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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
When clinicians refer to body fluid, they mean body water content. Sometimes, the terms body fluid volume and body volume are also used (e.g. ‘volume contracted’ or ‘volume overloaded’). Body water consists of water in cells (intracellular fluid) and water outside cells (extracellular fluid).Extracellular fluid consists of water in the circulation or vascular compartment (intravascular fluid) and water in the tissues or interstitial or extravascular compartment (extravascular fluid).Intravascular extracellular fluid is plasma.
In Vivo Observations of Tumor Blood Flow
Published in Hans-Inge Peterson, Tumor Blood Circulation: Angiogenesis, Vascular Morphology and Blood Flow of Experimental and Human Tumors, 2020
This mechanism has been studied most extensively by means of either fluid-balance (isogravimetric) methods in isolated limbs,31 or with radioisotopes (see Chapter 3). With regard to the extravascular fluid distribution in tumors, Figure 5 is of interest. Here one will note that in some areas in the tumor tissue there is a very rapid extravasation, while in others the extravasation rate is very low and resembles a physical dif-fusion process. The extravasation velocity of the fluorescent dye, as depicted in Figure 5, was found in a large number of measurements to range between 25 ¿¿m/sec to values lower than 1 jLtm/sec.10 There can be little doubt that the intensity of the extravascular fluid transport depends to a large extent on differences in intravascular pressure in the various parts of the microcirculatory network, with possibly some additional factors involved that may restrict diffusion. Such factors may be found in the permeability characteristics of the vessel wall, but the composition of the extravascular (interstitial) spaces will also be of influence. Moreover, one should consider the possibility that the rate of interstitial fluid transport may be impaired when the interstitial tissue pressure is increased. The latter will be rather high due to the proliferative properties of tumor cells, causing intratumoral expansion. For a mathematical treatise of the factors involved, see Chapter 10.
The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
The compensatory mechanisms can cope with loss of up to 25% of the blood volume. Arterioles constrict more than the venules, thereby lowering the hydrostatic pressure in the capillaries. Also, circulating cytokines cause capillary leakage (see below) and extravascular fluid enters the intravascular compartment. Tissue perfusion is, nevertheless, precarious and it is important to restore the blood volume by prompt intravenous administration of fluid. Macromolecular solutions, such as plasma or dextrans, maintain plasma osmotic pressure and retain fluid in the circulation. Blood transfusion is required when the loss exceeds 25% of blood volume. Blood pressure, haemoglobin, and haematocrit levels are poor indicators of the degree of hypovolaemia during the first 36 hours. Central venous pressure gives a more accurate indication and should be monitored in all cases of severe shock.
Effect of ondansetron for preventing of ovarian hyperstimulation syndrome: in an experimental rat model
Published in Gynecological Endocrinology, 2022
Şükrü Bakırcı, Nevin Sağsöz, Tuba Devrim, Yaşar Şahin, Murat Bulanık, Hilal Gözüyukarı
About 10–15% of couples in society have infertility problems [1]. Ovulatory disorders are identified in 18 to 25 percent of couples presenting with infertility [2]. The use of gonadotropins for ovulation induction in ovulation dysfunction has increased considerably in the last 30 years. However, ovarian hyperstimulation syndrome (OHSS), which is a serious iatrogenic complication, can develop during the use of these drugs [3]. The clinical manifestations of OHSS are massive extravascular fluid accumulation and hemoconcentration. Renal failure, hypovolemic shock, thromboembolic attacks, and adult respiratory distress syndrome (ARDS) may occur in these patients. In this syndrome, an increase in capillary permeability occurs with the secretion of vasoactive substances by the ovaries under stimulation of human chorionic gonadotropin (hCG). Agents such as hCG, Vascular endothelial growth factor (VEGF), estradiol, progesterone, renin-angiotensin system, kinin-kallikrein system, prostaglandins, cytokines, and nitric oxide have been implicated in the development of OHSS in humans [4]. OHSS occurs with ovarian hypersecretion because of increased vascular permeability (VP) due to VEGF activating vascular endothelial growth factor receptor-2 (VEGFR-2) [5]. There is no specific treatment available for OHSS. Although the pathophysiology is not fully understood, there is an increase in permeability in the peri ovarian vessels [6].
Pressure-driven accumulation of Mn-doped mesoporous silica nanoparticles containing 5-aza-2-deoxycytidine and docetaxel at tumours with a dry cupping device
Published in Journal of Drug Targeting, 2021
Yongwei Hao, Cuixia Zheng, Qingxia Song, Hongli Chen, Wenbin Nan, Lei Wang, Zhenzhong Zhang, Yun Zhang
Recently, several external devices were been reported to enhance delivery due to the disruption of the physiological barriers [6–9]. Moreover, iontophoresis, electroporation, microneedle and microwave active technologies are also promising in improving drug delivery [10–13]. Weissleder et al. suggested that local tumour irradiation with the radiation device could lead to a sixfold increase of therapeutic accumulation in the tumour because that treatment made the tumour-associated macrophages become the nanoparticle drug depots [14]. Subsequently, Jaffray et al. further demonstrated that radiation and heat could enhance the therapeutic nanoparticles transport within tumours by regulating intratumoural fluid dynamics [15]. Moreover, two studies also showed that vascular bursts could change permeability of tumour blood vessels, which resulted in improving nanoparticles delivery [16,17]. Although many devices reported previously could improve nanomedicine accumulation to tumours, these inconvenient treatments sometimes also induced adverse side effects, such as thermal damage. Recently, one research have found that greater accumulation appeared when fluid flow induced by pressure differences of less than 1 mm Hg across the tumour blood vessels walls forms [18]. However, how to make the pressure differences between circulating blood and the extravascular fluid has not been reported. Accordingly, a negative pressure drainage strategy aiming at changing the tumour perfusion as well as modulation of tumour vessel permeability for delivering therapeutic nanoparticles as much as possible was proposed here.
Multimodal Imaging of Annular Choroidal Detachment in a Patient with Vogt–Koyanagi–Harada Disease
Published in Ocular Immunology and Inflammation, 2021
Jae Hyuck Kwak, Jiwon Baek, Ho Ra
Nonetheless, pathophysiologic mechanisms that can cause choroidal detachments in uveal effusion syndrome can be applied to explain the phenomenon in the current case. Vortex vein compression was suggested as a possible mechanism of uveal effusion in nanophthalmic eyes following glaucoma filtration surgery by Schaffer in 1975.6 Choroidal detachment in uveal effusion syndrome is considered to be caused by relative obstruction of venous outflow which may cause congestion of the choriocapillaris and alter the transmural hydrostatic pressure gradient, favoring increased retention of fluid in the suprachoroidal space. Choroidal detachment in the current case may be explained as follows. First, choroidal inflammation that causes hyperpermeability of choriocapillaris in VKH may allow extravasation of fluid and albumin to the extravascular space and eventually to suprachoroidal space.3 Second, vortex vein compression might lead to increased extravascular fluid retention and choroidal detachment. Many vortex ampullae were not observed in the UWF ICGA in the current case. Mechanical compression of the vortex veins by the adjacent thickened choroid might have caused choroidal outflow obstruction. This was evidenced by dilated choroidal veins in the UWF ICGA in the current case. Hasegawa et al.4 previously reported a VKH case with choroidal detachment, and their ICGA also revealed dilated choroidal veins at inferotemporal and inferonasal quadrant.