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Neurocritical Care Aug 2023Aneurysmal subarachnoid hemorrhage is a medical emergency that necessitates direct transfer to a tertiary referral center specialized in the diagnosis and treatment of...
Aneurysmal subarachnoid hemorrhage is a medical emergency that necessitates direct transfer to a tertiary referral center specialized in the diagnosis and treatment of this condition. The initial hours after aneurysmal rupture are critical for patients with aneurysmal subarachnoid hemorrhage, both in terms of rebleeding and combating the effect of early brain injury. No good treatment options are available to reduce the risk of rebleeding before aneurysm occlusion. Lowering the blood pressure may reduce the risk of rebleeding but carries a risk of inducing delayed cerebral ischemia or aggravating the consequences of early brain injury. Early brain injury after aneurysmal rupture has an important effect on final clinical outcome. Proper cerebral perfusion is pivotal in these initial hours after aneurysmal rupture but threatened by complications such as neurogenic pulmonary edema and cardiac stunning, or by acute hydrocephalus, which may necessitate early drainage of cerebrospinal fluid.
Topics: Humans; Subarachnoid Hemorrhage; Intracranial Aneurysm; Hydrocephalus; Brain Ischemia
PubMed: 37344653
DOI: 10.1007/s12028-023-01757-7 -
Multimedia Manual of Cardiothoracic... Sep 2023This case presents a Commando procedure with posterior atrioventricular groove reconstruction in a patient after double-valve replacement performed in another hospital...
This case presents a Commando procedure with posterior atrioventricular groove reconstruction in a patient after double-valve replacement performed in another hospital with a posterior atrioventricular groove patch due to mitral annular calcification for aortomitral Streptococcus agalactiae endocarditis. The patient was transferred to our institution on postoperative day 6 under femoro-axillary venoarterial extracorporeal membrane oxygenation with cardiogenic shock and pulmonary oedema due to patch dehiscence and severe periprosthetic mitral leak. To control pulmonary oedema and decrease myocardial tension, left atrial venting was performed in the intensive care unit through a redo sternotomy. After 24 hours, repeat reconstruction surgery was performed after improvement of pulmonary infiltrates and contractility. We alternate operative images with a porcine wet-lab model to facilitate understanding of this advanced reconstruction.
Topics: Humans; Animals; Swine; Pulmonary Edema; Heart Atria; Heart Diseases; Shock, Cardiogenic; Atrial Appendage
PubMed: 37707308
DOI: 10.1510/mmcts.2023.062 -
Journal of Investigative Surgery : the... Dec 2023Septic patients are especially vulnerable to acute lung injury (ALI). Calycosin (CAL) has various promising pharmacological activities. This paper aims to expound on...
Septic patients are especially vulnerable to acute lung injury (ALI). Calycosin (CAL) has various promising pharmacological activities. This paper aims to expound on the role of CAL in mice with sepsis-induced ALI and the associated mechanisms. Mouse models of sepsis-induced ALI were established using lipopolysaccharide (LPS). Pulmonary histopathological changes were observed by HE staining. Cell apoptosis was assessed by TUNEL staining. Pulmonary edema was evaluated by measuring wet/dry weight. Bronchoalveolar lavage fluid (BALF) was collected to count inflammatory cells. In vitro LPS models were established using MLE-12 cells. expression was determined by RT-qPCR. Cell viability and apoptosis were assessed by MTT assay and flow cytometry. Levels of inflammatory cytokines were determined by ELISA. The target relationship between and ROCK2 was analyzed by the dual-luciferase assay. ROCK2 protein level was determined by Western blot. was weakly-expressed in mice with sepsis-induced ALI, and CAL treatment elevated expression. CAL treatment mitigated pulmonary tissue damage and edema, decreased apoptosis and inflammatory cells, downregulated levels of pro-inflammatory cytokines, and upregulated levels of anti-inflammatory cytokines in mice with sepsis-induced ALI. CAL treatment increased MLE-12 cell viability and decreased apoptosis and inflammation in MLE-12 cells. Inhibition of partially abrogated CAL-mediated protective action on MLE-12 cells. attenuated LPS-induced MLE-12 cell injury by targeting ROCK2. CAL upregulates to target ROCK2, thus protecting against sepsis-induced ALI in mice.
Topics: Mice; Animals; Lipopolysaccharides; Acute Lung Injury; MicroRNAs; Cytokines; Sepsis
PubMed: 37400250
DOI: 10.1080/08941939.2023.2211166 -
Global Cardiology Science & Practice Aug 2023Lung transplantation volumes and survival rates continue to increase worldwide. Primary graft dysfunction (PGD) and acute kidney injury (AKI) are common early... (Review)
Review
Lung transplantation volumes and survival rates continue to increase worldwide. Primary graft dysfunction (PGD) and acute kidney injury (AKI) are common early postoperative complications that significantly affect short-term mortality and long-term outcomes. These conditions share overlapping risk factors and are driven, in part, by circulatory derangements. The prevalence of severe PGD is up to 20% and is the leading cause of early death. Patients with pulmonary hypertension are at a higher risk. Prevention and management are based on principles learned from acute lung injury of other causes. Targeting the lowest effective cardiac filling pressure will reduce alveolar edema formation in the setting of increased pulmonary capillary permeability. AKI is reported in up to one-half of lung transplant recipients and is strongly associated with one-year mortality as well as long-term chronic kidney disease. Optimization of renal perfusion is critical to reduce the incidence and severity of AKI. In this review, we highlight key early post-transplant pulmonary, circulatory, and renal perturbations and our center's management approach.
PubMed: 37575284
DOI: 10.21542/gcsp.2023.18 -
Frontiers in Pharmacology 2023Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening lung diseases with high mortality rates, predominantly attributable to acute...
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening lung diseases with high mortality rates, predominantly attributable to acute and severe pulmonary inflammation. Lomerizine (LMZ) is a calcium channel blocker previously used in preventing and treating migraine. Here, we found that LMZ inhibited inflammatory responses and lung pathological injury by reducing pulmonary edema, neutrophil infiltration and pro-inflammatory cytokine production in lipopolysaccharide (LPS)-induced ALI mice. In experiments, upon treating with LMZ, the expression of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was attenuated in macrophages. The phosphorylation of p38 MAPK, ERK1/2, JNK, and NF-κB p65 was inhibited after LMZ treatment. Furthermore, LPS-induced Ca influx was reduced by treating with LMZ, which correlated with inhibition of pro-inflammatory cytokine production. And L-type Ca channel agonist Bay K8644 (BK) could restore cytokine generation. In conclusion, our study demonstrated that LMZ alleviates LPS-induced ALI and is a potential agent for treating ALI/ARDS.
PubMed: 37693893
DOI: 10.3389/fphar.2023.1236469 -
Proceedings of the National Academy of... Oct 2023parasites cause malaria with disease outcomes ranging from mild illness to deadly complications such as severe malarial anemia (SMA), pulmonary edema, acute renal...
parasites cause malaria with disease outcomes ranging from mild illness to deadly complications such as severe malarial anemia (SMA), pulmonary edema, acute renal failure, and cerebral malaria. In young children, SMA often requires blood transfusion and is a major cause of hospitalization. Malaria parasite infection leads to the destruction of infected and noninfected erythrocytes as well as dyserythropoiesis; however, the mechanism of dyserythropoiesis accompanied by splenomegaly is not completely understood. Using 17XNL as a model, we show that both a defect in erythroblastic island (EBI) macrophages in supporting red blood cell (RBC) maturation and the destruction of reticulocytes/RBCs by the parasites contribute to SMA and splenomegaly. After malaria parasite infection, the destruction of both infected and noninfected RBCs stimulates extramedullary erythropoiesis in mice. The continuous decline of RBCs stimulates active erythropoiesis and drives the expansion of EBIs in the spleen, contributing to splenomegaly. Phagocytosis of malaria parasites by macrophages in the bone marrow and spleen may alter their functional properties and abilities to support erythropoiesis, including reduced expression of the adherence molecule CD169 and inability to support erythroblast differentiation, particularly RBC maturation in vitro and in vivo. Therefore, macrophage dysfunction is a key mechanism contributing to SMA. Mitigating and/or alleviating the inhibition of RBC maturation may provide a treatment strategy for SMA.
Topics: Child; Humans; Animals; Mice; Child, Preschool; Erythropoiesis; Plasmodium yoelii; Splenomegaly; Anemia; Erythrocytes; Malaria, Cerebral; Macrophages
PubMed: 37748059
DOI: 10.1073/pnas.2311557120 -
Revista Brasileira de Enfermagem 2023to develop a nursing diagnosis proposal focused on venous return. (Review)
Review
OBJECTIVES
to develop a nursing diagnosis proposal focused on venous return.
METHODS
this is a concept analysis according to the model proposed by Walker and Avant, which is operationalized through an integrative review. The study was carried out according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses protocol recommendations.
RESULTS
the analysis of the 131 studies allowed identifying attributes, antecedents and consequences. The most common attribute was decreased venous flow. The antecedents most frequently found were structural and/or functional valve deficiency, advanced age and peripheral venous thrombosis. The most common consequences were peripheral edema, venous ulcer and pain in the extremity.
CONCLUSIONS
the formulated nursing diagnosis was proposed as part of Domain 4, Activity/rest, in Class 4, Cardiovascular/pulmonary responses, with eight defining characteristics, five related factors, six at-risk populations and four associated conditions.
Topics: Humans; Nursing Diagnosis; Concept Formation
PubMed: 38018610
DOI: 10.1590/0034-7167-2022-0426 -
Frontiers in Physiology 2023High altitude exposure may lead to high altitude pulmonary hypertension (HAPH) and high altitude pulmonary edema (HAPE). The pathophysiologic processes of both entities...
High altitude exposure may lead to high altitude pulmonary hypertension (HAPH) and high altitude pulmonary edema (HAPE). The pathophysiologic processes of both entities have been linked to decreased nitric oxide (NO) availability. We studied the effect of acute high altitude exposure on the plasma concentrations of asymmetric (ADMA) and symmetric dimethylarginine (SDMA), L-arginine, L-ornithine, and L-citrulline in two independent studies. We further investigated whether these biomarkers involved in NO metabolism were related to HAPH and HAPE, respectively. Fifty (study A) and thirteen (study B) non-acclimatized lowlanders were exposed to 4,559 m for 44 and 67 h, respectively. In contrast to study A, the participants in study B were characterized by a history of at least one episode of HAPE. Arterial blood gases and biomarker concentrations in venous plasma were assessed at low altitude (baseline) and repeatedly at high altitude. HAPE was diagnosed by chest radiography, and HAPH by measuring right ventricular to atrial pressure gradient (RVPG) with transthoracic echocardiography. AMS was evaluated with the Lake Louise Score (LLS) and the AMS-C score. In both studies SDMA concentration significantly increased at high altitude. ADMA baseline concentrations were higher in individuals with HAPE susceptibility (study B) compared to those without (study A). However, upon high altitude exposure ADMA only increased in individuals without HAPE susceptibility, while there was no further increase in those with HAPE susceptibility. We observed an acute and transient decrease of L-ornithine and a more delayed but prolonged reduction of L-citrulline during high altitude exposure. In both studies SDMA positively correlated and L-ornithine negatively correlated with RVPG. ADMA was significantly associated with the occurrence of HAPE (study B). ADMA and SDMA were inversely correlated with alveolar PO, while L-ornithine was inversely correlated with blood oxygenation and haemoglobin levels, respectively. In non-acclimatized individuals ADMA and SDMA, two biomarkers decreasing endothelial NO production, increased after acute exposure to 4,559 m. The observed biomarker changes suggest that both NO synthesis and arginase pathways are involved in the pathophysiology of HAPH and HAPE.
PubMed: 38093907
DOI: 10.3389/fphys.2023.1297636 -
Respiratory Research Apr 2024The success of lung transplantation is limited by the high rate of primary graft dysfunction due to ischemia-reperfusion injury (IRI). Lung IRI is characterized by a... (Review)
Review
The success of lung transplantation is limited by the high rate of primary graft dysfunction due to ischemia-reperfusion injury (IRI). Lung IRI is characterized by a robust inflammatory response, lung dysfunction, endothelial barrier disruption, oxidative stress, vascular permeability, edema, and neutrophil infiltration. These events are dependent on the health of the endothelium, which is a primary target of IRI that results in pulmonary endothelial barrier dysfunction. Over the past 10 years, research has focused more on the endothelium, which is beginning to unravel the multi-factorial pathogenesis and immunologic mechanisms underlying IRI. Many important proteins, receptors, and signaling pathways that are involved in the pathogenesis of endothelial dysfunction after IR are starting to be identified and targeted as prospective therapies for lung IRI. In this review, we highlight the more significant mediators of IRI-induced endothelial dysfunction discovered over the past decade including the extracellular glycocalyx, endothelial ion channels, purinergic receptors, kinases, and integrins. While there are no definitive clinical therapies currently available to prevent lung IRI, we will discuss potential clinical strategies for targeting the endothelium for the treatment or prevention of IRI. The accruing evidence on the essential role the endothelium plays in lung IRI suggests that promising endothelial-directed treatments may be approaching the clinic soon. The application of therapies targeting the pulmonary endothelium may help to halt this rapid and potentially fatal injury.
Topics: Humans; Lung; Reperfusion Injury; Endothelium; Lung Transplantation; Lung Injury
PubMed: 38637760
DOI: 10.1186/s12931-024-02776-4