Evaluate the role of mercury chloride in the development of toxic pulmonary edema in laboratory animals during intoxication with substances of acylating action

2021 ◽  
Vol 20 (4) ◽  
pp. 55-61
Author(s):  
Pavel G. Tolkach ◽  
Vadim A. Basharin ◽  
Sergey V. Chepur ◽  
Darya T. Sizova ◽  
Nicolay G. Vengerovich
Keyword(s):  
Pulmonary Edema ◽  
Carbonic Acid ◽  
Oxygenation Index ◽  
Laboratory Animals ◽  
Mercury Chloride ◽  
Lung Edema ◽  
Acid Base ◽  
Acid Dichloride ◽  
And Function

Relevance. Intoxication of acylate pulmonotoxicants causes disturbance of structure and function of air-blood barrier, the output of liquid in the interstitial and alveolar space and manifestation of lung edema. Aquaporins play an important role in the transportation of fluid through the alveolar-capillary membrane, including pathological conditions. Water permeability through aquaporins is blocked by mercury ions. Using mercury chloride may reduce severity of the acute lung edema after intoxication of the pulmonotoxicants. Intention. The goal is to evaluate the role of mercury dichloride in the development of toxic pulmonary edema in laboratory animals during intoxication with pulmonotoxicants with an acylating effect. Methodology. Laboratory animals (rats and rabbits) were exposed to inhalation intoxication of carbonic acid dichloride and perfluoroisobutylene at concentrations of 1,5LC50. In 30 minutes after exposure were administrated of 0,3LD50 mercury chloride to the animals subcutaneously. The oxygenation index, acid-base state, pulmonary coefficient, histological changes in lung was investigated in 6 hours after exposure. Results. It was found that intoxication with carbonic acid dichloride and perfluoroisobutylene at concentrations of 1,5LC50 led to the development of toxic pulmonary edema in rats and rabbits 6 hours following exposure. The administration mercury chloride to 30 minutes following exposure to the pulmonotoxicants under study, led to a decrease (p 0.05) in the pulmonary coefficient, an increase (p 0.05) in the oxygenation index and normalization of the acid-base state according to compared with animals receiving 0.9 % NaCl following intoxication. When conducting a histological examination, in animals treated with mercury chloride less pronounced changes in the histoarchitectonics of the lung tissue were noted. Conclusion. Considering the fact that the administration of mercury chloride to animals led to a decrease in the manifestations of pulmonary edema in animals, it was suggested that aquaporins play an important role in the pathogenesis of toxic pulmonary edema caused by intoxication with pulmonotoxicants with an acylating effect. The use of selective blockers of aquaporins (less toxic than mercury chloride) may be a new direction in the pathogenetic therapy of toxic pulmonary edema due to exposure to pulmonotoxicants.

Role of the Splanchnic Nerve and the Adrenal Medulla in the Genesis of ‘Preoptic Pulmonary Edema’

1956 ◽  
Vol 184 (2) ◽  
pp. 351-355 ◽  
Author(s):  
Frederick W. Maire ◽  
Harry D. Patton
Keyword(s):  
Body Weight ◽  
Protective Effect ◽  
Pulmonary Edema ◽  
Adrenal Medulla ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
Lung Edema ◽  
Splanchnic Nerves ◽  
Intact Rats

The pulmonary edema which follows preoptic lesions in rats is prevented by antecedent bilateral section of the splanchnic nerves. Intravenous epinephrine in doses exceeding 0.0125 mg/100 gm body weight causes fatal lung edema in rats comparable to that produced by preoptic lesions. Moreover, extracted pressor amines from rat adrenal glands cause lung edema, often fatal, when injected into the donor or into intact rats. However, adrenal demedullation does not prevent lung edema following preoptic lesions. Hence the protective effect of splanchnectomy against preoptic lesions is not wholly due to adrenal denervation. It is tentatively suggested that preoptic lung edema results from overloading of the pulmonary circuit owing to splanchnic mediated constriction of visceral venous reservoirs. Liver and spleen weights of animals dying from preoptic lung edema were significantly less than normal.

Increased cardiac output increases shunt: role of pulmonary edema and perfusion

1985 ◽  
Vol 59 (4) ◽  
pp. 1313-1321 ◽  
Author(s):  
P. H. Breen ◽  
P. T. Schumacker ◽  
J. Sandoval ◽  
I. Mayers ◽  
L. Oppenheimer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Edema ◽  
Base Line ◽  
Lung Water ◽  
Arteriovenous Fistulas ◽  
Anesthetized Dogs ◽  
The Right

In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6–29%, O2 technique) and extravascular thermal volume (ETV, 2.6–7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.

scholarly journals Sphingomyelin synthase 2 (SMS2) deficiency attenuates LPS-induced lung injury

2011 ◽  
Vol 300 (3) ◽  
pp. L430-L440 ◽  
Author(s):  
Satish Gowda ◽  
Calvin Yeang ◽  
Sunil Wadgaonkar ◽  
Fatima Anjum ◽  
Natalia Grinkina ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Lung Edema ◽  
Wild Type Littermate ◽  
Littermate Control ◽  
Sphingomyelin Synthase ◽  
Membrane Microdomain ◽  
Permeability Pulmonary Edema

Sphingomyelin synthase (SMS) catalyzes the synthesis of sphingomyelin (SM) and is required for maintenance of plasma membrane microdomain fluidity. Of the two isoforms of mammalian SMS, SMS1 is mostly present in the trans-Golgi apparatus, whereas SMS2 is predominantly found at the plasma membrane. SMS2 has a role in receptor mediated response to inflammation in macrophages, however, the role of SMS2 in vascular permeability, pulmonary edema, and lung injury have not been investigated. To define the role of SMS activation in lung injury, we utilized a lipopolysaccharide (LPS)-induced lung edema model. SMS activity was measured and correlated with the severity of lung injury. Within 4 h of LPS treatment, SMS activity was increased significantly and remained upregulated up to 24 h. Comparison of LPS-induced lung injury in SMS2 knockout (SMS2−/−) and wild-type littermate control mice showed that inflammation, cytokine induction, and lung injury were significantly inhibited in SMS2−/− mice. Our results suggest that a deficiency of SMS2 can diminish the extent of pulmonary edema and lung injury. Furthermore, we show that depletion of SMS2 was sufficient to decrease MAP kinase-JNK activation, severity of LPS-induced pulmonary neutrophil influx, and inflammation, suggesting a novel role of SMS2 activation in lung injury.

Continuous enteral nutrition attenuates pulmonary edema in rats exposed to 100% oxygen

2000 ◽  
Vol 89 (5) ◽  
pp. 1759-1765 ◽  
Author(s):  
Phillip Factor ◽  
Karen Ridge ◽  
John Alverdy ◽  
Jacob I. Sznajder
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Dry Weight ◽  
Lung Edema ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Sprague Dawley Rats ◽  
Lung Liquid ◽  
And Function ◽  
Protective Proteins

Adult rats exposed to hyperoxia develop anorexia, weight loss, and a lung injury characterized by pulmonary edema and decreased lung liquid clearance. We hypothesized that maintenance of nutrition during hyperoxia could attenuate hyperoxia-induced pulmonary edema. To test this hypothesis, we enterally fed adult male Sprague-Dawley rats via gastrostomy tubes and exposed them to oxygen (inspired O2 fraction >0.95) for 64 h. In contrast to controls, enterally fed hyperoxic animals did not lose weight and had smaller pleural effusions and wet-to-dry weight ratios (a measure of lung edema) that were not different from room air controls. Enterally fed rats exposed to hyperoxia had increased levels of mRNA for the Na+-K+-ATPase α1- and β1-subunits and glutathione peroxidase. These findings suggest that maintenance of nutrition during an oxidative lung injury reduces lung edema, perhaps by allowing for continued expression and function of protective proteins such as the Na+-K+-ATPase.

scholarly journals Structure and function of bacteriophage CBA120 ORF211 (TSP2), the determinant of phage specificity towards E. coli O157:H7

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Julia Greenfield ◽  
Xiaoran Shang ◽  
Heng Luo ◽  
Yan Zhou ◽  
Sara B. Linden ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Structure And Function ◽  
Acid Base ◽  
E Coli ◽  
Close Proximity ◽  
Catalytic Role ◽  
And Function ◽  
Branched Structure ◽  
Partner Proteins

Abstract The genome of Escherichia coli O157:H7 bacteriophage vB_EcoM_CBA120 encodes four distinct tailspike proteins (TSPs). The four TSPs, TSP1-4, attach to the phage baseplate forming a branched structure. We report the 1.9 Å resolution crystal structure of TSP2 (ORF211), the TSP that confers phage specificity towards E. coli O157:H7. The structure shows that the N-terminal 168 residues involved in TSPs complex assembly are disordered in the absence of partner proteins. The ensuing head domain contains only the first of two fold modules seen in other phage vB_EcoM_CBA120 TSPs. The catalytic site resides in a cleft at the interface between adjacent trimer subunits, where Asp506, Glu568, and Asp571 are located in close proximity. Replacement of Asp506 and Asp571 for alanine residues abolishes enzyme activity, thus identifying the acid/base catalytic machinery. However, activity remains intact when Asp506 and Asp571 are mutated into asparagine residues. Analysis of additional site-directed mutants in the background of the D506N:D571N mutant suggests engagement of an alternative catalytic apparatus comprising Glu568 and Tyr623. Finally, we demonstrate the catalytic role of two interacting glutamate residues of TSP1, located in a cleft between two trimer subunits, Glu456 and Glu483, underscoring the diversity of the catalytic apparatus employed by phage vB_EcoM_CBA120 TSPs.

Scanning electron microscopic study of collagen fibrillogenesis and extracellular compartmentalization in the chick embryo tendon

1986 ◽  
Vol 44 ◽  
pp. 208-209
Author(s):  
Grace C.H. Yang
Keyword(s):  
Chick Embryo ◽  
Extracellular Space ◽  
Fibroblast Cell ◽  
Collagen Fibrils ◽  
Electron Microscopic ◽  
Voltage Electron ◽  
Scanning Electron Microscopic Study ◽  
Microscopic Studies ◽  
And Function

The size and organization of collagen fibrils in the extracellular matrix is an important determinant of tissue structure and function. The synthesis and deposition of collagen involves multiple steps which begin within the cell and continue in the extracellular space. High-voltage electron microscopic studies of the chick embryo cornea and tendon suggested that the extracellular space is compartmentalized by the fibroblasts for the regulation of collagen fibril, bundle, and tissue specific macroaggregate formation. The purpose of this study is to gather direct evidence regarding the association of the fibroblast cell surface with newly formed collagen fibrils, and to define the role of the fibroblast in the control and the precise positioning of collagen fibrils, bundles, and macroaggregates during chick tendon development.

Role of the Cilia Membrane in Control of Microtubule Sliding

1980 ◽  
Vol 38 ◽  
pp. 612-615
Author(s):  
Edna S. Kaneshiro
Keyword(s):  
Control Mechanism ◽  
Beat Frequency ◽  
Surface Membrane ◽  
Ciliary Membrane ◽  
Ciliary Beating ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
Reversal Mechanism ◽  
And Function

It is currently believed that ciliary beating results from microtubule sliding which is restricted in regions to cause bending. Cilia beat can be modified to bring about changes in beat frequency, cessation of beat and reversal in beat direction. In ciliated protozoans these modifications which determine swimming behavior have been shown to be related to intracellular (intraciliary) Ca2+ concentrations. The Ca2+ levels are in turn governed by the surface ciliary membrane which exhibits increased Ca2+ conductance (permeability) in response to depolarization. Mutants with altered behaviors have been isolated. Pawn mutants fail to exhibit reversal of the effective stroke of ciliary beat and therefore cannot swim backward. They lack the increased inward Ca2+ current in response to depolarizing stimuli. Both normal and pawn Paramecium made leaky to Ca2+ by Triton extrac¬tion of the surface membrane exhibit backward swimming only in reactivating solutions containing greater than IO-6 M Ca2+ Thus in pawns the ciliary reversal mechanism itself is left operational and only the control mechanism at the membrane is affected. The topographic location of voltage-dependent Ca2+ channels has been identified as a component of the ciliary mem¬brane since the inward Ca2+ conductance response is eliminated by deciliation and the return of the response occurs during cilia regeneration. Since the ciliary membrane has been impli¬cated in the control of Ca2+ levels in the cilium and therefore is the site of at least one kind of control of microtubule sliding, we have focused our attention on understanding the structure and function of the membrane.

POPDC proteins and cardiac function

2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand
Keyword(s):  
Potential Role ◽  
Striated Muscle ◽  
Short Review ◽  
Effector Proteins ◽  
Muscle Disease ◽  
Disease Genes ◽  
Protein Protein Interaction ◽  
Interaction Partners ◽  
And Function

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.

Role of the 807 C/T Polymorphism of the α2 Gene in Platelet GP Ia Collagen Receptor Expression and Function

1999 ◽  
Vol 81 (06) ◽  
pp. 951-956 ◽  
Author(s):  
J. Corral ◽  
R. González-Conejero ◽  
J. Rivera ◽  
F. Ortuño ◽  
P. Aparicio ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Cell Types ◽  
Receptor Expression ◽  
Case Control Studies ◽  
Platelet Surface ◽  
Vitro Analysis ◽  
And Function ◽  
In Vitro Analysis

SummaryThe variability of the platelet GP Ia/IIa density has been associated with the 807 C/T polymorphism (Phe 224) of the GP Ia gene in American Caucasian population. We have investigated the genotype and allelic frequencies of this polymorphism in Spanish Caucasians. The T allele was found in 35% of the 284 blood donors analyzed. We confirmed in 159 healthy subjects a significant association between the 807 C/T polymorphism and the platelet GP Ia density. The T allele correlated with high number of GP Ia molecules on platelet surface. In addition, we observed a similar association of this polymorphism with the expression of this protein in other blood cell types. The platelet responsiveness to collagen was determined by “in vitro” analysis of the platelet activation and aggregation response. We found no significant differences in these functional platelet parameters according to the 807 C/T genotype. Finally, results from 3 case/control studies involving 302 consecutive patients (101 with coronary heart disease, 104 with cerebrovascular disease and 97 with deep venous thrombosis) determined that the 807 C/T polymorphism of the GP Ia gene does not represent a risk factor for arterial or venous thrombosis.

Von Willebrand disease and Weibel-Palade bodies

2010 ◽  
Vol 30 (03) ◽  
pp. 150-155 ◽  
Author(s):  
J. W. Wang ◽  
J. Eikenboom
Keyword(s):  
Platelet Adhesion ◽  
Coagulation Factor ◽  
Von Willebrand Disease ◽  
Inflammatory Factors ◽  
Limited Data ◽  
Storage Organelle ◽  
And Function ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryVon Willebrand factor (VWF) is a pivotal haemostatic protein mediating platelet adhesion to injured endothelium and carrying coagulation factor VIII (FVIII) in the circulation to protect it from premature clearance. Apart from the roles in haemostasis, VWF drives the formation of the endothelial cell specific Weibel-Palade bodies (WPBs), which serve as a regulated storage of VWF and other thrombotic and inflammatory factors. Defects in VWF could lead to the bleeding disorder von Willebrand disease (VWD).Extensive studies have shown that several mutations identified in VWD patients cause an intracellular retention of VWF. However, the effects of such mutations on the formation and function of its storage organelle are largely unknown. This review gives an overview on the role of VWF in WPB biogenesis and summarizes the limited data on the WPBs formed by VWD-causing mutant VWF.

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