Disorders of oxygenation: hypoxemia and tissue hypoxia

2022 ◽  
pp. 65-84
Author(s):  
John G. Toffaletti ◽  
Craig R. Rackley
Keyword(s):  
Tissue Hypoxia

Tissue Hypoxia and Ischemia

1978 ◽  
Vol 6 (6) ◽  
pp. 1411-1411
Author(s):  
ROY G. SPECTOR
Keyword(s):  
Tissue Hypoxia

scholarly journals Neurovascular Coupling and Epilepsy: Hemodynamic Markers for Localizing and Predicting Seizure Onset

2007 ◽  
Vol 7 (4) ◽  
pp. 91-94 ◽  
Author(s):  
Theodore H. Schwartz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurovascular Coupling ◽  
Epileptic Activity ◽  
Tissue Hypoxia ◽  
Epileptic Focus ◽  
Seizure Onset

Hemodynamic surrogates of epileptic activity are being used to map epileptic foci with PET, SPECT, and fMRI. However, there are few studies of neurovascular coupling in epilepsy. Recent data indicate that cerebral blood flow, although focally increased at the onset of a seizure, may be temporarily inadequate to meet the metabolic demands of both interictal and ictal epileptic events. Transient focal tissue hypoxia and hyperperfusion may be excellent markers for the epileptic focus and may even precede the onset of the ictal event.

The synthesis and radiolabelling of novel markers of tissue hypoxia of the iodinated azomycin nucleoside class.

1997 ◽  
Vol 39 (7) ◽  
pp. 541-557 ◽  
Author(s):  
R. F. Schneider ◽  
E. L. Engelhardt ◽  
C. C. Stobbe ◽  
M. C. Fenning ◽  
J. D. Chapman
Keyword(s):  
Tissue Hypoxia

Abstract 3680: Transfusion-Induced Tissue Hypoxia is Ameliorated by S -nitrosohemoglobin Repletion of Stored Red Blood Cells

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Diana L Diesen ◽  
Jonathan S Stamler
Keyword(s):  
Animal Models ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Tissue Oxygenation ◽  
Ex Vivo ◽  
Tissue Hypoxia ◽  
Mouse Blood ◽  
Mortality And Morbidity ◽  
Stored Blood ◽  
Related Mortality

Transfusion of stored red blood cells (RBCs) is associated with a decrease in tissue oxygenation in animal models and with increased mortality and morbidity in patients. Recent studies have demonstrated that stored RBCs are deficient in vasodilatory ability and depleted of S -nitrosohemoglobin (SNO-Hb), and that renitrosylation ex vivo can increase SNO-Hb levels and restore vasoactivity. We have examined in a mouse model the extent to which transfusion impairs tissue oxygenation and whether SNO-Hb repletion can ameliorate that impairment. We report here that transfusion of (mouse) RBCs stored for 1 day or 1 week results in tissue hypoxia that is largely prevented by SNO-Hb repletion prior to transfusion ( 1 day stored blood : % decrease in oxygenation 58+/−10% untreated vs. 92+/−0.7% SNO-Hb repleted, p<0.05, n=3– 6; 1 week stored blood : % decrease in oxygenation 66+/−10% untreated vs. 91+/−2.8% SNO-Hb repleted, p<0.05, n=3– 6). Storage of mouse blood beyond human expiration-equivalents (1 month) resulted in substantial lysis and the death of all mice transfused (native and SNO-Hb repleted blood, n=5). In conclusion, repletion of SNO-Hb ameliorates the decrease in tissue oxygenation that results from transfusion of untreated stored blood. Therefore, SNO-Hb repletion may provide a simple and efficacious method to reduce transfusion-related mortality and morbidity.

Update on Chronic-Venous-Insufficiency-Induced Inflammatory Processes

Angiology ◽  
2001 ◽  
Vol 52 (1_suppl) ◽  
pp. S35-S42 ◽  
Author(s):  
Philip D. Coleridge Smith
Keyword(s):  
Growth Factor ◽  
Ischemia Reperfusion ◽  
Tissue Hypoxia ◽  
Chronic Venous Disease ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Venous Disease ◽  
Venous Ulceration ◽  
Transcutaneous Oxygen ◽  
Sequence Of Events ◽  
Inflammatory Processes

The causes of venous ulceration remain unclear. Twentieth-century hypotheses concentrated on the possibility that this problem was caused by failure of oxygen delivery to the skin. However, it has been difficult to substantiate these predictions in practice. Although the presence of tissue hypoxia has been suggested by studies in which transcutaneous oxygen tension has been assessed with transducers heated to unphysiological temperatures, when oxygen measurements are made at room temperature there is little evidence of tissue hypoxia. This has led to the assessment of alternative mechanisms of ulcer development. There has been considerable interest in recent years in the inflammatory processes that surround venous ulceration. A complex sequence of events appears to surround the develop ment of leg ulceration. Increased leukocyte activation has been shown in patients with venous disease as well as increased expression of soluble endothelial adhesion molecules. Histologic studies of the skin in patients with chronic venous disease show a perivascular infiltration of the capillaries of the papillary plexus (the most superficial part of the dermis) with monocytes, macrophages, and connective tissue proteins including fibrin. Fibrosis of the skin and subcutaneous tissues may be initiated by increased gene expression and production of transforming growth factor-β 1. Vascular endothelial growth factor may be involved in the capillary proliferation that has been reported in the skin by a number of authors. Increased expression of several tissue metallo proteinases has been reported both in liposclerotic skin and periulcer skin. The tissue inhibitors of metalloproteinases are also increased and the net result is unclear. Treatment of venous disease using micronized purified flavonoid fraction moderates some of the inflammatory markers, including leukocyte ligand expression and endothelial adhesion molecule shedding. These compounds have also been shown to reduce leukocyte-endothelial adhesion in animal models of ischemia-reperfusion injury. Many inflammatory processes have now been shown to be involved in the development of the skin changes in patients with chronic venous disease. However, the precise sequence of events that leads to leg ulceration is still unclear. Pharmacologic treatments aimed at moderating some of these inflammatory processes are now under investigation as potential ways of treating patients with the more advanced stages of venous disease.

Adipose tissue hypoxia and insulin resistance

2016 ◽  
Vol 64 (4) ◽  
pp. 830-832 ◽  
Author(s):  
Neda Rasouli
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Hypoxia ◽  
Sequence Of Events ◽  
Adipose Tissue Dysfunction ◽  
Underlying Mechanisms ◽  
Key Events

Despite the well-established association of obesity with insulin resistance and inflammation, the underlying mechanisms and sequence of events leading to inflammation and insulin resistance remain unknown. Adipose tissue hypoxia has been proposed as one of the possible key events during the process of fat expansion that leads to adipose tissue dysfunction. The focus of this paper is reviewing the evidence on adipose tissue hypoxia in obesity and its relation to insulin resistance.

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