoconia, regulation of membranous labyrinth pressure, acid/basic transport, and secretion of substances. Its anatomy is not very variable, since in most studies no more than 20mm separates the location of the ES in the samples, in any direction. Conclusion The human ES has vital functions in the inner ear, and its anatomy is rarely variable. Knowing that, and the importance of this area for neurosurgery, the present study elucidates the exact location of the ES and the lost functions that a lesion in this structure must cause.

Computational and experimental investigations of a microfluidic mixer for efficient iodine extraction using carbon tetrachloride enhanced with gas bubbles

Numerous studies have been conducted on microfluidic mixers in various microanalysis systems, which elucidated the manipulation and control of small fluid volumes within microfluidic chips. These studies have demonstrated the ability to control fluids and samples precisely at the microscale. Microfluidic mixers provide high sensitivity for biochemical analysis due to their small volumes and high surface-to-volume ratios. A promising approach in drug delivery is the rapid microfluidic mixer-based extraction of elemental iodine at the micro level, demonstrating the versatility and the potential to enhance diagnostic imaging and accuracy in targeted drug delivery. Micro-mixing inside microfluidic chips plays a key role in biochemical analysis. The experimental study describes a microfluidic mixer for extraction of elemental iodine using carbon tetrachloride with a gas bubble mixing process. Gas bubbles are generated inside the microcavity to create turbulence and micro-vortices resulting in uniform mixing of samples. The bubble mixing of biochemical samples is analyzed at various pressure levels to validate the simulated results in computational fluid dynamics (CFD). The experimental setup includes a high-resolution camera and an air pump to observe the mixing process and volume at different pressure levels with time. The bubble formation is controlled by adjusting the inert gas flow inside the microfluidic chip. Microfluidic chip-based gas bubble mixing effects have been elaborated at various supplied pressures.

What a Neurosurgeon Should Know About the Endolymphatic Sac: Part 2 – Diagnosis and Management of the Endolymphatic Sac Tumors

Abstract Objective This article is divided into three parts. In the second part of this review, the authors focus on describing the endolymphatic sac tumor and presenting illustrative cases. Methods A review of previous studies, from 1957 to 2021, from basic and translational research using human and animal endolymphatic sac (ES) tissue or cells, as well as other reviews on this theme. Results The ES is an inner ear structure, which is responsible for the homeostatic regulation, as well as endolymphatic fluid volume control, immune response etc. One of the possible alterations of the ES is the ELST, a low-grade malign neoplasm that originates from the epithelium of the endolymphatic duct and sac. The clinical presentation of the ELST includes hearing loss, tinnitus, headache, and vertigo. The diagnosis in the early stages is rare, given that this group of symptoms is very similar to other, more common, diseases such as the Meniere syndrome. Its diagnosis is made by computed tomography (CT), magnetic resonance imaging (MRI), immunohistochemistry, and confirmed by histopathology. However, none of these examinations are part of the pathological guidelines for ELST. The treatment for ELST in the early stages has a high rate of success. Conclusion The ELST is a very difficult diagnosis due to its presentation. Furthermore, the interactions between ELST and the Von Hippel-Lindau disease usually result in a more aggressive condition. Despite the difficulty of the diagnosis, doing it early increases the chances of successful treatment.

AW-APSH-1: TARGETING WINDOWS OF PLASTICITY TO PREVENT HYPERTENSION.

Failing lifestyle interventions, there are many classes of anti-hypertensive drugs that are highly effective in most patients if taken appropriately. But multiple agents taken daily may be required to achieve target blood pressure (BP). The problem is that the majority of patients are non-compliant: they do not take their drugs continuously, choose to only take some, or stop taking them completely. It is time to focus on interventions that do not require lifelong daily medications, and this requires understanding and treating the causative factors. For decades, it has been understood that the kidney, under the influence of both the renin-angiotensin-aldosterone system and sympathetic nerves, has a dominant role in the long-term control of extracellular fluid volume and BP. The kidney is an important target for the treatment of hypertension. Early postnatal life is a period of remarkable plasticity and is a neglected window of opportunity to prevent disease onset. Our aim is to preserve and protect function of existing nephrons. If born with reduced renal mass (less nephrons), the compensatory response is to increase the filtration rate of each individual nephron so that GFR is maintained. Clinically, the degree of nephron overload is linked to faster age and disease related reduction in renal functional reserve, glomerular damage, albuminuria and hypertension. By targeting the postnatal period of maturation, our aim is to prevent maladaptive compensatory hypertrophy and hyperfiltration to preserve kidney health-span without the need for lifelong drug therapy. Our studies in a large animal model of congenital renal mass reduction demonstrate the long-term therapeutic potential of a brief period of angiotensin converting enzyme inhibition early in life to alter the trajectory of renal and cardiovascular disease.

Cryo-EM structure of the human sodium-chloride cotransporter NCC.

The sodium-chloride cotransporter NCC mediates the coupled import of sodium and chloride across the plasma membrane, playing vital roles in kidney extracellular fluid volume and blood pressure control. Here, we present the full-length structure of human NCC, with 2.9 Å for the transmembrane domain and 3.8 Å for the carboxyl-terminal domain. NCC adopts an inward-open conformation and a domain-swap dimeric assembly. Conserved ion binding sites among the cation-chloride cotransporters and the Na2 site are observed in our structure. A unique His residue in the substrate pocket in NCC potentially interacts with Na1 and Cl1 and might also mediate the coordination of Na2 through a Ser residue. Putative observed water molecules are indicated to participate in the coordination of ions and TM coupling. Together with transport activity assays, our structure provides the first glimpse of NCC and defines ion binding sites, promoting drug development for hypertension targeting on NCC.

Physiological Mechanisms of Hypertension and Cardiovascular Disease in End-Stage Kidney Disease.

In this article, we summarize recent advances in understanding hypertension and cardiovascular disease in patients with end-stage kidney disease. Factors such as anemia, valvular and vascular calcification, vasoconstrictors, uremic toxins, hypoglycemia, carbamylated proteins, oxidative stress, and inflammation have all been associated with the progression of cardiovascular disease in end-stage kidney disease but the causality of these mechanisms has not been proven. The high risk of cardiovascular mortality has not improved as in the general population despite many advancements in cardiovascular care over the last two decades. Mechanisms that increase hypertension risk in these patients are centered on the control of extracellular fluid volume; however, over-correction of volume with dialysis can increase risks of intradialytic hypotension and death in these patients. This review presents both recent and classic work that increases our understanding of hypertension and cardiovascular disease in end-stage kidney disease.

The rationale and clinical potential of on-line hemodiafiltration as renal replacement therapy.

On-line hemodiafiltration (ol-HDF) was developed in the 1980s in response to the unmet medical needs observed with conventional low- and high-flux hemodialysis. Firstly, the limited overall efficacy of conventional HD treatment programs as compared to native kidney function has been consistently documented over the broad MW spectrum of uremic toxins as well as fluid volume and hemodynamic control. Secondly, the unphysiological profile of intermittent treatment leading to repetitive dialysis-induced hemodynamic stress is now a well-recognized component of cardiovascular disease and end organ damage. Thirdly, the bioincompatibility of patient-dialysis system leading to dialysis-induced biological reactions also identified as contributing to dialytic morbidity and mortality. To overcome these limitations and pitfalls, alternative convective-based therapies (hemofiltration and hemodiafiltration), using higher hemoincompatible membranes and ultrapure dialysis fluid, were proposed as a solution to enhance and enlarge MW spectrum of uremic compounds cleared and to reduce dialysis-patient biological interactions. In this context, online HDF appeared soon as the best viable and efficient renal replacement modality to cover these needs. Clinical development and implementation of ol-HDF showed also that dialytic convective dose matters with a threshold point (23 L/1.73 m2 in postdilution mode) to observe clinical benefits and outcomes improvements.

Apelin-13 Decreases Epithelial Sodium Channel (ENaC) Expression and Activity in Kidney Collecting Duct Cells.

Apelin and its G protein-coupled receptor APLNR (also known as APJ) are widely expressed within the central nervous system and peripheral organs including heart, lung and kidney. Several studies have shown that the apelin/APJ system is involved in various important physiological processes such as energy metabolism, cardiovascular functions and fluid homeostasis. In the kidney, the apelin/APJ system performs a wide range of activities. We recently demonstrated that apelin antagonises the hydro-osmotic effect of vasopressin on aquaporin-2 water channel (AQP-2) expression by reducing its mRNA and protein levels in collecting duct principal cells. The central role of these cells in water and sodium transport is governed by AQP-2 and the epithelial sodium channel (ENaC). The coordination of these channels is essential for the control of extracellular fluid volume, sodium homeostasis and blood pressure. This study aimed at investigating the role of apelin in the regulation of sodium balance in the distal nephron, and more specifically its involvement in modulating the expression and activity of ENaC in collecting duct principal cells. mpkCCD cells were incubated in the presence of aldosterone and treated with or without apelin-13. Transepithelial Na+ current was measured and the changes in ENaC expression determined by RT-PCR and immunoblotting. Our data show that apelin-13 reduces the transepithelial sodium amiloride-sensitive current in collecting duct principal cells after 8h and 24h treatment. This effect was associated with a decrease in αENaC subunit expression and mediated through the ERK pathway as well as SGK1 and Nedd4-2. Our findings indicate that apelin is involved in the fine regulation of sodium balance in the renal collecting duct by opposing the effects of aldosterone, likely by activation of ENaC ubiquitination.

Ефективність антагоністів альдостерону у хворих на інфаркт міокарда, ускладнений гострою лівошлуночковою недостатністю із збереженою систолічною функцією лівого шлуночка

Актуальність. Гострий інфаркт міокарда (ГІМ) залишається провідною причиною смертності в Україні та світі загалом. Мета. Аналіз впливу еплеренону на перебіг захворювання у хворих на ГІМ, ускладнений розвитком гострої лівошлуночкової недостатності (ГЛШН) із збереженою фракцією викиду лівого шлуночка. Матеріали та методи. Обстежено 137 хворих на ГІМ з елевацією сегмента SТ, ускладнений ГЛШН. Пацієнти розподілені на дві групи: 1-ша група — 65 хворих, які отримували еплеренон, 2-га група — 72 хворих, які не приймали препаратів із групи антагоністів альдостерону. Усі хворі отримували базисну терапію. З них 87 хворим проведена тромболітична терапія. Оцінено клінічні прояви серцевої недостатності (СН), результати ЕхоКС, концентрації N-термінальної мозкової фракції натрійуретичного пропептиду (NT-pro BNP). Результати. Доведений регрес клінічної симптоматики СН, який корелював із позитивною динамікою NT-pro BNP і розмірів камер серця на фоні прийому препарату у складі комплексної терапії ГІМ. Крім того, на фоні тривалого систематичного прийому еплеренону відзначена достовірна позитивна динаміка прогностичних маркерів перебігу післяінфарктного періоду у досліджуваних пацієнтів. Висновки. Застосування еплеренону спричинює гальмування процесів ремоделяції ЛШ у хворих на ГІМ, сприяє контролю об’єму рідини, що зумовлює зменшення та поступовий регрес проявів СН навіть після перенесеної ГЛШН.

Contextualizing the FHN Nocturnal Trial a Decade Later: How Nocturnal Home Hemodialysis Is Performed Matters to Outcomes.

Long, frequent hemodialysis (HD) was thought to be a sound treatment because of improved clearance of uremic toxins and control of extracellular fluid volume. After all, no solute or volume control is tantamount to no dialysis, and whatever its shortcomings, dialysis does keep people alive. The

Temporal changes in dialysate [Na+] prescription from 1996 to 2018 and their clinical significance as judged from a meta‐regression of clinical trials

Over the last two decades, the clinical care of dialysis patients has refocused sharply on fluid volume control. Dialysate [Na+] is a key, albeit under-investigated, clinical tool for manipulation of fluid volume on dialysis. In the article, we firstly use data from the Dialysis Outcomes and Practice Patterns Study to document the global decrease in dialysate [Na+] that has occurred from 1996 to 2018, and demonstrate the virtual disappearance of [Na+] profiling from routine dialysis practice over the same period. Second, we used data from previously synthesized randomized clinical trial evidence combined with that of a more recently published trail to assess the clinical significance of these changes, estimating the effects of different levels of low dialysate [Na+] on key clinical outcomes. Our analyses suggest that current levels of dialysate [Na+] in some health jurisdictions are possibly causing harm to many patients, especially given that real world populations are significantly less robust and more vulnerable than clinical trial ones. To quote a recent editorial, "more evidence needed before lower dialysate sodium concentrations can be recommended." That evidence is coming, and no further changes should be made to default customary practice until it is available.

Cardiovascular Benefits of Extended-Time Nocturnal Hemodialysis.

Hemodialysis (HD) remains the most utilized treatment for End-Stage Kidney Disease (ESKD) globally, mainly as conventional HD administered in 4 h sessions thrice weekly. Despite advances in HD delivery, patients with ESKD carry a heavy cardiovascular morbidity and mortality burden. This is associated with cardiac remodeling, left ventricular hypertrophy (LVH), myocardial stunning, hypertension, decreased heart rate variability, sleep apnea, coronary calcification and endothelial dysfunction. Therefore, intensive HD regimens closer to renal physiology were developed. They include longer, more frequent dialysis or both. Among them, Nocturnal Hemodialysis (NHD), carried out at night while asleep, provides efficient dialysis without excessive interference with daily activities. This regimen is closer to the physiology of the native kidneys. By providing increased clearance of small and middle molecular weight molecules, NHD can ameliorate uremic symptoms, control hyperphosphatemia and improve quality of life by allowing a liberal diet and free time during the day. Lastly, it improves reproductive biology leading to successful pregnancies. Conversion from conventional to NHD is followed by improved blood pressure control with fewer medications, regression of LVH, improved LV function, improved sleep apnea, and stabilization of coronary calcifications. These beneficial effects have been associated, among others, with better extracellular fluid volume control, improved endothelial- dependent vasodilation, decreased total peripheral resistance, decreased plasma norepinephrine levels and restoration of heart rate variability. Some of these effects represent improvements in outcomes used as surrogates of hard outcomes related to cardiovascular morbidity and mortality. In this review, we consider the cardiovascular effects of NHD.

HEART REMODELING, TREATMENT OF MYOCARDIAL INFARCTION WITH DIABETES MELLITUS 2ND TYPE AND HEART FAILURE

Scientific 42 articles were analyzed, which for analysis were taken from scientometric databases: Web of Science, Scopus, PubMed, Medline, on topics related to: heart remodeling, treatment of myocardial infarction with type 2 diabetes mellitus and heart failure. Analysis of current medical studies and the data obtained indicate both availability in the usage of new HF biological markers - suppressor of tumorigenesis 2 (ST2), and the efficiency in the use of antagonists of miniralocorticoid receptors and sodium-glucose linked transporter-2 inhibitors, which is complicated by HF and type 2 diabetes by slowing down the processes of LV myocardial remodeling, which promotes control of blood pressure and fluid volume and causes a decrease and gradual regression of HF regardless of its origin.

Hipertensión arterial y riñón

Cardiac output and peripheral resistances are the arterial blood pressure determinants. Kidney, through complex mechanisms, acts on both. Thus, cardiac output is modify by the kidney's capacity for the control of extracellular fluid volume, adjusting urinary sodium and water excretion. On the other hand, kidney works on peripheral resistances by the synthesis of vasoconstrictors and vasodilators which modulate both vascular wall tone and structure. In current update the main kidney mechanisms involved on arterial blood pressure modulation, will be reviewed; emphasizing those having more importance in conditions associated with hypertension. Knowing them we will understand the mechanism of action of hypotensive drugs.

The Rational Use of Diuretics in the Management of Cirrhotic Ascites in Japan

In cirrhosis, portal hypertension and hypoalbuminemia due to decreased albumin synthetic capacity and hormonal imbalance due to increased renin-angiotensin-aldosterone and vasopressin systems cause fluid retention and electrolyte abnormalities. Diuretics are indispensable for the control of body fluid volume in liver cirrhosis, and aldosterone antagonists and loop diuretics have been widely used until now. In Japan, tolvaptan, a vasopressin V2 receptor antagonists, became available in September 2013, expanding treatment options. This drug has been reported to be effective in improving hyponatremia and ascites in combination with aldosterone antagonists and loop diuretics without markedly affecting renal function. Excessive diuretic use should be avoided because it can cause deterioration of the renal function, which influences the vital prognosis of liver cirrhosis. Therefore, it is important to choose the appropriate diuretics to protect of the renal function.

Increased Frequency of In-Center Hemodialysis as Rescue Therapy: Impact on Hospitalization for Acute Cardiovascular Events

Background: The intermittency of conventional hemodialysis (HD) leads to an increase in cardiovascular events. Objective: We aimed to evaluate the effect of in-center frequent HD (FHD, 4–6 times a week) as a rescue option for cardiovascular events. Method: Patients who failed to achieve fluid volume control with conventional HD (thrice a week) were administered FHD. A total of 52 patients were divided into 2 groups by left ventricular ejection fraction (LVEF): low ejection fraction (LEF [n = 26], LVEF < 55%) and normal ejection fraction (NEF [n = 26], LVEF ≥55%). Mortality and hospitalization rates were evaluated. Results: All-cause mortality tended to be higher in the LEF than in the NEF group (p = 0.09). The 1-year hospitalization rate for acute cardiovascular events decreased in both LEF (1.24–0.89; p = 0.049) and NEF (0.36–0.16; p = 0.01) groups. In Cox regression models, LVEF < 55% (hazard ratio 3.81; 95% CI 1.15–12.66; p = 0.03) was identified as the risk factor for hospitalization for acute cardiovascular events. Conclusion: In-center FHD may decrease acute cardiovascular events.

Role of AMPA and NMDA receptors on vasopressin and oxytocin secretion induced by hypertonic extracellular volume expansion.

Vasopressin (AVP) and oxytocin (OT) are essential for the control of extracellular fluid osmolality and volume. Secretion of these hormones is modulated by several mechanisms, including NMDA and AMPA L-glutamate receptors in magnocellular cells of paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei. Thus, to better understand the participation of L-glutamate on the neuroendocrine control of AVP and OT, this work evaluated the effects of intracerebroventricular (icv) NMDA and AMPA receptor antagonists on plasma AVP and OT levels induced by extracellular volume expansion (EVE). Cannulated rats received icv NMDA (AP5) and AMPA (NBQX) antagonists in 10 and 30nmol/5μl/rat doses and were subjected to either isotonic (0.15 M NaCl, 2ml/100g) or hypertonic (0.30 M NaCl, 2ml/100g) EVE. Blood samples were collected for plasma AVP and OT determination. Isotonic EVE did not change plasma AVP and OT levels, but hypertonic EVE increased both AVP and OT plasma levels. AP5 reduced plasma AVP, but it did not change the OT level induced by hypertonic EVE. On the other hand, NBQX reduced plasma OT, but did not alter the AVP plasma level. Our data shows that L-glutamate controls the secretion of neurohypophyseal hormones through the NMDA receptor for AVP release, and through the AMPA receptor for OT release, both in response to hypertonic EVE. This article is protected by copyright. All rights reserved.

Pretransplant Nephrectomy for Large Polycystic Kidneys in ADPKD (Autosomal Dominant Polycystic Kidney Disease) Patients

Introduction and Background Autosomal Dominant Polycystic Kidney Disease (ADPKD) is characterized by relentless development and growth of cysts causing progressive kidney enlargement and progressive renal failure. Diuresis and fluid volume control is often preserved also during the dialytic period. Some recent studies have proposed peritoneal dialysis (PD) as a valid alternative even for ADPKD, which was once considered a relative contraindication because of the possible limited intraperitoneal space and the risk of hernia. Native kidneys are not routinely removed before transplantation in consideration of the significant morbidity and mortality associated to the procedure. Indications for nephrectomy include recurrent or severe infection, symptomatic nephrolithiasis, recurrent or severe bleeding, intractable pain, suspicion of renal cancer and space restrictions prior to transplantation. Considering that after a trans-peritoneal nephrectomy the peritoneum often results damaged and unsuitable for PD, the aim of this study is to assess if and how long after nephrectomy PD may be effectively resumed. Materials and Method A retrospective analysis of ADPKD patients in waiting list for kidney transplant which underwent nephrectomy in our trasplant surgery department between December 2012 and October 2017 was carried out. All patients were included, male and female, and the indications for nephrectomy were symptoms (pain, urinary tract infections or hematuria) or steric hindrance. In all cases the surgical procedure was performed with meticoulus technique by laparotomic access with subcostal incision with recostruction of the posterior peritoneal flap in order to preserve peritoneal cavity avoiding visceral adhesions and for future peritoneal dialysis recovery. Results and Discussion From December 2012 to October 2017 30 ADPKD patients underwent nephrectomy in our transplant surgery department. The patients were 18 (63%) males and 12 (37%) females, with a mean age of 54±8. 9 patients were in peritoneal dialysis, 19 in hemodialysis and 2 were affected by stage 5 chronic renal failure. 4 patients underwent nephrectomy after trasplantation. The indication for nephrectomy was steric hindrance in 43,3% of cases, while 56,6% of patients had symptoms (52,9% UTI, 35,3% haematuria and 11,7% pain). No complications were reported after surgery. Among patients treated with peritoneal dialysis before nephrectomy 3 underwent nephrectomy after trasplantation, 3 started hemodialysis and 3 resumed peritoneal dialysis 30 days after surgery. Conclusions Monolateral nephrectomy with a laparotomic approach seems to be a safe and feasible procedure also for very large kidneys. A meticulous technique with accurate peritoneal preservation avoids commons postsurgical complications and may allow a rapid peritoneal dialysis resume.

Integrin αV β3 can substitute for collagen-binding β1 -integrins in vivo to maintain a homeostatic interstitial fluid pressure.

New Findings What is the central question of this study? Collagen‐binding β1‐integrins function physiologically in cellular control of dermal interstitial fluid pressure (P IF) in vivo and thereby participate in control of extravascular fluid volume. During anaphylaxis, simulated by injection of compound 48/80, integrin αVβ3 takes over this physiological function. Here we addressed the question whether integrin αVβ3 can replace collagen‐binding β1‐integrin to maintain a long‐term homeostatic P IF. What is the main finding and its importance? Mice lacking the collagen‐binding integrin α11β1 show a complex dermal phenotype with regard to the interstitial physiology apparent in the control of P IF. Notably dermal P IF is not lowered with compound 48/80 in these animals. Our present data imply that integrin αVβ3 is the likely candidate that has taken over the role of collagen‐binding β1‐integrins for maintaining a steady‐state homeostatic P IF. A better understanding of molecular processes involved in control of P IF is instrumental for establishing novel treatment regimens for control of oedema formation in anaphylaxis and septic shock. Accumulated data indicate that cell‐mediated contraction of reconstituted collagenous gels in vitro can serve as a model for cell‐mediated control of interstitial fluid pressure (P IF) in vivo. A central role for collagen‐binding β1‐integrins in both processes has been established. Furthermore, integrin αVβ3 takes over the role of collagen‐binding β1‐integrins in mediating contraction after perturbations of collagen‐binding β1‐integrins in vitro. Integrin αVβ3 is also instrumental for normalization of dermal P IF that has been lowered due to mast cell degranulation with compound 48/80 (C48/80) in vivo. Here we demonstrate a role of integrin αVβ3 in maintaining a long term homeostatic dermal P IF in mice lacking the collagen‐binding integrin α11β1 (α11−/− mice). Measurements of P IF were performed after circulatory arrest. Furthermore, cell‐mediated integrin αVβ3‐directed contraction of collagenous gels in vitro depends on free access to a collagen site known to bind several extracellular matrix (ECM) proteins that form substrates for αVβ3‐directed cell attachment, such as fibronectin and fibrin. A streptococcal collagen‐binding protein, CNE, specifically binds to and blocks this site on the collagen triple helix. Here we show that whereas CNE perturbed αVβ3‐directed and platelet‐derived growth factor BB‐induced normalization of dermal P IF after C48/80, it did not affect αVβ3‐dependent maintenance of a homeostatic dermal P IF. These data imply that dynamic modification of the ECM structure is needed during acute patho‐physiological modulations of P IF but not for long‐term maintenance of a homeostatic P IF. Our data thus show that collagen‐binding β1‐integrins, integrin αVβ3 and ECM structure are potential targets for novel therapy aimed at modulating oedema formation and hypovolemic shock during anaphylaxis.

Factors associated with reduction of left ventricular mass in children on peritoneal dialysis.

This study aimed to investigate sensitive factors involved in left ventricular mass reduction in children with end-stage renal disease (ESRD) undergoing peritoneal dialysis. Thirty-five subjects on peritoneal dialysis were enrolled. Two successive echocardiographic and clinical data for each subject were obtained. Blood pressure and left ventricular mass index (LVMI) were indexed through a division with the normal 95th percentile value. Differences in numeric data between two datasets were calculated. The mean age was 12.9±4.6years. Predictors of left ventricular hypertrophy and its persistence were systolic blood pressure index (P=0.019 and P=0.046) and E' velocity (P=0.035 and P=0.031) in univariate analysis. However, differences in these predictors between the datasets were not related to the change in indexed LVMI. Reduction in indexed LVMI was correlated to a reduction of indexed left atrial volume (R=0.638, P=0.001), trans-mitral A velocity (R=0.443, P=0.011), and serum blood urea nitrogen level (R=0.372, P=0.028) and an elevation of haemoglobin level (R=-0.374, P=0.027). The extent of circulating volume expansion is potentially the main predictive factor for change of LVMI, because the volume dependent diastolic functional variables correlate to the change of LVMI. Further study with a large number of ESRD children including a group under fluid volume control is needed to investigate the role of volume expansion on the change of LVMI.