scholarly journals Effects of acid aspiration-induced acute lung injury on kidney function

2008 ◽  
Vol 294 (4) ◽  
pp. F900-F908 ◽  
Author(s):  
Jeffrey B. Hoag ◽  
Manchang Liu ◽  
R. Blaine Easley ◽  
Martin F. Britos-Bray ◽  
Priya Kesari ◽  
...  

Acute lung injury (ALI) in combination with acute kidney injury carries a mortality approaching 80% in the intensive care unit. Recently, attention has focused on the interaction of the lung and kidney in the setting of ALI and mechanical ventilation (MV). Small animal models of ALI and MV have demonstrated changes in inflammatory mediators, water channels, apoptosis, and function in the kidney early in the course of injury. The purpose of this investigation was to test the hypothesis that ALI and injurious MV cause early, measurable changes in kidney structure and function in a canine HCl aspiration model of ALI when hemodynamics and arterial blood gas tensions are carefully controlled. Intratracheal HCl induced profound ALI as demonstrated by increased shunt fraction and airway pressures compared with sham injury. Sham-injured animals had similar mean arterial pressure and arterial Pco2 and HCO3 levels compared with injured animals. Measurements of renal function including renal blood flow, urine flow, serum creatinine, glomerular filtration rate, urine albumin-to-creatinine ratio, and kidney histology scores were not different between groups. With maintenance of hemodynamic parameters and alveolar ventilation, ALI and injurious MV do not alter kidney structure and function early in the course of injury in this acid aspiration canine model. Kidney injury in large animal models may be more similar to humans and may differ from results seen in small animal models.

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Ryan McGinn ◽  
Dean A. Fergusson ◽  
Duncan J. Stewart ◽  
Arnold S. Kristof ◽  
Carly C. Barron ◽  
...  

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Peter Nordbeck ◽  
Leoni Bönhof ◽  
Karl-Heinz Hiller ◽  
Sabine Voll ◽  
Paula Arias ◽  
...  

Background: Surgical procedures in small animal models of heart disease, such as artificial ligation of the coronary arteries for experimental myocardial infarction, can evoke alterations in cardiac morphology and function. Such alterations might induce artificial early or long term effects in vivo that might account for a significant bias in basic cardiovascular research, and, therefore, could potentially question the meaning of respective studies in small animal models of heart disease. Methods: Female Wistar rats were matched for weight and distributed to sham left coronary artery ligation or untreated control. Cardiac parameters were then investigated in vivo by high-field MRI over time after the surgical procedure, determining left and right ventricular morphology and function. Additionally, the time course of several metabolic and inflammatory blood parameters was determined. Results: Rats after sham surgery showed a lower body weight for up to 8 weeks after the intervention compared to healthy controls. Left and right ventricular morphology and function were not different in absolute measures in both groups 1 week after surgery. However, there was a confined difference in several cardiac parameters normalized to the body weight (bw), such as myocardial mass (2.19±0.30/0.83±0.13 vs. 1.85±0.22/0.70±0.07 mg left/right per g bw, p<0.05), or enddiastolic ventricular volume (1.31±0.36/1.21±0.31 vs. 1.14±0.20/1.07±0.17 µl left/right per g bw, p<0.05). Vice versa, after 8 weeks, cardiac masses, volumes, and output showed a trend for lower values in the sham operated rats compared to the controls in absolute measures (782.2±57.2/260.2±33.2 vs. 805.9±84.8/310.4±48.5 mg, p<0.05 for left/right ventricular mass), but not normalized to body weight. Matching these findings, blood testing revealed prolonged metabolic and inflammatory changes after surgery not related to cardiac disease. Conclusion: There is a small distinct impact of cardio-thoracic surgical procedures on the global integrity of the organism, which in the long term also includes circumscribed repercussions on cardiac morphology and function. This impact has to be considered when analyzing data from respective studies and transferring the findings to conditions in patients.


2008 ◽  
Vol 295 (3) ◽  
pp. L379-L399 ◽  
Author(s):  
Gustavo Matute-Bello ◽  
Charles W. Frevert ◽  
Thomas R. Martin

Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.


PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e68275 ◽  
Author(s):  
Peter Nordbeck ◽  
Leoni Bönhof ◽  
Karl-Heinz Hiller ◽  
Sabine Voll ◽  
Paula Arias-Loza ◽  
...  

2004 ◽  
Vol 30 (5) ◽  
pp. 641-650 ◽  
Author(s):  
Amiya K. Panda ◽  
Kaushik Nag ◽  
Robert R. Harbottle ◽  
Karina Rodriguez-Capote ◽  
Ruud A. W. Veldhuizen ◽  
...  

2019 ◽  
Vol 316 (6) ◽  
pp. F1227-F1235 ◽  
Author(s):  
Yu Qi Lee ◽  
Emma L. Beckett ◽  
Dean V. Sculley ◽  
Kym M. Rae ◽  
Clare E. Collins ◽  
...  

Maternal undernutrition during pregnancy is prevalent across the globe, and the origins of many chronic diseases can be traced back to in utero conditions. This systematic review considers the current evidence in animal models regarding the relationship between maternal global nutrient restriction during pregnancy and offspring kidney structure and function. CINAHL, Cochrane, EMBASE, MEDLINE, and Scopus were searched to November 2017. Preferred Reporting Items for Systematic Reviews and Meta-analysis guidelines were followed, and articles were screened by two independent reviewers. Twenty-eight studies met the inclusion criteria: 16 studies were on rats, 9 on sheep, 2 on baboons, and 1 on goats. The majority of the rat studies had maternal global nutrient restriction during pregnancy at 50% of ad libitum while restriction for sheep and baboon studies ranged from 50% to 75%. Because of the heterogeneity of outcome measures and the large variation in the age of offspring at followup, no meta-analysis was possible. Common outcome measures included kidney weight, nephron number, glomerular size, glomerular filtration rate, and creatinine clearance. To date, there have been no studies assessing kidney function in large animal models. Most studies were rated as having a high or unknown risk of bias. The current body of evidence in animals suggests that exposure to maternal global nutrient restriction during pregnancy has detrimental effects on offspring kidney structure and function, such as lower kidney weight, lower nephron endowment, larger glomerular size, and lower glomerular filtration rate. Further long-term followup of studies in large animal models investigating kidney function through to adulthood are warranted.


2021 ◽  
Vol 8 (1) ◽  
pp. e000879
Author(s):  
Premila Devi Leiphrakpam ◽  
Hannah R Weber ◽  
Tobi Ogun ◽  
Keely L Buesing

BackgroundAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a lethal disease with limited therapeutic options and an unacceptably high mortality rate. Understanding the complex pathophysiological processes involved in the development of ALI/ARDS is critical for developing novel therapeutic strategies. Smoke inhalation (SI) injury is the leading cause of morbidity and mortality in patients with burn-associated ALI/ARDS; however, to our knowledge few reliable, reproducible models are available for pure SI animal model to investigate therapeutic options for ALI/ARDS without the confounding variables introduced by cutaneous burn or other pathology.ObjectiveTo develop a small animal model of pure SI-induced ALI and to use this model for eventual testing of novel therapeutics for ALI.MethodsRats were exposed to smoke using a custom-made smoke generator. Peripheral oxygen saturation (SpO2), heart rate, arterial blood gas, and chest X-ray (CXR) were measured before and after SI. Wet/dry weight (W/D) ratio, lung injury score and immunohistochemical staining of cleaved caspase 3 were performed on harvested lung tissues of healthy and SI animals.ResultsThe current study demonstrates the induction of ALI in rats after SI as reflected by a significant, sustained decrease in SpO2 and the development of diffuse bilateral pulmonary infiltrates on CXR. Lung tissue of animals exposed to SI showed increased inflammation, oedema and apoptosis as reflected by the increase in W/D ratio, injury score and cleaved caspase 3 level of the harvested tissues compared with healthy animals.ConclusionWe have successfully developed a small animal model of pure SI-induced ALI. This model is offered to the scientific community as a reliable model of isolated pulmonary SI-induced injury without the confounding variables of cutaneous injury or other systemic pathology to be used for study of novel therapeutics or other investigation.


Sign in / Sign up

Export Citation Format

Share Document