Introduction: Acute hemorrhage results in perfusion deficit and regional hypoxia. Since failure of intestinal integrity seem to be the linking element between hemorrhage, delayed multi organ failure, and mortality, it is crucial to maintain intestinal microcirculation in acute hemorrhage. During critical bleeding physicians increase FiO to raise total blood oxygen content. Likewise, a systemic hypercapnia was reported to maintain microvascular oxygenation (μHbO). Both, O and CO, may have adverse effects when applied systemically that might be prevented by local application. Therefore, we investigated the effects of local hyperoxia and hypercapnia on the gastric and oral microcirculation.
Methods: Six female foxhounds were anaesthetized, randomized into eight groups and tested in a cross-over design. The dogs received a local CO-, O-, or N-administration to their oral and gastric mucosa. Hemorrhagic shock was induced through a withdrawal of 20% of estimated blood volume followed by retransfusion 60 min later. In control groups no shock was induced. Reflectance spectrophotometry and laser Doppler were performed at the gastric and oral surface. Oral microcirculation was visualized by incident dark field imaging. Systemic hemodynamic parameters were recorded continuously. Statistics were performed using a two-way-ANOVA for repeated measurements and analysis was conducted by Bonferroni testing ( < 0.05).
Results: The gastric μHbO decreased from 76 ± 3% to 38 ± 4% during hemorrhage in normocapnic animals. Local hypercapnia ameliorated the decrease of μHbO from 78 ± 4% to 51 ± 8%. Similarly, the oral μHbO decreased from 81 ± 1% to 36 ± 4% under hemorrhagic conditions and was diminished by local hypercapnia (54 ± 4%). The oral microvascular flow quality but not the total microvascular blood flow was significantly improved by local hypercapnia. Local O-application failed to change microvascular oxygenation, perfusion or flow quality. Neither CO nor O changed microcirculatory parameters and macrocirculatory hemodynamics under physiological conditions.
Discussion: Local hypercapnia improved microvascular oxygenation and was associated with a continuous blood flow in hypercapnic individuals undergoing hemorrhagic shock. Local O application did not change microvascular oxygenation, perfusion and blood flow profiles in hemorrhage. Local gas application and change of microcirculation has no side effects on macrocirculatory parameters.
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http://dx.doi.org/10.3389/fmed.2022.867298 | DOI Listing |
J Transl Med
December 2024
Institut de Recherche Biomédicale Des Armées (IRBA), 1, Rue du Lieutenant Raoul Batany, 92141, Clamart, France.
Background: Hemorrhagic shock (HS) corresponds to absolute hypovolemia creating an imbalance between oxygen supply and consumption. This causes an impaired hemostasis, a systemic inflammatory response, and microvascular permeability which can lead to multiple organ failure (MOF). There is no specific treatment for the endothelial dysfunction that plays a major role in the evolution towards MOF.
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December 2024
Department of Encephalopathy, Shenzhen Luohu Hospital of Traditional Chinese Medicine, Shenzhen, Guangdong 518000, China; Department of Encephalopathy, Shenzhen Hospital of Shanghai University of Traditional Chinese Medicine, Shenzhen, Guangdong 518000, China. Electronic address:
Ischaemic stroke is one of the major diseases affecting human health, involving complex and diverse pathological mechanisms, including inflammatory response, oxidative stress and angiogenesis. Sodium ferulate (SF) exerts a protective effect on cerebral ischaemia/reperfusion and when combined with bone marrow mesenchymal stem cells (BMSCs), has a considerable therapeutic effect on brain injury in rats. Here, we speculate that SF also exerts cerebroprotective effects.
View Article and Find Full Text PDFExp Neurol
December 2024
Department of Neurology, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Chuoku, Niigata 951-8585, Japan. Electronic address:
Background: Despite advances in reperfusion therapies, ischemic stroke remains a major cause of long-term disability due to residual hypoxic lesions persisting after macrovascular reperfusion. These residual hypoxic lesions, caused by microvascular dysfunction, represent an important therapeutic target. We previously demonstrated that oxygen-glucose-deprived peripheral blood mononuclear cells (OGD-PBMCs) migrate to ischemic brain regions and promote functional recovery after stroke.
View Article and Find Full Text PDFNeurobiol Dis
December 2024
Department of Bioengineering, University of Maryland, College Park, MD 20742, United States of America. Electronic address:
Niemann Pick Disease Type C (NP-C), a rare neurogenetic disease with no known cure, is caused by mutations in the cholesterol trafficking protein NPC1. Brain microvascular endothelial cells (BMEC) are thought to play a critical role in the pathogenesis of several neurodegenerative diseases; however, little is known about how these cells are altered in NP-C. In this study, we investigated how NPC1 inhibition perturbs BMEC metabolism in human induced pluripotent stem cell-derived BMEC (hiBMEC).
View Article and Find Full Text PDFMedicine (Baltimore)
December 2024
Department of Neurology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Emergency intravascular interventional therapy is the most effective approach to rapidly restore blood flow and manage occlusion of major blood vessels during the initial phase of acute ischemic stroke. Nevertheless, several patients continue to experience ineffective reperfusion or cerebral no-reflow phenomenon, that is, hypoperfusion of cerebral blood supply after treatment. This is primarily attributed to downstream microcirculation disturbance.
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