Effect of Varying the Hematocrit Ratio on the Susceptibility to Hemorrhagic Shock

1957 ◽  
Vol 192 (1) ◽  
pp. 171-174 ◽  
Author(s):  
Jack W. Crowell ◽  
Sara H. Bounds ◽  
W. W. Johnson
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Natural Variation ◽  
Time Lapse ◽  
Arterial Blood ◽  
Time Required

By the use of a) acetyl phenylhydrazine, b) hemorrhage, c) transfusion, and d) natural variation, 67 dogs with hematocrit ratios varying from 12 to 56 were obtained. These dogs were subjected to hemorrhagic shock by lowering their arterial blood pressure to 30 mm Hg, and the time lapse between the initial production of hypotension and the beginning deterioration of the animal determined. This time lapse is a measure of the resistance of the animal to the development of irreversible shock. A graph of initial hematocrit versus the time required for the development of irreversible shock shows that an increase in the hematocrit ratio from 12 to 35 increases the resistance of the animals by a factor of approximately 5; however, increasing the hematocrit ratio above 35 decreases the resistance of the animal to the development of irreversible shock.

Corticosteroids for reversal of hemorrhagic shock in rats

1965 ◽  
Vol 209 (4) ◽  
pp. 815-818 ◽  
Author(s):  
Max Harry Weil ◽  
Howard Whigham
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Adrenal Glands ◽  
Pharmacological Action ◽  
Therapeutic Benefit ◽  
Dosage Range ◽  
Arterial Blood ◽  
Adrenalectomized Animal ◽  
Adrenocortical Hormone

Corticosteroids administered in amounts more than 100 times those required to sustain a fully adrenalectomized animal were highly effective in increasing survival following hemorrhagic shock. In rats with intact adrenal glands, hemorrhagic shock was produced by maintaining arterial blood pressure at 35 mm Hg for 240 min. Glucocorticoids and aldosterone were administered only after blood was reinfused. The therapeutic benefit is due to a pharmacological action of the adrenocortical hormone. Aldosterone had a lesser and relatively narrow dosage range of effectiveness.

Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock

1977 ◽  
Vol 232 (3) ◽  
pp. H283-H287
Author(s):  
D. J. Loegering
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Liver Slice ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Shed Blood ◽  
Arterial Blood

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

scholarly journals Sympathetic innervation of the splanchnic region mediates the beneficial hemodynamic effects of 8-OH-DPAT in hemorrhagic shock

2012 ◽  
Vol 303 (5) ◽  
pp. R527-R538 ◽  
Author(s):  
Ruslan Tiniakov ◽  
Kalipada Pahan ◽  
Karie E. Scrogin
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Sympathetic Innervation ◽  
Hypovolemic Shock ◽  
Pressor Effect ◽  
Venous Tone ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Splanchnic Nerves

Administration of the 5-HT1A receptor agonist, 8-OH-DPAT, improves cardiovascular hemodynamics and tissue oxygenation in conscious rats subjected to hypovolemic shock. This effect is mediated by sympathetic-dependent increases in venous tone. To determine the role of splanchnic nerves in this response, effects of 8-OH-DPAT (30 nmol/kg iv) were measured following fixed-arterial blood pressure hemorrhagic shock (i.e., maintenance of 50 mmHg arterial pressure for 25 min) in rats subjected to bilateral splanchnic nerve denervation (SD). Splanchnic denervation decreased baseline venous tone as measured by mean circulatory filling pressure (MCFP) and accelerated the onset of hypotension during blood loss. Splanchnic denervation did not affect the immediate pressor effect of 8-OH-DPAT but did reverse the drug's lasting pressor effect, as well as its ability to increase MCFP and improve metabolic acidosis. Like SD, adrenal demedullation (ADMX) lowered baseline MCFP and accelerated the hypotensive response to blood withdrawal but also reduced the volume of blood withdrawal required to maintain arterial blood pressure at 50 mmHg. 8-OH-DPAT raised MCFP early after administration in ADMX rats, but the response did not persist throughout the posthemorrhage period. In a fixed-volume hemorrhage model, 8-OH-DPAT continued to raise blood pressure in ADMX rats. However, it produced only a transient and variable rise in MCFP compared with sham-operated animals. The data indicate that 8-OH-DPAT increases venoconstriction and improves acid-base balance in hypovolemic rats through activation of splanchnic nerves. This effect is due, in part, to activation of the adrenal medulla.

Renovascular reactivity measured by near-infrared spectroscopy

2012 ◽  
Vol 113 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Christopher J. Rhee ◽  
Kathleen K. Kibler ◽  
R. Blaine Easley ◽  
Dean B. Andropoulos ◽  
Marek Czosnyka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Hemorrhagic Shock ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Laser Doppler ◽  
Arterial Blood

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.

scholarly journals Exceptional Cause of Hemorrhagic Shock in Intensive Care by Arterial Blood Pressure Catheter Disconnection

2021 ◽  
Vol 7 (4) ◽  
pp. 168-169
Author(s):  
  A. Elmoqaddem ◽  
N. Mrani Alaoui ◽  
T. Cherrad ◽  
M. Hmidi ◽  
F. Choumi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intensive Care ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Pressure Catheter

Nitric oxide does not contribute to the hypotension of heatstroke

2001 ◽  
Vol 90 (3) ◽  
pp. 961-970 ◽  
Author(s):  
Kathy L. Ryan ◽  
Maria R. Tehrany ◽  
James R. Jauchem
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Survival Time ◽  
Arterial Blood Pressure ◽  
Synthesis Inhibitor ◽  
End Point ◽  
Arterial Blood ◽  
Time Required ◽  
Colonic Temperature ◽  
Time Point

The purpose of this study was to determine whether nitric oxide (NO) contributes to the hypotensive state induced by prolonged environmental heat (EH) stress. Ketamine-anesthetized rats were instrumented for the measurement of arterial blood pressure, electrocardiogram, and temperature at four sites. Rats were exposed to EH (ambient temperature, 40 ± 1°C) until mean arterial blood pressure (MAP) decreased to 75 mmHg, which was arbitrarily defined as the induction of heatstroke. In addition to cardiovascular and temperature measurements, the time required to reach this MAP end point and the subsequent survival time were measured. In three separate experimental series, the competitive NO synthesis inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) was administered (0, 10, or 100 mg/kg) either before, during (30 min after initiation of EH), or immediately after EH. l-NAME administered at any of these times transiently increased MAP. l-NAME infusion either before or during EH did not alter the EH time required to decrease MAP to 75 mmHg, butl-NAME pretreatment did decrease the colonic temperature at which this MAP end point was reached. l-NAME infusion before or after EH did not affect subsequent survival time, butl-NAME administered during EH significantly decreased survival time. The administration of l-NAME at any time point, therefore, did not prove beneficial in either preventing or reversing heatstroke. Taken together, these data suggest that NO does not mediate the hypotension associated with heatstroke.

Diaphragmatic Function Is Preserved during Severe Hemorrhagic Shock in the Rat

2014 ◽  
Vol 120 (2) ◽  
pp. 425-435 ◽  
Author(s):  
Serge Carreira ◽  
Matthieu Lê Dinh ◽  
Marc Soubeyrand ◽  
Marie-Pierre Poloujadoff ◽  
Bruno Riou ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Proinflammatory Cytokine ◽  
Diaphragmatic Function ◽  
Arterial Blood ◽  
Cytokine Levels ◽  
Tetanic Tension

Abstract Background: Acute diaphragmatic dysfunction has been reported in septic and cardiogenic shock, but few data are available concerning the effect of hemorrhagic shock on diaphragmatic function. The authors examined the impact of a hemorrhagic shock on the diaphragm. Methods: Four parallel groups of adult rats were submitted to hemorrhagic shock induced by controlled exsanguination targeting a mean arterial blood pressure of 30 mmHg for 1 h, followed by a 1-h fluid resuscitation with either saline or shed blood targeting a mean arterial blood pressure of 80 mmHg. Diaphragm and soleus strip contractility was measured in vitro. Blood flow in the muscle microcirculation was measured in vivo using a Laser Doppler technique. Muscle proinflammatory cytokine concentrations were also measured. Results: Hemorrhagic shock was characterized by a decrease in mean arterial blood pressure to 34 ± 5 mmHg (−77 ± 4%; P< 0.05) and high plasma lactate levels (7.6 ± 0.9 mM; P < 0.05). Although tetanic tension of the diaphragm was not altered, hemorrhagic shock induced dramatic impairment of tetanic tension of the soleus (−40 ± 19%; P < 0.01), whereas proinflammatory cytokine levels were low and not different between the two muscles. Resuscitation with either blood or saline did not further modify either diaphragm or soleus performance and proinflammatory cytokine levels. The shock-induced decrease in blood flow was much more pronounced in the soleus than in the diaphragm (−75 ± 13% vs. −17 ± 10%; P = 0.02), and a significant interaction was observed between shock and muscle (P < 0.001). Conclusion: Diaphragm performance is preserved during hemorrhagic shock, whereas soleus performance is impaired, with no further impact of either blood or saline fluid resuscitation.

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