scholarly journals Detrimental effects of complement activation in hemorrhagic shock

2001 ◽  
Vol 90 (2) ◽  
pp. 441-446 ◽  
Author(s):  
John G. Younger ◽  
Nobuyoshi Sasaki ◽  
Michael D. Waite ◽  
Holt N. Murray ◽  
Edward F. Saleh ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Complement Activation ◽  
Metabolic Effects ◽  
Acute Blood Loss ◽  
Serum Bicarbonate ◽  
Hemorrhage Volume ◽  
Carboxypeptidase N ◽  
The Complement System

The complement system has been implicated in early inflammatory events and a variety of shock states. In rats, we measured complement activation after hemorrhage and examined the hemodynamic and metabolic effects of complement depletion before injury and worsening of complement activation after hemorrhage and resuscitation [with a carboxypeptidase N inhibitor (CPNI), which blocks the clearance of C5a]. Rats were bled to a mean arterial pressure of 30 mmHg for 50 min and were then resuscitated for 2 h. Shock resulted in significant evidence of complement consumption, with serum hemolytic activity being reduced by 33% ( P < 0.05). Complement depletion before injury did not affect hemorrhage volume (complement depleted = 28 ± 1 ml/kg, complement intact = 29 ± 1 ml/kg, P = 0.74) but improved postresuscitation mean arterial pressure by 37 mmHg ( P < 0.05) and serum bicarbonate levels (complement depleted = 22 ± 3 meq/ml, complement intact = 13 ± 8 meq/ml, P < 0.05). Pretreatment with CPNI was lethal in 80% of treated animals vs. the untreated hemorrhaged group in which no deaths occurred ( P < 0.05). In this model of hemorrhagic shock, complement activation appeared to contribute to progressive hypotension and metabolic acidosis seen after resuscitation. The lethality of CPNI during acute blood loss suggests that the anaphylatoxins are important in the pathophysiological events involved in hemorrhagic shock.

Evidence for enhanced uptake of ATP by liver and kidney in hemorrhagic shock

1977 ◽  
Vol 233 (3) ◽  
pp. R83-R88 ◽  
Author(s):  
I. H. Chaudry ◽  
M. M. Sayeed ◽  
A. E. Baue
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Beneficial Effect ◽  
Hemorrhagic Shock ◽  
Kidney Slices ◽  
Atp Levels ◽  
Salutary Effect ◽  
Liver And Kidney ◽  
In Vitro Uptake

It has been shown that infusion of ATP-MgCl2 proved beneficial in the treatment of shock; however, it is not known whether this effect is due to improvement in the microcirculation or direct provision of energy or a combination of the above or other effects. To elucidate the mechanism of the salutary effect of ATP-MgCl2, we have now examined the in vitro uptake of ATP by liver and kidney of animals in shock. Rats were bled to a mean arterial pressure of 40 Torr and so maintained for 2 hrs. After the rats were killed, liver and kidney were removed and slices of tissue (0.3-0.5 mm thick) were incubated for 1 h in 1.0 ml of Krebs-HCO3 buffer containing 10 mM glucose, 5 mM MgCl2, and 5 mM [8-14C]ATP or 5 mM [8-14C]ADP, or 5 mM [8-14C]AMP, or 5 mM [8-14C]adenosine in 95% O2-5% CO2 and then homogenized. Tissue and medium samples were subjected to electrophoresis to separate and measure the various nucleotides. The uptake of [14C]ATP but not that of [14C]ADP or [14C]adenosine by liver and kidney slices from animals in shock was 2.5 times greater than the corresponding uptake by control slices. Thus, the beneficial effect of ATP-MgCl2 in shock could be due to provision of energy directly to tissue in which ATP levels were lowered.

Blood pressure and metabolic effects of 9α-fluorocorticosterone and 9α-fluorodeoxycorticosterone in sheep

1985 ◽  
Vol 104 (2) ◽  
pp. 291-294 ◽  
Author(s):  
B. A. Scoggins ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
P. J. McCarthy ◽  
R. T. Mason ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Urine Volume ◽  
Plasma Potassium ◽  
Metabolic Effect ◽  
Metabolic Effects

ABSTRACT 9α-Fluorocortisol has been postulated to have 'hypertensinogenic' as well as 'mineralocorticoid' and 'glucocorticoid' activity. The present study examined the blood pressure and metabolic effect in sheep of the structurally related steroids 9α-fluorodeoxycorticosterone (9α-FDOC) and 9α-fluorocorticosterone (9α-FB). Infusions of these fluorinated steroids at 0·63 and 0·67 mg/day respectively for 5 days produced falls in plasma potassium, but only 9α-FB increased urine volume. 9α-FDOC raised mean arterial pressure by 11 mmHg and 9α-FB raised it by 14 mmHg. Addition of a 9α-fluoro group appears to increase both 'mineralocorticoid' and 'hypertensinogenic' steroid potencies. J. Endocr. (1985) 104, 291–294

scholarly journals Responsiveness to different volume therapies following hemodilution and hemorrhagic shock: a comparative experimental study in rats

2007 ◽  
Vol 22 (5) ◽  
pp. 355-360 ◽  
Author(s):  
Riad Naim Younes ◽  
Fernanda Deutsch ◽  
Mario Itinoshe ◽  
Belchor Fontes ◽  
Renato Poggetti ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Hypertonic Saline ◽  
Hypovolemic Shock ◽  
Isotonic Saline ◽  
High Volume ◽  
Subsequent Treatment ◽  
Volume Replacement ◽  
Trauma Patients

Guidelines for volume replacement for acutely hemorrhaged and hemodiluted trauma patients have not been well established. Purpose: To evaluate the effects of acute hemodilution on mean arterial pressure (MAP), and responsiveness of acutely hemodiluted and subsequently hemorrhaged rats to different volume therapies. Methods: 180 rats were hemodiluted to simulate hemorrhaged trauma patients with persistent bleeding after high volume replacement with isotonic solutions. Thirty hemodiluted [Anemia (ANE) group] animals received no further treatment. The remaining 150 animals were subjected to hypovolemic shock and randomized into five groups, according to the treatment option employed: Control (CTL) animals did not receive subsequent treatment after hemorrhagic hypovolemia, SAL4 animals received isotonic saline 4 mL/kg, SAL32 animals received isotonic saline 32 mL/kg, HS animals received hypertonic saline 4 mL/kg and BLD animals received re-infusion of drawn blood. Results: Highest mean arterial pressure (MAP) was achieved by BLD, followed by SAL32 and HS. MAP after treatment of BLD, HS, SAL32 and ANE were higher than CTL (p=0.036). At 85 and 95 minutes of experiment, SAL4, SAL32 and HS presented the lowest hematocrit levels (p<0.01). At day 3, ANE, CTL and HS had the highest hematocrit. SAL4 and CTL groups presented the highest mortality rates. Conclusion: Hypertonic saline is an effective and safe initial therapy for hemodiluted rats undergoing hemorrhagic shock, with an overall outcome comparable to blood replacement or high volume isotonic saline administration.

scholarly journals Prolonged severe hemorrhagic shock at a mean arterial pressure of 40 mmHg does not lead to brain damage in rats

2018 ◽  
Vol 5 (4) ◽  
pp. 350-357 ◽  
Author(s):  
Ryosuke Mihara ◽  
Akira Takasu ◽  
Kentaro Maemura ◽  
Toshiaki Minami
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Brain Damage

Recombinant Human Hemoglobin with Reduced Nitric Oxide–scavenging Capacity Restores Effectively Pancreatic Microcirculatory Disorders in Hemorrhagic Shock

2004 ◽  
Vol 100 (6) ◽  
pp. 1484-1490 ◽  
Author(s):  
Ernst von Dobschuetz ◽  
Joerg Hutter ◽  
Tomas Hoffmann ◽  
Konrad Messmer
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Hydroxyethyl Starch ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Human Hemoglobin ◽  
Scavenging Capacity ◽  
Area Functional

Background Scavenging of nitric oxide by hemoglobin-based oxygen carriers could aggravate microcirculatory failure in splanchnic organs after hemorrhagic shock as a consequence of vasoconstrictive side effects. The aim of this study was to compare the effects of two recombinant human hemoglobin solutions, a second-generation product bearing reduced nitric oxide-scavenging properties (rHb2.0) due to site directed mutagenesis of the heme pocket and a first-generation recombinant hemoglobin (rHb1.1) with scavenging capacity similar to native hemoglobin, on the pancreatic microcirculation after hemorrhagic shock. Methods Twenty-eight pentobarbital-anesthetized rats were bled to a mean arterial pressure of 40 mmHg and maintained at this level for 1 h. Using an intravital microscope, the length of erythrocyte-perfused pancreatic capillaries per observation area (functional capillary density) were measured in animals resuscitated by volumes of hydroxyethyl starch, rHb1.1, or rHb2.0 equivalent to the shed blood volume. Animals without shock induction served as control. Results As compared with control (438 +/- 10 cm(-1)), animals treated with hydroxyethyl starch (315 +/- 44 cm(-1)) and rHb1.1 (288 +/- 67 cm(-1)) showed a significant reduction of functional capillary density after 2 h of resuscitation. rHb2.0 was able to restore functional capillary density (410 +/- 42 cm(-1)) and mean arterial pressure to baseline values. Conclusion rHb2.0 was effectively able to restore pancreatic microcirculation after hemorrhagic shock. This may be related to the compound's effective lack of nitric oxide-scavenging properties. This hemoglobin solution or ones similar to it might be uniquely valuable for resuscitation from hemorrhagic shock.

Reversal of Insulin Resistance by ATP in Hemorrhagic Shock

1975 ◽  
Vol 53 (5) ◽  
pp. 859-865 ◽  
Author(s):  
Irshad H. Chaudry ◽  
Mohammed M. Sayeed ◽  
Arthur E. Baue
Keyword(s):  
Insulin Resistance ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Glucose Uptake ◽  
Insulin Concentration ◽  
Insulin Effect ◽  
Intracellular Atp ◽  
Basal Glucose Uptake ◽  
Stimulation Of

Hemorrhagic shock was produced by bleeding rats to a mean arterial pressure of 40 mm Hg (1 mm Hg = 133 N/m2), which was maintained for 2 h. Muscles from these animals ('shock' muscles) showed resistance to the stimulation of glucose uptake by insulin. Addition of 1 mM ATP–MgCl2 to the medium had no effect on basal glucose uptake in either group of muscles, but it permitted insulin to exert its stimulatory effect in 'shock' muscles. An optimal insulin effect on glucose uptake in 'shock' muscles incubated without ATP was observed at an insulin concentration of 0.2 Unit/ml. When 1 mM ATP–MgCl2 was added to the medium, optimal insulin effect in 'shock' muscles was observed at an insulin concentration of 0.007 Unit/ml. Increasing the concentration of ATP–MgCl2 to 2.5 mM in the medium resulted in an optimal insulin effect at an insulin concentration of 0.001 Unit/ml in 'shock' muscles. Following 1 h incubation in Krebs–HCO3 medium, intracellular ATP contents of 'shock' muscles were approximately 50% lower than in control muscles. Addition of 1 mM ATP–MgCl2 to the incubation medium had no effect on the intracellular ATP contents of either group of muscles following incubation; however, 2.5 mM ATP–MgCl2 elevated intracellular ATP contents of 'shock' muscles but had no effect in control muscles. Possible mechanisms for this reversal of insulin resistance by ATP-MgCl2 in shock are discussed.

Sign in / Sign up

Export Citation Format

Share Document