Fluid resuscitation with O2 vs. non-O2 carriers after 2 h of hemorrhagic shock in conscious hamsters

1997 ◽  
Vol 272 (1) ◽  
pp. H525-H537 ◽  
Author(s):  
H. Kerger ◽  
A. G. Tsai ◽  
D. J. Saltzman ◽  
R. M. Winslow ◽  
M. Intaglietta
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Whole Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Dextran 70 ◽  
Autologous Whole Blood ◽  
Tissue Po2

Efficacy of a cell-free o-raffinose cross-linked and oligomerized hemoglobin (Hemo-link) solution in restoring macro- and microcirculatory conditions after 2 h of hemorrhagic shock (40 mmHg) was compared with conventional treatment with autologous whole blood, Ringer lactate (RL), and Dextran 70. Studies were conducted in the dorsal skinfold microcirculation of conscious hamsters. Initial infusion was equivalent to shed blood volume (SBV) for RL and 50% of SBV for remaining solutions. After 2 h all animals received blood at 50% of SBV. Vessel diameter, functional capillary density, microvascular red blood cell velocity, and flow were measured. Arteriolar, venular, and tissue PO2 were determined by phosphorescence decay. Systemic parameters included mean arterial blood pressure, heart rate, arterial blood gases, pH, and base excess. Autologous whole blood and Hemolink, but not Dextran 70 and RL, restored mean arterial blood pressure, systemic blood gas, and metabolic parameters. Tissue PO2 recovered to 40–50% with blood and Hemolink but remained significantly lower (10-15% of control) with Dextran 70 and RL. Initial volume replacement after shock with blood or Hemolink yields equivalent macro- and microhemodynamic improvements not attainable with non-O2-carrying plasma expanders.

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.

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.

Vasopressin, but Not Fluid Resuscitation, Enhances Survival in a Liver Trauma Model with Uncontrolled and Otherwise Lethal Hemorrhagic Shock in Pigs

2003 ◽  
Vol 98 (3) ◽  
pp. 699-704 ◽  
Author(s):  
Karl H. Stadlbauer ◽  
Horst G. Wagner-Berger ◽  
Claus Raedler ◽  
Wolfgang G. Voelckel ◽  
Volker Wenzel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Fluid Resuscitation ◽  
Liver Trauma ◽  
Experimental Therapy ◽  
Midline Laparotomy ◽  
Arterial Blood ◽  
Trauma Model

Background The authors compared the effects of vasopressin fluid resuscitation on survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs. Methods A midline laparotomy was performed on 23 domestic pigs, followed by an incision, and subsequent finger fraction across the right medial liver lobe. During hemorrhagic shock, animals were randomly assigned to receive either 0.4 U/kg vasopressin (n = 9), or fluid resuscitation (n = 7), or saline placebo (n = 7), respectively. A continuous infusion of 0.08 U x kg(-1) x min(-1) vasopressin in the vasopressin group, or normal saline was subsequently administered in the fluid resuscitation and saline placebo group, respectively. After 30 min of experimental therapy, bleeding was controlled by surgical intervention, and blood transfusion and rapid fluid infusion were subsequently performed. Results Maximum mean arterial blood pressure during experimental therapy in the vasopressin-treated animals was significantly higher than in the fluid resuscitation and saline placebo groups (mean +/- SD, 72 +/- 26 vs 38 +/- 16 vs 11 +/- 7 mmHg, respectively; P< 0.05). Subsequently, mean arterial blood pressure remained at approximately 40 mmHg in all vasopressin-treated animals, whereas mean arterial blood pressure in all fluid resuscitation and saline placebo pigs was close to aortic hydrostatic pressure (approximately 15 mmHg) within approximately 20 min of experimental therapy initiation. Total blood loss was significantly higher in the fluid resuscitation pigs compared with vasopressin or saline placebo after 10 min of experimental therapy (65 +/- 6 vs 42 +/- 4 vs 43 +/- 6 ml/kg, respectively; P< 0.05). Seven of seven fluid resuscitation, and seven of seven saline placebo pigs died within approximately 20 min of experimental therapy, while 8 of 9 vasopressin animals survived more than 7 days (P < 0.05). Conclusions Vasopressin, but not fluid resuscitation or saline placebo, ensured survival with full recovery in this liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.

Liberal vs. conservative vasopressor use to maintain mean arterial blood pressure during resuscitation of septic shock: an observational study

2007 ◽  
Vol 34 (1) ◽  
pp. 157-162 ◽  
Author(s):  
Sanjay Subramanian ◽  
Murat Yilmaz ◽  
Ahmer Rehman ◽  
Rolf D. Hubmayr ◽  
Bekele Afessa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Observational Study ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Arterial Blood ◽  
Vasopressor Use

Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Neurosurgical Procedures ◽  
Shr Rats ◽  
Mr Microscopy ◽  
Content Type ◽  
Wky Rats ◽  
Arterial Blood ◽  
Fine Print

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

Cerebroelectrical Depression Following Surfactant Treatment in Preterm Neonates

PEDIATRICS ◽  
1992 ◽  
Vol 89 (4) ◽  
pp. 643-647 ◽  
Author(s):  
Lena Hellström-Westas ◽  
Nils W. Svenningsen ◽  
Angela H. Bell ◽  
Liselotte Skov ◽  
Gorm Greisen
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Intraventricular Hemorrhage ◽  
Preterm Neonates ◽  
Cerebral Function ◽  
Surfactant Treatment ◽  
Arterial Blood ◽  
Cerebral Dysfunction ◽  
Almost All

During surfactant treatment of respiratory distress syndrome, 23 premature newborns were investigated with continuous amplitude-integrated electroencephalography (cerebral function monitors). Simultaneously, arterial blood pressure and transcutaneous blood gas values were recorded. A short(<10 minutes) but significant decrease in cerebral activity was seen in almost all neonates immediately after the surfactant instillation, in spite of an improved pulmonary function. In 21 of 23 neonates, a transient fall in mean arterial blood pressure of 9.3 mm Hg (mean) occurred coincidently with the cerebral reaction. Neonates in whom intraventricular hemorrhage developed tended to have lower presurfactant mean arterial blood pressure (P> .05), but they had a significantly lower mean arterial blood pressure after surfactant instillation (P < .05). No other differences were found between neonates in whom intraventricular hemorrhage developed and those without intraventricular hemorrhage. The present findings demonstrate that an acute cerebral dysfunction may occur after surfactant instillation. In some vulnerable neonates with arterial hypotension and severe pulmonary immaturity,the fall in mean arterial blood pressure may increase the risk of cerebral complications and could be related to an unchanged rate of intraventricular hemorrhage after surfactant treatment.

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