Rapid and Persistent Decrease in Brain Tissue Oxygenation in Ovine Gram-negative Sepsis

2021 ◽  
Author(s):  
Nobuki Okazaki ◽  
Yugeesh R Lankadeva ◽  
Rachel M Peiris ◽  
Ian E Birchall ◽  
Clive N. May
Keyword(s):  
Oxygen Tension ◽  
Cerebral Perfusion ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Brain Perfusion ◽  
Tissue Perfusion ◽  
Brain Dysfunction ◽  
Cerebral Tissue ◽  
Brain Tissue Oxygenation ◽  
Conscious Sheep

The changes in brain perfusion and oxygenation in critical illness, which are thought to contribute to brain dysfunction, are unclear due to the lack of methods to measure these variables. We have developed a technique to chronically measure cerebral tissue perfusion and oxygen tension in unanesthetised sheep. Using this technique, we have determined the changes in cerebral perfusion and PO2 during the development of ovine sepsis. In adult Merino ewes, fibre-optic probes were implanted in the brain, renal cortex and renal medulla to measure tissue perfusion, oxygen tension (PO2) and temperature and flow probes were implanted on the pulmonary and renal arteries. Conscious sheep were infused with live Escherichia coli for 24-hr, which induced hyperdynamic sepsis; mean arterial pressure decreased (85.2±5.6 to 71.5±8.7 mmHg), while cardiac output (4.12±0.70 to 6.15±1.26 L/min) and total peripheral conductance (48.9±8.5 to 86.8±11.5 mL/min/mmHg) increased (n=8, all P<0.001) and arterial PO2 decreased (104±8 to 83±10 mmHg; P<0.01). Cerebral perfusion tended to decrease acutely, although this did not reach significance, but there was a significant and sustained decrease in cerebral tissue PO2 (32.2±10.1 to 18.8±11.7 mmHg) after 3 h and to 22.8±5.2 mmHg after 24-hr of sepsis (P<0.02). Sepsis induced large reductions in both renal medullary perfusion and PO2 but had no effect in the renal cortex. In ovine sepsis, there is an early decrease in cerebral PO2 that is maintained for 24-hours despite minimal changes in cerebral perfusion. Cerebral hypoxia may be one of the factors causing sepsis-induced malaise and lethargy.

Long-term measurement of renal cortical and medullary tissue oxygenation and perfusion in unanesthetized sheep

2015 ◽  
Vol 308 (10) ◽  
pp. R832-R839 ◽  
Author(s):  
Paolo Calzavacca ◽  
Roger G. Evans ◽  
Michael Bailey ◽  
Yugeesh R. Lankadeva ◽  
Rinaldo Bellomo ◽  
...  
Keyword(s):  
Renal Artery ◽  
Fiber Optic ◽  
Renal Cortex ◽  
Tissue Perfusion ◽  
Fiber Optic Probes ◽  
Medullary Tissue ◽  
Time Flow ◽  
Conscious Sheep ◽  
Long Term Measurement

The role of renal cortical and medullary hypoxia in the development of acute kidney injury is controversial, partly due to a lack of techniques for the long-term measurement of intrarenal oxygenation and perfusion in conscious animals. We have, therefore, developed a methodology to chronically implant combination probes to chronically measure renal cortical and medullary tissue perfusion and oxygen tension (tPo2) in conscious sheep and evaluated their responsiveness and reliability. A transit-time flow probe and a vascular occluder were surgically implanted on the left renal artery. At the same operation, dual fiber-optic probes, comprising a fluorescence optode to measure tPo2 and a laser-Doppler probe to assess tissue perfusion, were inserted into the renal cortex and medulla. In recovered conscious sheep ( n = 8) breathing room air, mean 24-h cortical and medullary tPo2 were similar (31.4 ± 0.6 and 29.7 ± 0.7 mmHg, respectively). In the renal cortex and medulla, a 20% reduction in renal blood flow (RBF) decreased perfusion (14.6 ± 8.6 and 41.2 ± 8.5%, respectively) and oxygenation (48.1 ± 8.5 and 72.4 ± 8.5%, respectively), with greater decreases during a 50% reduction in RBF. At autopsy, minimal fibrosis was observed around the probes. In summary, we have developed a technique to chronically implant fiber-optic probes in the renal cortex and medulla for recording tissue perfusion and oxygenation over many days. In normal resting conscious sheep, cortical and medullary tPo2 were similar. The responses to and recovery from renal artery occlusion, together with the consistent measurements over a 24-h period, demonstrate the responsiveness and stability of the probes.

scholarly journals Accounting for oxygen in the renal cortex: a computational study of factors that predispose the cortex to hypoxia

2017 ◽  
Vol 313 (2) ◽  
pp. F218-F236 ◽  
Author(s):  
Chang-Joon Lee ◽  
Bruce S. Gardiner ◽  
Jennifer P. Ngo ◽  
Saptarshi Kar ◽  
Roger G. Evans ◽  
...  
Keyword(s):  
Oxygen Tension ◽  
Renal Cortex ◽  
Computational Study ◽  
Ischemia Reperfusion ◽  
Sodium Reabsorption ◽  
Model Parameters ◽  
Arterial Blood ◽  
Increased Risk ◽  
Renal Oxygen Consumption ◽  
Renal Oxygen

We develop a pseudo-three-dimensional model of oxygen transport for the renal cortex of the rat, incorporating both the axial and radial geometry of the preglomerular circulation and quantitative information regarding the surface areas and transport from the vasculature and renal corpuscles. The computational model was validated by simulating four sets of published experimental studies of renal oxygenation in rats. Under the control conditions, the predicted cortical tissue oxygen tension ([Formula: see text]) or microvascular oxygen tension (µPo2) were within ±1 SE of the mean value observed experimentally. The predicted [Formula: see text] or µPo2 in response to ischemia-reperfusion injury, acute hemodilution, blockade of nitric oxide synthase, or uncoupling mitochondrial respiration, were within ±2 SE observed experimentally. We performed a sensitivity analysis of the key model parameters to assess their individual or combined impact on the predicted [Formula: see text] and µPo2. The model parameters analyzed were as follows: 1) the major determinants of renal oxygen delivery ([Formula: see text]) (arterial blood Po2, hemoglobin concentration, and renal blood flow); 2) the major determinants of renal oxygen consumption (V̇o2) [glomerular filtration rate (GFR) and the efficiency of oxygen utilization for sodium reabsorption (β)]; and 3) peritubular capillary surface area (PCSA). Reductions in PCSA by 50% were found to profoundly increase the sensitivity of [Formula: see text] and µPo2 to the major the determinants of [Formula: see text] and V̇o2. The increasing likelihood of hypoxia with decreasing PCSA provides a potential explanation for the increased risk of acute kidney injury in some experimental animals and for patients with chronic kidney disease.

scholarly journals An immunohistochemical study of aspartate, glutamate, and taurine in rat kidney.

1994 ◽  
Vol 42 (5) ◽  
pp. 621-626 ◽  
Author(s):  
N Ma ◽  
E Aoki ◽  
R Semba
Keyword(s):  
Amino Acids ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Loop Of Henle ◽  
Immunoperoxidase Method ◽  
Collecting Tubules ◽  
Convoluted Tubules ◽  
Thin Portion ◽  
Intrarenal Distribution

Biochemical studies have revealed considerable amounts of free amino acids in the kidney. We examined the intrarenal distribution of three amino acids (aspartate, glutamate, and taurine) in the rat kidney with an immunoperoxidase method. In the renal cortex, all three amino acids were concentrated in the renal corpuscles and in the epithelia of the collecting tubules. Immunostaining of the collecting tubules was more intense in the principal cells than in the intercalated cells. The distal convoluted tubules were also immunostained with aspartate- and glutamate- specific antibodies but not with the taurine-specific antibody. In the renal medulla, the immunoreactivity specific for aspartate and for glutamate was similar; it was weak in the thick portion of the loop of Henle and strong in the collecting tubules. Immunoreactivity specific for taurine was restricted to regions within the epithelia of the thin portion of the loop of Henle and the collecting tubules. The significance of the accumulated amino acids as osmoregulatory agents is discussed.

scholarly journals Total Cerebral Blood Flow and Total Brain Perfusion in the General Population: The Rotterdam Scan Study

2007 ◽  
Vol 28 (2) ◽  
pp. 412-419 ◽  
Author(s):  
Meike W Vernooij ◽  
Aad van der Lugt ◽  
Mohammad Arfan Ikram ◽  
Piotr A Wielopolski ◽  
Henri A Vrooman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
General Population ◽  
Cerebral Perfusion ◽  
Brain Volume ◽  
Measurement Techniques ◽  
White Matter Lesions ◽  
Brain Perfusion ◽  
Linear Regression Models ◽  
Total Brain

Reduced cerebral perfusion may contribute to the development of cerebrovascular and neurodegenerative diseases. Little is known on cerebral perfusion in the general population, as most measurement techniques are too invasive for application in large groups of healthy individuals. Total cerebral blood flow (tCBF) can be noninvasively measured by magnetic resonance imaging (MRI) but is highly correlated with brain volume. We calculated total brain perfusion by dividing tCBF by brain volume, and we investigated determinants of total brain perfusion in comparison with tCBF. Secondly, we studied whether persons with a low tCBF or low total brain perfusion have a larger volume of white matter lesions (WML). This study is based on 892 persons aged 60 to 91 years from the Rotterdam Study, a population-based cohort study. We performed two-dimensional (2D) phase-contrast MRI for tCBF measurement. Brain volume and WML volume were quantitatively assessed. Cardiovascular determinants were assessed by interview and physical examination. We assessed associations between cardiovascular determinants and flow measures with linear regression models, adjusted for age and sex. Associations between tCBF or total brain perfusion and WML volume were assessed using general linear models. We found that determinants of tCBF and total brain perfusion differed largely due to the large influence of brain volume on tCBF values. Persons with low total brain perfusion had a significantly larger WML volume compared with those with high total brain perfusion. Prospective studies are required to unravel whether hypoperfusion contributes to WML formation or that tissue damage, manifested by WML, leads to brain hypoperfusion.

Abstract P219: Losartan Prevents The Recruitment Of Renal M1-like Macrophages And Dendritic Cells In Medulla Of Angiotensin Ii Hypertensive Mice

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Patricio A Araos ◽  
Andrés Guzmán ◽  
Stefanny M Figueroa ◽  
Javier Reyes ◽  
Cristián A Amador
Keyword(s):  
Dendritic Cells ◽  
Immune Cells ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Ang Ii ◽  
Mhc Ii ◽  
Treatment Changes ◽  
Antigen Presenting

Immune cells play a major role in the development and progression of hypertension. Previous studies have shown that antigen presenting cells (APCs), such as macrophages (Mø) and dendritic cells (DCs) are particularly abundant in kidney. However, the relevance of these renal APCs on hypertension and whether their distribution change during the anti-hypertensive treatment remain unknow. We evaluated whether losartan (Los) treatment changes the abundance of APCs in the renal cortex and medulla in Angiotensin (Ang) II-infused mice.Male C57BL/6 mice (8-12wo) were treated with AngII (490ng/Kg/min), AngII+Los (20mg/Kg/day) or Vehicle for 14 days (n=4-6). Systolic blood pressure (SBP) was measured by the tail cuff method, and renal cortex/medulla were isolated for the measurements of: APCs (MHC-II + :CD11c + ), DCs (APCs:F4/80 - :CD64 - /CD103 + for type-1 DCs, or APCs:F4/80 - :CD64 - :CD11b + for type-2 DCs), and M1-like Mø (APCs:F4/80 - :CD64 + :CD11b + ), by flow cytometry.Los treatment prevented the increased SBP (AngII+Los=118.8±6.4 mmHg vs. AngII=158.0±21.1 mmHg; p<0.001), and the APCs recruitment in renal cortex (AngII+Los=23.2±2.7 vs. AngII=36.0±5.9%; p<0.01) and in renal medulla (Veh=16.3±7.7; AngII=26.3±4,7; AngII+Los=14.9±3.3%; p<0.05) induced by AngII. In addition, we observed an increase of DC2 and M1-like Mø recruitments in renal medulla of AngII mice (DC2 Veh =29.0±5.0 vs. DC2 AngII =45.5±7.3%; p<0.05; M1 Veh =44.8±7.5 vs. M1 AngII =58.3±5.3%; p<0.05), which were prevented by Los treatment (DC2 AngII+Los =27.1±6.8%; p<0.05; M1 AngII+Los =47.0±3.5%; p<0.05). Interestingly, we did not observe differences between groups on M1-like Mø, and DC2 populations in renal cortex. However, Los treatment prevented the increase of DC1 on renal cortex (Veh=2.1±1.4; AngII=5.2±2.4; AngII+Los=2.1±0.8%; p<0.05), without differences between groups at medullar level.Our results show that Los treatment has a differential effect on the APCs populations in renal cortex and medulla, suggesting that renal APCs have different participations on hypertension according their microenvironment.Supported by Fondecyt #1201251 and #3201016

Management of raised intracranial pressure

2020 ◽  
pp. 3892-3897
Author(s):  
David K. Menon
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Brain Oedema ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Brain Perfusion ◽  
Normal Brain ◽  
Intracranial Volume ◽  
Nervous System Diseases

Normal intracranial pressure is between 5 and 15 mm Hg in supine subjects. Intracranial hypertension (ICP >20 mm Hg) is common in many central nervous system diseases and in fatal cases is often the immediate cause of death. Increases in intracranial volume and hence—given the rigid skull—intracranial pressure may be the consequence of brain oedema, increased cerebral blood volume, hydrocephalus, and space-occupying lesions. Brain perfusion depends on the cerebral perfusion pressure which is mean arterial pressure minus intracranial pressure. The normal brain autoregulates cerebral blood flow down to a lower limit of cerebral perfusion pressure of about 50 mm Hg in healthy subjects, and perhaps 60–70 mm Hg in disease. Cerebral perfusion pressure reduction to below these values results in cerebral ischaemia.

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