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PubMed1993

Myocardial hypercarbic acidosis reduces cardiac resuscitability.

BACKGROUND: The severity of spontaneous myocardial hypercarbic acidosis during cardiac arrest previously has been predictive of the likelihood of restoring spontaneous circulation. The present study investigated whether hypercarbia itself impairs cardiac resuscitation. Since coronary perfusion pressure is the overriding determinant of cardiac resuscitability, we used a porcine model of cardiac arrest in which coronary perfusion pressure was controlled. METHODS: In 31 domestic pigs anesthetized with pentobarbital, the lungs were mechanically ventilate. Myocardial carbon dioxide tension and hydrogen ion concentration were measured by sensors advanced into the myocardium. After 15 min of untreated ventricular fibrillation, venoarterial extracorporeal circulation was initiated. Animals were randomized to receive a carbon dioxide gas fraction in the extracorporeal perfusate of 0.00, 0.10, 0.30, or 0.50 with oxygen concentration maintained constant at 0.50. Extracorporeal flow was adjusted to maintain a coronary perfusion pressure in the range of 60-80 mmHg, a level of predictive resuscitability. RESULTS: The proportion of animals successfully resuscitated and the proportion of animals maintaining spontaneous circulation for 60 min or longer decreased with increasing perfusate PCO2 and concurrent increases in myocardial CO2 tension in the absence of altered oxygen utilization (P < .01). CONCLUSIONS: Hypercarbia, in this experimental setting, was therefore a quantitative determinant of both myocardial resuscitability and the restoration of spontaneous circulation.

Acidosis↗
PubMed2005

Intercellular adhesion molecule-1 inhibition attenuates neurologic and hepatic damage after resuscitation in mice.

BACKGROUND: Cardiac arrest and cardiopulmonary resuscitation may result in multiorgan damage after global hypoxia due to neutrophil recruitment. Patients display all signs of a systemic inflammatory response syndrome. Reducing neutrophil recruitment may thus preserve organ function. METHODS: Mice were subjected to cardiac arrest and resuscitation. CD18/CD11b expression on circulating neutrophils was assessed by flow cytometry. Intercellular adhesion molecule-1 expression was analyzed by Western blot and immunofluorescence. Neutrophil recruitment was quantified by immunohistochemistry. Neurologic function was assessed by a balance test. For liver and kidney function, plasma alanine aminotransferase activity and creatinine concentrations were determined. To reduce neutrophil recruitment, mice received 100 microg anti-intercellular adhesion molecule-1 antibody intraperitoneally. RESULTS: Resuscitation led to severe hypoxia, acidosis, and hypercarbia. Adhesion molecule expression and neutrophil recruitment were increased in the liver, kidney, and brain. Neurologic performance was impaired 24 h after cardiac arrest. Creatinine and alanine aminotransferase concentrations were significantly increased. Immunoneutralization of intercellular adhesion molecule-1 attenuated neutrophil influx in the liver along with alanine aminotransferase activity, whereas creatinine concentrations and neutrophil influx in the kidney remained unchanged. Neurologic function was improved in the treatment group. CONCLUSIONS: Global hypoxia induces activation of the endothelium in the brain, liver, and kidney. The resulting damage to the brain and liver are due to infiltration of neutrophils, whereas kidney damage is not, because reduction of neutrophil recruitment after cardiopulmonary resuscitation improves recovery of neurologic and hepatic but not renal function. Inhibition of intercellular adhesion molecule-1 after global hypoxia may be beneficial in patients experiencing cardiac arrest and resuscitation.

Animals↗
PubMed2007

Milrinone combined with vasopressin improves cardiac index after cardiopulmonary resuscitation in a pig model of myocardial infarction.

BACKGROUND: Milrinone used for acute cardiac insufficiency could be of interest during cardiopulmonary resuscitation because of its positive inotropic effects. In this study, the combination of milrinone-vasopressin was compared with epinephrine and vasopressin, as well as with the combination of epinephrine-vasopressin, in reference to hemodynamics. METHODS: Thirty-two pigs underwent ligation of the circumflex coronary artery and induction of ventricular fibrillation lasting for 4 min. Cardiopulmonary resuscitation was performed after randomization to one of four groups: epinephrine (30-microg/kg bolus), vasopressin (0.4-U/kg bolus), epinephrine-vasopressin (15-microg/kg epinephrine bolus, 0.2-U/kg vasopressin bolus), or milrinone-vasopressin (0.4-U/kg vasopressin bolus, 50-microg/kg milrinone bolus over 5 min and a continuous infusion of 0.4 microg.kg.min). The hemodynamic variables were measured before cardiopulmonary resuscitation as well as 4, 8, 15, and 30 min after return of spontaneous circulation. RESULTS: All animals were resuscitated successfully. The animals of the milrinone-vasopressin group displayed significantly (P<0.05) higher cardiac index values (30 min after return of spontaneous circulation: epinephrine, 65.8+/-13.2; vasopressin, 70.7+/-18.3; epinephrine-vasopressin, 69.1+/-36.2; milrinone-vasopressin, 120.7+/-34.8 ml.min.kg) without a decrease in mean arterial pressure or coronary perfusion pressure. CONCLUSIONS: The combination of vasopressin-milrinone as compared with epinephrine during cardiopulmonary resuscitation leads to an improved cardiac index without relevant decrease of mean arterial pressure or coronary perfusion pressure.

Animals↗
PubMed1974

Extravascular lung water following hemorrhagic shock in the baboon: Comparison between resuscitation with Ringer's lactate and Plasmanate.

Baboons were subjected to deep hemorrhagic shock by using a membrane potential of -65 mv as an endpoint. They were then resuscitated with either Plasmanate plus their shed blood or Ringer's lactate plus their shed blood. As compared with their own preshock values, the Plasmanate-resuscitated animals accumulated more extravascular lung water than the Ringer's lactate-resuscitated animals. Another group of baboons resuscitated from deep shock demonstrated significant extravasation of albumin on postmortem analysis of lung composition. This increased tendency for extravasation of albumin after shock partially explains why resuscitation with Plasmanate gave no protection against the formation of pulmonary edema. The authors believe that Plasmanate, and probably other colloidal solutions, should be used sparingly in the initial treatment of deep hemorrhagic shock.

Albumins↗
PubMed1980

Initial experience with a "code-no code" resuscitation system in cancer patients.

A "code-no code" resuscitation classification was recently instituted at Memorial Sloan Kettering Cancer Center. Physician compliance was voluntary. Of 48 subsequent cardiopulmonary arrests, 7 patients (14.6%) were discharged from hospital. They included 4 of 17 patients (23.5%) previously assigned "code" status and 1 of 27 patients (3%) whose resuscitation status had not been designated. Reluctance on the part of the primary physician to withhold resuscitation was clearly evident in this group, of whom more than half had widespread malignancy. Stage of disease did not influence the 50% rate of successful resuscitations but no patient with metastatic or uncontrolled cancer left hospital. The discharge rate among arrest patients with recently diagnosed or localized cancer was 32%. These observations justify continued efforts to restrict cardiopulmonary resuscitation (CPR) to those with a reasonable prognosis for worthwhile palliation or cure.

Adolescent↗
PubMed1983

Drug therapy in resuscitation from electromechanical dissociation.

Electromechanical dissociation (EMD) (organized ECG activity without myocardial contractions) is thought to be rare and associated with poor prognosis. Epinephrine, calcium chloride, and atropine are recommended during attempted resuscitation. Epinephrine's effectiveness in other forms of cardiac arrest is due to its alpha-adrenergic action. Its beta-adrenergic effect may be a disadvantage which is not characteristic of methoxamine, a pure alpha-agonist. Forty anesthetized dogs were asphyxiated until asystolic. Five min later each had slow organized ECG activity. Ventilation with air and sternal compressions were started; 10 dogs each received saline, atropine, calcium chloride, or methoxamine iv. Resuscitation was discontinued after 10 min. Two dogs were resuscitated after saline. Results were not significantly better after atropine or calcium chloride. All 10 which received methoxamine were resuscitated; methoxamine, given at the end of the protocol to all dogs not resuscitated with atropine or calcium chloride, promptly restored spontaneous circulation.

Animals↗
PubMed1985

Effects on cerebral hemodynamics of resuscitation from endotoxic shock with hypertonic saline versus lactated Ringer's solution.

This study was carried out to determine whether 7.5% hypertonic saline (HSS) and lactated Ringer's solution restore cerebral hemodynamics comparably when used for resuscitation from endotoxic shock. Endotoxic shock was produced in 13 dogs by the iv administration of 1.5 mg/kg Escherichia coli endotoxin. After 90 min of shock, seven animals were resuscitated with lactated Ringer's solution, 60 ml/kg iv, and six with 7.5% HSS, 6 ml/kg iv. Both solutions increased cardiac output and mean arterial pressure. With HSS, intracranial pressure was lower immediately after resuscitation (p less than .001) and one hour later (p less than .01). However, cerebral blood flow was not increased by either fluid and, due to hemodilution, cerebral oxygen transport decreased during resuscitation in both groups of animals. Thus, HSS restored systemic hemodynamics and maintained a lower intracranial pressure during resuscitation from endotoxic shock, but failed, as did lactated Ringer's solution, to restore cerebral blood flow and oxygen transport.

Animals↗
PubMed1986

Cerebral hemodynamics after hemorrhagic shock: effects of the type of resuscitation fluid.

Cerebral blood flow (CBF), cerebral oxygen delivery, and intracranial pressure were measured in 12 dogs subjected to hemorrhagic shock and then resuscitated with lactated Ringer's solution or 6% hetastarch. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure (MAP) of 40 mm Hg with BP maintained at that level for 30 min. Six animals were resuscitated with lactated Ringer's solution, 60 ml/kg iv, and six with 6% hetastarch, 20 ml/kg iv. Both solutions effectively restored systemic hemodynamic stability, increasing cardiac output and MAP. Intracranial pressure was significantly (p less than .05) lower after resuscitation in the hetastarch group, but CBF, which had decreased during shock, was not normalized by either fluid, and cerebral oxygen transport fell further with resuscitation secondary to a hemodilutional reduction of hemoglobin. Although 6% hetastarch may improve systemic hemodynamics and maintain a low intracranial pressure during resuscitation, it fails, as does lactated Ringer's solution, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Animals↗
PubMed1988

Some futuristic possibilities for resuscitation.

Future possibilities for resuscitation must take into account our still limited understanding of the reperfusion syndrome. Clinical resuscitation research must incorporate the use of prolonged life-support techniques. These may depend on the use of cardiopulmonary bypass to provide improved reperfusion of vital organs and to permit the time necessary to evaluate and treat the mediators and modifiers of the reperfusion syndrome. It is likely that some patients who require prolonged life support will need replacement organs or, should their brains fail to survive resuscitation, become organ donors. Physicians involved in resuscitation and transplantation must come to grips with the logistic problems of techniques for prolonged resuscitation.

Blood Circulation↗
PubMed1991

Acute ethanol intoxication decreases the likelihood of resuscitation from cardiac arrest in rats.

BACKGROUND AND METHODS: Acute ethanol intoxication has been shown to depress myocardial performance in both laboratory and clinical studies. The present study was designed to examine the effect of acute ethanol intoxication on resuscitation of rats subjected to cardiac arrest. Rats were given 1.2 g ("moderately intoxicated") or 2.4 g ("highly intoxicated") of ethanol/kg, or distilled water ("nonintoxicated" rats). Using a standardized technique, we induced cardiac arrest. CPR was then attempted using chest compressions interposed with abdominal compressions. Resuscitation was said to be successful if BP returned spontaneously within 6 mins of institution of chest compressions interposed with abdominal compressions, and if systolic BP was 50% of its prearrest level within 10 mins of discontinuation of chest compressions interposed with abdominal compressions. Mean +/- SD serum ethanol levels were 121.3 +/- 12.9 mg/dL (26.3 +/- 2.8 mmol/L) (moderately intoxicated rats) and 254.4 +/- 34.6 mg/dL (55.2 +/- 7.5 mmol/L) (highly intoxicated rats). RESULTS: Resuscitation was successful in 75% (15/20) of nonintoxicated rats, 46.7% (7/15) of moderately intoxicated rats, and 33.3% (5/15) of highly intoxicated rats. The difference in resuscitation rates was significant for nonintoxicated rats compared with either intoxicated rats as a group (p = .021) or highly intoxicated rats (p = .019), but was not significant for nonintoxicated rats compared with moderately intoxicated rats. CONCLUSION: Acute ethanol intoxication appears to decrease the likelihood of successful resuscitation in a dose-dependent fashion.

Alcoholic Intoxication↗
PubMed1991

Hypercarbic acidosis reduces cardiac resuscitability.

BACKGROUND AND METHODS: Marked increases in myocardial hypercarbia and acidosis accompany cardiac arrest and resuscitation. To investigate whether hypercarbic acidosis independent of oxygenation is of itself detrimental to cardiac resuscitation, three groups of six Sprague-Dawley rats were ventilated with gas mixtures containing concentrations of inspired CO2 (FICO2) of 0.0, 0.3, or 0.5, with oxygen fractions held constant at 0.5. After 4 mins of ventricular fibrillation, mechanical chest compressions were initiated with a pneumatic thumper; 2 mins later, transthoracic defibrillation was attempted. RESULTS: Each animal ventilated with FICO2 of 0.0 or 0.3 was successfully resuscitated. However, none of the animals ventilated with FICO2 of 0.5, in which aortic pH was less than 6.67 and aortic PCO2 was greater than 200 torr (greater than 26.7 kPa), was resuscitated (p less than .001). This finding contrasted with a second control group of seven identically treated animals which, in the absence of cardiac arrest, demonstrated no adverse effects after ventilation with an FICO2 of 0.5. CONCLUSIONS: Increases in FICO2 to levels of 0.5 under conditions of constant arterial oxygenation and controlled coronary perfusion pressure preclude successful resuscitation in this rodent model of CPR.

Acidosis, Respiratory↗
PubMed1992

Diltiazem improves resuscitation from experimental ventricular fibrillation in dogs.

OBJECTIVE: To determine the effect of diltiazem on survival immediately after cardiac arrest and cardiopulmonary resuscitation (CPR) in dogs. DESIGN: Prospective, double-blind, randomized trial. SETTING: Laboratory at a large, university-affiliated medical center. SUBJECTS: Twenty-eight mongrel dogs, weighing 12 to 16 kg. INTERVENTIONS: After the administration of anesthesia, catheters were placed in the pulmonary artery, aortic arch, left ventricle, right ventricle, and great cardiac vein (12 dogs) for sample collection, pressure determinations, and induction of ventricular fibrillation. Dogs were randomized to receive either diltiazem, calcium chloride, or placebo (saline) either before or early during CPR. Dogs underwent 3 mins of unassisted fibrillatory arrest followed by 10 mins of standard CPR using a pneumatic device. After 13 mins of ventricular fibrillation, defibrillation was attempted repeatedly for less than or equal to 10 mins. Successful resuscitation was defined as an organized rhythm with an unassisted systolic BP of greater than 60 mm Hg for greater than or equal to 2 mins. MEASUREMENTS AND MAIN RESULTS: The resuscitation rate was significantly greater in diltiazem-treated animals (100%) than in those dogs receiving calcium (57%) or placebo (29%). Diltiazem-treated animals were resuscitated faster and required fewer defibrillation attempts than did dogs in the other groups. During CPR, coronary artery perfusion pressure and blood gases (arterial, venous, and myocardial) were similar among treatment groups. CONCLUSIONS: Diltiazem improves the resuscitation from experimentally induced ventricular fibrillation when administered before or early during CPR. This response may have important clinical implications in the treatment of patients undergoing cardiac arrest and CPR.

Analysis of Variance↗
PubMed1993

Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation.

OBJECTIVE: To define changes in intramyocardial pH and PCO2 during cardiac arrest and resuscitation. DESIGN: Prospective and observational trial. SETTING: Mammalian research laboratory utilizing a porcine model of cardiac arrest. SUBJECTS: Sixteen domestic pigs. INTERVENTIONS: Ventricular fibrillation was induced by an alternating current delivered to the epicardium. Precordial compression was begun after 3 mins of untreated cardiac arrest and was initially adjusted to produce a coronary perfusion pressure of 10 mm Hg. Electrical defibrillation was attempted after an additional 8 mins of precordial compression. MEASUREMENTS AND MAIN RESULTS: A rapid-response, ion-selective field effect transistor sensor was adapted for measurement of intramyocardial PCO2. Intramyocardial PCO2 progressively increased from 54 to 346 torr (7.2 to 46.1 kPa) during the 11-min interval of cardiac arrest. Intramyocardial hydrogen ion concentrations were simultaneously measured with a glass electrode. The intramyocardial hydrogen ion value increased from 65 nmol/L (pH 7.20) to 441 nmol/L (pH 6.38) over the same interval. The increases in myocardial PCO2 were inversely correlated with coronary perfusion pressure and with the likelihood of successful resuscitation. Within 30 mins after successful cardiac resuscitation, myocardial PCO2 had almost completely returned to prearrest levels. CONCLUSIONS: Striking increases in myocardial PCO2 and hydrogen ion values accompany the global myocardial ischemia of cardiac arrest. The increases in myocardial PCO2, rather than decreases in pH, reflected more precisely the hemodynamic efficacy of the resuscitation effort, correlated inversely with coronary perfusion pressure, and predicted the likelihood of successful resuscitation.

Acidosis, Respiratory↗
PubMed1994

Dopamine infusion during resuscitation of experimental hemorrhagic shock.

OBJECTIVE: To compare the effects of starting dopamine administration early or late on organ perfusion by measuring tissue oxygen tensions during standard volume resuscitation of hemorrhagic shock. DESIGN: Randomized, control trial. SUBJECTS: Thirteen piglets (mean weight, 19 kg). INTERVENTIONS: The animals were bled to a state of hemorrhagic shock and resuscitated using crystalloid solution. Cardiac outputs and mean arterial pressures were measured as indicators of volume filling over a period of 80 mins. Dopamine was administered by infusion at 5 micrograms/kg/min from the start of volume correction (early-dopamine group, n = 7) or after the volume deficit was corrected (late-dopamine group, n = 6). MEASUREMENTS AND MAIN RESULTS: Blood pressures and cardiac output were measured. Tissue oxygen tensions were continuously recorded in the liver, conjunctiva, and via subcutaneous and transcutaneous electrodes in the abdominal region. Mean arterial pressure decreased from 111 +/- 5 (SEM) to 44 +/- 2 mm Hg with the induction of hemorrhagic shock. Cardiac output decreased by 78% during shock. During resuscitation, mean arterial pressure increased to near baseline values in both groups. Cardiac output recovered completely in the late-dopamine group and almost completely in the early-dopamine group. Liver oxygen tension increased to above baseline during resuscitation in the early-dopamine group. Liver oxygen tension in the early-dopamine group was significantly higher than in the late-dopamine group. Similar changes were observed in subcutaneous and transcutaneous oxygen tensions, but not in conjunctival oxygen tensions. CONCLUSIONS: Starting dopamine administration early during volume resuscitation in a model of experimental hemorrhagic shock led to higher liver, subcutaneous, and transcutaneous tissue oxygen levels. This finding indicates enhanced tissue oxygen perfusion, especially in the liver.

Animals↗
PubMed1994

Effects of trauma, duration of hypotension, and resuscitation regimen on cellular immunity after hemorrhagic shock.

OBJECTIVE: To determine the effects of: a) surgical trauma, b) crystalloid resuscitation, and c) different durations of hypotension on cellular immunity after hemorrhagic shock. DESIGN: Prospective, multiexperimental, randomized, controlled studies. SETTING: University research laboratory. SUBJECTS: Inbred C3H/HeN (endotoxin-sensitive) mice, aged 6 to 7 wks, weighing 18 to 23 g. INTERVENTIONS: Crystalloid resuscitation, with and without blood, after hemorrhage. MEASUREMENTS AND MAIN RESULTS: Mice which did or did not undergo laparotomy were subjected to hypotension of 35 mm Hg for 60 or 90 mins. Crystalloid resuscitation with and without blood was then provided. Animals were killed at 2 hrs after hemorrhage and cytokine concentrations in supernatants of splenocytes, splenic macrophages, and serum were assessed by bioassays. The cellular release of interleukin (IL)-2, IL-3, IL-6, tumor necrosis factor, and the splenocyte proliferative capacity were significantly and similarly depressed in all groups. Conversely, circulating IL-6 concentrations were significantly increased in all groups. CONCLUSIONS: Cellular immunity was depressed at 2 hrs after simple hemorrhage and no further depression occurred if hemorrhage was coupled with trauma, pure crystalloid resuscitation was provided, or the shock period was prolonged. Thus, the early immunodepression after hemorrhage was mainly dependent on the severity rather than the duration of shock, resuscitation regimen, or tissue trauma.

Animals↗
PubMed1995

Attenuation of shock-induced hepatic microcirculatory disturbances by the use of a starch-deferoxamine conjugate for resuscitation.

OBJECTIVE: To determine the effects of a hydroxyethyl starch-deferoxamine conjugate on hepatic microcirculation in an isobaric, anesthetized rat model of hemorrhagic shock and asanguineous resuscitation. DESIGN: Prospective, randomized, controlled study. SETTING: Laboratory at a university hospital. SUBJECTS: Twenty-three female, inbred Lewis rats (190 to 215 g). INTERVENTIONS: After anesthesia (pentobarbital-sodium; 50 mg/kg), tracheotomy, and cannulation, animals were assigned to a hemorrhagic shock (mean arterial pressure at 40 +/- 3 mm Hg for 45 mins) or a time-matched sham protocol. Rats in the shock groups received either hydroxyethyl starch or a starch-deferoxamine conjugate for resuscitation. Liver microcirculation was assessed in vivo 60 mins after onset of volume therapy by epifluorescence microscopy. MEASUREMENTS AND MAIN RESULTS: Conventional resuscitation with the starch-vehicle failed to restore sinusoidal blood flow compared with either time-matched controls (71% of control value; p < .01) or the starch-deferoxamine-treated animals (89% of control value; p < .05 compared with starch-vehicle), although a comparable restoration of central hemodynamics was achieved with both starch preparations. Additionally, treatment with the starch-deferoxamine conjugate resulted in a significant attenuation of sinusoidal leukocyte margination (sham 72.4 +/- 11.0/mm2; starch-vehicle 194.5 +/- 19.0/mm2 [p < .01 compared with controls]; starch-deferoxamine conjugate 135.9 +/- 12.1/mm2 [p < .02 compared with sham and starch-vehicle]). CONCLUSIONS: Asanguineous resuscitation with conventional hydroxyethyl starch failed to restore hepatic microvascular blood flow, despite otherwise effective resuscitation. In contrast, the starch-deferoxamine conjugate improved volumetric blood flow and attenuated leukocyte margination in hepatic sinusoids compared with starch-vehicle, suggesting involvement of iron-dependent, oxygen-derived radicals in shock-induced hepatic microcirculatory disturbances.

Animals↗
PubMed1999

Right ventricular rupture during closed-chest cardiopulmonary resuscitation after pneumonectomy with pericardiotomy: a case report.

SETTING: The collapse of a patient immediately after right pneumonectomy with right pericardiotomy resulted in closed-chest cardiopulmonary resuscitation, subsequent thoracotomy, and demise secondary to right ventricular rupture. INTERVENTIONS: Closed-chest resuscitation with opened and closed chest tubes and medical and fluid interventions were inadequate, necessitating subsequent thoracotomy. MAIN RESULTS AND CONCLUSIONS: Right ventricular rupture during resuscitation was found during subsequent thoracotomy. This rupture and inadequacy of closed-chest resuscitation were felt to be associated with the operative pneumonectomy and pericardiotomy. Pathophysiology and the role of open-heart vs. closed-chest resuscitative measures are discussed.

Cardiopulmonary Resuscitation↗
PubMed2000

Human neutrophil activation and increased adhesion by various resuscitation fluids.

OBJECTIVE: To determine whether activated neutrophils play a major role in secondary tissue injury after resuscitation in trauma. We hypothesized that human neutrophil activation and adhesion vary, depending on the type and amount of resuscitation fluid used. SETTING: University-based research facility. SUBJECTS: Ten healthy adult volunteers. DESIGN: Whole blood from volunteers was serially diluted in polypropylene tubes with various resuscitation fluids. Fluids tested were phosphate-buffered saline, normal saline, lactated Ringer's solution, dextran, hespan, 5% human albumin, 25% human albumin, 3.5% hypertonic saline, and 7.5% hypertonic saline. Neutrophil activation (intracellular oxidative burst activity with dichlorofluorescin diacetate staining) and adhesion (integrin cell surface expression of CD18) were measured with flow cytometry (fluorescence-activated cell sorting). Blood was diluted with hypertonic saline by controlling for sodium content equal to normal saline. dose-related increase in neutrophil oxidative burst activity as the result of dilution followed with crystalloid fluids and artificial colloids (dextran and hespan). The increase was 12-18 x baseline at the 75% dilution. The increase with 5% human albumin was only 2.2 x baseline, and 25% albumin did not demonstrate any increased intracellular activity. A similar significant increase in the neutrophil adhesion expression (CD18) occurred with artificial colloids (p<.05) and, to a lesser extent, with crystalloids, but not with albumin. Hypertonic saline caused a decrease in CD18 cell surface expression. CONCLUSIONS: This study suggests that the neutrophil activation and adhesion may vary, depending on the type of resuscitative fluid used. All artificial resuscitative fluids may not be similar or innocuous, as demonstrated by the dose-related increase in neutrophil activation and adhesion.

Adult↗