Hemorrhagic Shock: Metabolic Effects

Science ◽  
1963 ◽  
Vol 141 (3580) ◽  
pp. 536-542 ◽  
Author(s):  
F. A. Simeone
1998 ◽  
Vol 12 (5) ◽  
pp. 416-420 ◽  
Author(s):  
M. Steinman ◽  
L. E. da Silva ◽  
I. J. C. Coelho ◽  
R. S. Poggetti ◽  
R. G. Bevilacqua ◽  
...  

1967 ◽  
Vol 166 (1) ◽  
pp. 29-38 ◽  
Author(s):  
ARTHUR E. Baue ◽  
EUGENE T. THAGUS ◽  
SIDNEY K. WOLFSON ◽  
ALICE L. CARY ◽  
WILLIAM M. PARKINS

2014 ◽  
Vol 120 (4) ◽  
pp. 926-934 ◽  
Author(s):  
Antoine Kimmoun ◽  
Nicolas Ducrocq ◽  
Nacira Sennoun ◽  
Khodr Issa ◽  
Charlène Strub ◽  
...  

Abstract Background: Lactic acidosis is associated with cardiovascular failure. Buffering with sodium bicarbonate is proposed in severe lactic acidosis. Bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. The authors thus investigated the cardiovascular and metabolic effects of an adapted sodium bicarbonate therapy, including prevention of carbon dioxide increase with hyperventilation and ionized calcium decrease with calcium administration. Methods: Lactic acidosis was induced by hemorrhagic shock. Twenty animals were randomized into five groups: (1) standard resuscitation with blood retransfusion and norepinephrine (2) adapted sodium bicarbonate therapy (3) nonadapted sodium bicarbonate therapy (4) standard resuscitation plus calcium administration (5) hyperventilation. Evaluation was focused in vivo on extracellular pH, on intracellular pH estimated by P31 nuclear magnetic resonance and on myocardial contractility by conductance catheter. Aortic rings and mesenteric arteries were isolated and mounted in a myograph, after which arterial contractility was measured. Results: All animals in the hyperventilation group died prematurely and were not included in the statistical analysis. When compared with sham rats, shock induced extracellular (median, 7.13; interquartile range, [0.10] vs. 7.30 [0.01]; P = 0.0007) and intracellular acidosis (7.26 [0.18] vs. 7.05 [0.13]; P = 0.0001), hyperlactatemia (7.30 [0.01] vs. 7.13 [0.10]; P = 0.0008), depressed myocardial elastance (2.87 [1.31] vs. 0.5 [0.53] mmHg/μl; P = 0.0001), and vascular hyporesponsiveness to vasoconstrictors. Compared with nonadapted therapy, adapted bicarbonate therapy normalized extracellular pH (7.03 [0.12] vs. 7.36 [0.04]; P < 0.05), increased intracellular pH to supraphysiological values, improved myocardial elastance (1.68 [0.41] vs. 0.72 [0.44] mmHg/μl; P < 0.05), and improved aortic and mesenteric vasoreactivity. Conclusions: A therapeutic strategy based on alkalinization with sodium bicarbonate along with hyperventilation and calcium administration increases pH and improves cardiovascular function.


2001 ◽  
Vol 90 (2) ◽  
pp. 441-446 ◽  
Author(s):  
John G. Younger ◽  
Nobuyoshi Sasaki ◽  
Michael D. Waite ◽  
Holt N. Murray ◽  
Edward F. Saleh ◽  
...  

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.


1981 ◽  
Vol 241 (1) ◽  
pp. H12-H17 ◽  
Author(s):  
D. B. Hackel ◽  
E. M. Mikat ◽  
K. Reimer ◽  
G. Whalen

Myocardial blood flow and left ventricular oxygen utilization were studied in verapamil-treated and untreated pentobarbital-anesthetized dogs subjected to hemorrhagic shock. Blood loss was similar in both groups. The dogs treated with verapamil (n = 15) during shock had a slower heart rate and lower left ventricular oxygen utilization than the untreated dogs (n = 14). Nevertheless, the treated dogs had a significantly higher myocardial blood flow and were able to maintain a higher cardiac index. Thus, verapamil has beneficial hemodynamic and metabolic effects that preserve myocardial function. These effects may explain the improved survival and protection of the heart against anatomic lesions, which have been demonstrated previously in dogs treated with verapamil during hemorrhagic shock.


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