Red cell trapping after ischemia and long-term kidney damage. Influence of hematocrit

Hellberg, Pår; Bayati, A.; Källskog, Örjan; Wolgast, M.

doi:10.1038/ki.1990.107

Cited by 52 publications

(40 citation statements)

References 23 publications

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“…Other studies have demonstrated a regional variation of the hematocrit within the lung, and it is unclear whether the lung and peripheral hematocrits are equal (30,31). In this study, the lung hematocrit was estimated to 0.43 Ϯ 0.08 in the LPS group and to 0.55 Ϯ 0.06 in the control group, which reasonably agree with reported peripheral values of 0.45-0.50 in rats (32,33). However, the finding of a lower hematocrit in the LPS group disagrees with studies where the hematocrit was unaltered (31) or increased (34) after LPS challenge in rats.…”

Section: Rat Lung Spectroscopy Using Hyperpolarizedsupporting

confidence: 81%

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized ¹²⁹Xe

Månsson

Wolber

Driehuys³

et al. 2003

Magnetic Resonance in Med

106

156

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The ability to quantify pulmonary diffusing capacity and perfusion using dynamic hyperpolarized 129 Xe NMR spectroscopy is demonstrated. A model of alveolar gas exchange was developed, which, in conjunction with 129 Xe NMR, enables quantification of average alveolar wall thickness, pulmonary perfusion, capillary diffusion length, and mean transit time. The technique was employed to compare a group of naïve rats (n ‫؍‬ 10) with a group of rats with acute inflammatory lung injury (n ‫؍‬ 10), caused by instillation of lipopolysaccaride (LPS). The measured structural and perfusion-related parameters were in agreement with reported values from studies using non-NMR methods. Significant differences between the groups were found in total diffusion length (control 8.5 ؎ 0.5 m, LPS 9.9 ؎ 0.6 m, P < 0.001), in capillary diffusion length (control 2.9 ؎ 0.4 m, LPS 3.9 ؎ 1.0 m, P < 0.05), and in pulmonary hematocrit (control 0.55 ؎ 0.06, LPS 0.43 ؎ 0.08, P < 0.01), whereas no differences were observed in alveolar wall thickness, pulmonary perfusion, and mean transit time. These results demonstrate the ability of the method to distinguish two main aspects of lung function, namely, diffusing capacity and pulmonary perfusion. Key words: hyperpolarized gas NMR; xenon-129; lung function; diffusing capacity; pulmonary perfusion Gas transfer from ambient air to the blood involves different transport mechanisms. Alveolar ventilation is accomplished by convective transport. Gas transfer within the alveolus and from the alveolus into the blood stream occurs by diffusion along concentration gradients. The blood is then transported from the lungs to peripheral tissues by the pulmonary circulation. These transport processes are affected by a number of lung diseases. Convective transport in the airways is impaired in obstructive lung diseases (1). Diffusion impairment occurs in interstitial lung diseases as well as in pulmonary edema (2). The pulmonary vasculature is affected by both primary lung disease and by left heart failure, causing abnormalities in blood flow (3).The most common method of assessment of diffusion in the alveolar-capillary unit is measurement of the diffusing capacity for carbon monoxide, DL CO (4). The diffusing capacity is defined as the total rate of gas passage across the alveolar-capillary membrane per unit of partial pressure difference of the gas. The tracer gas carbon monoxide diffuses across the alveolar-capillary barrier and is tightly bound to hemoglobin in the erythrocytes. In addition to factors determining diffusion, e.g., the available surface area and the diffusion path length, DL CO therefore depends also on the availability of binding sites, i.e., on hemoglobin concentration and on perfusion. DL CO provides information about diffusion properties of the lung as a whole, but no regional information about function is obtained. By measurement at different partial pressures for oxygen, DL CO can be subdivided into the membrane conductance and a term reflecting the availability of binding sites. This is...

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Section: Rat Lung Spectroscopy Using Hyperpolarizedsupporting

confidence: 81%

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized ¹²⁹Xe

Månsson

Wolber

Driehuys³

et al. 2003

Magnetic Resonance in Med

106

156

View full text Add to dashboard Cite

show abstract

“…Previous studies have indicated that the RBC trapping occurs either during ischaemia [5,10] or in the very early recirculation phase [9,14], and disappears within less than 24 h [10,14]. It is evident from the results for the contra lateral intact kidneys in the present study that mannitol per se does not induce RBC trap ping.…”

Section: Discussionsupporting

confidence: 71%

Post-Ischaemic Administration of Hyperosmolar Mannitol Enhances Erythrocyte Trapping in Outer Medullary Vasculature in the Rat Kidney

Hellberg

Nygren

Hansell

et al. 1990

Kidney Blood Press Res

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Mannitol is widely used as a therapeutic agent in the management of acute renal failure. We sought to determine whether mannitol influences the trapping of red blood cells (RBCs) in renal microvasculature, as measured from the distribution of ⁵¹Cr-labelled RBCs, in the rat kidney after ischaemia. The results indicate that administration of hyperosmolar mannitol after an ischaemic insult increases RBC trapping in the outer renal medulla in a dose-dependent manner. This was found to occur even though parameters of nephron function were unaffected or even improved.

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“…28,29 Extensive trapping of erythrocytes was seen in the ISOM ( Figure 7B) and inner medulla ( Figure 7E) of saline-treated animals after 1-hour reperfusion after 45-minute ischemia. The trapping of erythrocytes was greatly reduced in ISOM ( Figure 7C) and the inner medulla ( Figure 7F) of SS-31 IR animals.…”

Section: Ss-31 Reduced Medullary Microvascular Congestionmentioning

confidence: 99%

Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury

Szeto

Liu

Soong

et al. 2011

Journal of the American Society of Nephrology

260

244

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The burst of reactive oxygen species (ROS) during reperfusion of ischemic tissues can trigger the opening of the mitochondrial permeability transition (MPT) pore, resulting in mitochondrial depolarization, decreased ATP synthesis, and increased ROS production. Rapid recovery of ATP upon reperfusion is essential for survival of tubular cells, and inhibition of oxidative damage can limit inflammation. SS-31 is a mitochondria-targeted tetrapeptide that can scavenge mitochondrial ROS and inhibit MPT, suggesting that it may protect against ischemic renal injury. Here, in a rat model of ischemia-reperfusion (IR) injury, treatment with SS-31 protected mitochondrial structure and respiration during early reperfusion, accelerated recovery of ATP, reduced apoptosis and necrosis of tubular cells, and abrogated tubular dysfunction. In addition, SS-31 reduced medullary vascular congestion, decreased IR-mediated oxidative stress and the inflammatory response, and accelerated the proliferation of surviving tubular cells as early as 1 day after reperfusion. In summary, these results support MPT as an upstream target for pharmacologic intervention in IR injury and support early protection of mitochondrial function as a therapeutic maneuver to prevent tubular apoptosis and necrosis, reduce oxidative stress, and reduce inflammation. SS-31 holds promise for the prevention and treatment of acute kidney injury. Acute kidney injury (AKI) develops in 5% of hospitalized patients and is associated with significant morbidity. Ischemia is the most common cause of AKI. Despite our current knowledge of the pathophysiology underlying renal ischemia-reperfusion (IR) injury, pharmacologic interventions have not reduced the mortality and morbidity associated with AKI.Rapid recovery of ATP after ischemia is essential for cell survival after IR injury. A profound reduction in intracellular ATP occurs early after onset of ischemia and leads to cytoskeletal derangements, membrane alterations, and cell death by apoptosis and necrosis. 1 Disruption of the cytoskeleton leads to redistribution of integrins and Na ϩ ,K ϩ -ATPase from the basal membrane, resulting in detachment of viable cells from the basement membrane and impairment of Na ϩ reabsorption. The mode of cell death depends on the duration of ischemia and the region of the nephron. Cell death is usually restricted to the outer medullary region where oxygen tension drops precipitously at the corticomedullary junction. 2 The proximal tubules are particularly susceptible to IR injury because they have minimal glycolytic capacity and must rely on mitochondrial metabolism for ATP synthesis. [3][4][5] Ischemia causes damage to all components of the mitochondrial electron transport chain (ETC), resulting in decreased oxidative phosphorylation upon reperfusion. 6 In addition, mitochondria are the primary source of reactive oxygen species (ROS). 6,7 Mitochondria can undergo further damage upon reperfusion because of mitochondrial permeability transition (MPT). During ischemia, elevated mitocho...

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Red cell trapping after ischemia and long-term kidney damage. Influence of hematocrit

Cited by 52 publications

References 23 publications

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized ¹²⁹Xe

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized ¹²⁹Xe

Post-Ischaemic Administration of Hyperosmolar Mannitol Enhances Erythrocyte Trapping in Outer Medullary Vasculature in the Rat Kidney

Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury

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Red cell trapping after ischemia and long-term kidney damage. Influence of hematocrit

Cited by 52 publications

References 23 publications

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized 129Xe

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized 129Xe

Post-Ischaemic Administration of Hyperosmolar Mannitol Enhances Erythrocyte Trapping in Outer Medullary Vasculature in the Rat Kidney

Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury

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Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized ¹²⁹Xe

Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized ¹²⁹Xe