Renal blood flow and renal clearances during hemorrhage and hemorrhagic shock

Shock ◽  
1962 ◽  
pp. 145-150 ◽  
Author(s):  
E. E. Selkurt
1966 ◽  
Vol 10 (3) ◽  
pp. 230???231
Author(s):  
R. C. CAMISHION ◽  
N. H. FISHMAN ◽  
Hebbel E. Hoff

2021 ◽  
Vol 12 ◽  
Author(s):  
Amaresh K. Ranjan ◽  
Zhong Zhang ◽  
Seema Briyal ◽  
Anil Gulati

Background: Centhaquine (CQ) (Lyfaquin®) is in late stage clinical development as a safe and effective first-in-class resuscitative agent for hemorrhagic shock patients (NCT02408731, NCT04056065, and NCT04045327). Acute kidney injury (AKI) is known to be associated with hemorrhagic shock. Hence, effect of CQ on protection of kidneys from damage due to hemorrhagic shock was investigated.Methods: To assess effect of CQ on AKI in shock, we created a rat model with hemorrhagic shock and AKI. Renal arteries were clamped and de-clamped to induce AKI like ischemia/reperfusion model and hemorrhage was carried out by withdrawing blood for 30 min. Rats were resuscitated with CQ (0.02 mg/kg) for 10 min. MAP, heart rate (HR), and renal blood flow (RBF) were monitored for 120 min.Results: CQ produced a significant improvement in RBF compared to vehicle (p< 0.003) even though MAP and HR was similar in CQ and vehicle groups. Blood lactate level was lower (p = 0.0064) in CQ than vehicle at 120 min post-resuscitation. Histopathological analysis of tissues indicated greater renal damage in vehicle than CQ. Western blots showed higher HIF-1α (p = 0.0152) and lower NGAL (p = 0.01626) levels in CQ vs vehicle. Immunofluorescence in the kidney cortex and medulla showed significantly higher (p< 0.045) expression of HIF-1α and lower expression of Bax (p< 0.044) in CQ. Expression of PHD 3 (p< 0.0001) was higher, while the expression of Cytochrome C (p = 0.01429) was lower in the cortex of CQ than vehicle.Conclusion: Results show CQ (Lyfaquin®) increased renal blood flow, augmented hypoxia response, decreased tissue damage and apoptosis following hemorrhagic shock induced AKI, and may be explored to prevent/treat AKI.Translational Statement: Centhaquine (CQ) is safe for human use and currently in late stage clinical development as a first-in-class resuscitative agent to treat hemorrhagic shock. In the current study, we have explored a novel role of CQ in protection from hemorrhagic shock induced AKI, indicating its potential to treat/prevent AKI.


1970 ◽  
Vol 2 (5) ◽  
pp. 333-340 ◽  
Author(s):  
S. Nagy ◽  
T. Barankay ◽  
G. Horpácsy

1952 ◽  
Vol 171 (2) ◽  
pp. 482-486 ◽  
Author(s):  
Martin Brandfonbrener ◽  
Herman M. Geller

1956 ◽  
Vol 186 (1) ◽  
pp. 74-78 ◽  
Author(s):  
E. D. Frank ◽  
H. A. Frank ◽  
S. Jacob ◽  
H. A. E. Weizel ◽  
H. Korman ◽  
...  

Norepinephrine infusion did not prolong the survival or effect the recovery of dogs in hemorrhagic shock unresponsive to replacement transfusion. During its pressor action in shock, either before or after replacement transfusion, norepinephrine infusion increased coronary, cerebral and adrenal blood flow, reduced renal blood flow, and did not change hepatic blood flow. Cardiac output was increased in oligemic shock but not after blood replacement. Pulmonary arterial pressure and right and left auricular pressures were raised by norepinephrine infusion in all phases of hemorrhagic shock, and calculated pulmonary vascular resistance was reduced.


2012 ◽  
Vol 113 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Christopher J. Rhee ◽  
Kathleen K. Kibler ◽  
R. Blaine Easley ◽  
Dean B. Andropoulos ◽  
Marek Czosnyka ◽  
...  

Hypotension and shock are risk factors for death, renal insufficiency, and stroke in preterm neonates. Goal-directed neonatal hemodynamic management lacks end-organ monitoring strategies to assess the adequacy of perfusion. Our aim is to develop a clinically viable, continuous metric of renovascular reactivity to gauge renal perfusion during shock. We present the renovascular reactivity index (RVx), which quantifies passivity of renal blood volume to spontaneous changes in arterial blood pressure. We tested the ability of the RVx to detect reductions in renal blood flow. Hemorrhagic shock was induced in 10 piglets. The RVx was monitored as a correlation between slow waves of arterial blood pressure and relative total hemoglobin (rTHb) obtained with reflectance near-infrared spectroscopy (NIRS) over the kidney. The RVx was compared with laser-Doppler measurements of red blood cell flux, and renal laser-Doppler measurements were compared with cerebral laser-Doppler measurements. Renal blood flow decreased to 75%, 50%, and 25% of baseline at perfusion pressures of 60, 45, and 40 mmHg, respectively, whereas in the brain these decrements occurred at pressures of 30, 25, and 15 mmHg, respectively. The RVx compared favorably to the renal laser-Doppler data. Areas under the receiver operator characteristic curves using renal blood flow thresholds of 50% and 25% of baseline were 0.85 (95% CI, 0.83–0.87) and 0.90 (95% CI, 0.88–0.92). Renovascular autoregulation can be monitored and is impaired in advance of cerebrovascular autoregulation during hemorrhagic shock.


2016 ◽  
Vol 2016 ◽  
pp. 1-6
Author(s):  
Maryam Maleki ◽  
Mehdi Nematbakhsh

Background.Angiotensin 1-7 (Ang1-7) plays an important role in renal circulation. Hemorrhagic shock (HS) may cause kidney circulation disturbance, and this study was designed to investigate the renal blood flow (RBF) response to Ang1-7 after HS.Methods. 27 male Wistar rats were subjected to blood withdrawal to reduce mean arterial pressure (MAP) to 45 mmHg for 45 min. The animals were treated with saline (group 1), Ang1-7 (300 ng·kg−1 min−1), Ang1-7 in hypertonic sodium chloride 7.5% (group 3), and hypertonic solution alone (group 4).Results. MAP was increased in a time-related fashion (Ptime<0.0001) in all groups; however, there was a tendency for the increase in MAP in response to hypertonic solution (P=0.09). Ang1-7, hypertonic solution, or combination of both increased RBF in groups 2-4, and these were significantly different from saline group (P=0.05); that is, Ang1-7 leads to a significant increase in RBF to 1.35 ± 0.25 mL/min compared with 0.55 ± 0.12 mL/min in saline group (P<0.05).Conclusion. Although Ang1-7 administration unlike hypertonic solution could not elevate MAP after HS, it potentially could increase RBF similar to hypertonic solution. This suggested that Ang1-7 recovers RBF after HS when therapeutic opportunities of hypertonic solution are limited.


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