摘要:

ObjectiveTo study the effect of graded crystalloid fluid resuscitation on central hemodynamics and outcome after intra-abdominal hemorrhage.MethodsTen minutes after a 5-mm long laceration was produced in the infrarenal aorta, 32 pigs were randomized to receive either no fluid or Ringer's solution in the proportion 1:1, 2:1, or 3:1 to the expected amount of blood lost per hour (26 mL kg sup -1) over 2 hours. The hemodynamics were studied using arterial and pulmonary artery catheters and four blood flow probes placed over major blood vessels.ResultsDuring the first 40 minutes after the injury, the respective blood flow rates in the distal aorta were 39% (no fluid), 41% (1:1), 56% (2:1), and 56% (3:1) of the baseline flow. Fluid resuscitation increased cardiac output but had no effect on arterial pressure, oxygen consumption, pH, or base excess. Rebleeding occurred only with the 2:1 and 3:1 fluid programs. Survival was highest with the 1:1 and 2:1 programs.ConclusionsCrystalloid fluid therapy improved the hemodynamic status but increased the risk of rebleeding. Therefore, a moderate fluid program offered the best chance of survival.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectiveIncreased intra-abdominal pressure (IAP) compromises cardiopulmonary function and visceral perfusion. Our goal was to characterize acute changes in these subsystems associated with operative abdominal decompression.Patient Population25 mm Hg).Main Outcome MeasuresStudied hemodynamic variables included pulmonary artery occlusion pressure (PAOP), right ventricular end-diastolic volume index (RVEDVI), and cardiac index (CI). Pulmonary variables included shunt fraction (Qs/Qt) and dynamic compliance (Cdyn). Visceral perfusion was assessed using hourly urine output 4 hours before and after decompression (UOP) and gastric intramucosal pH (pHi). Mean values before and after decompression were compared using the paired t test. Linear regression and Fisher's z transformation were used to evaluate the relationships between RVEDVI, PAOP, CI, and IAP. IAP was transduced via bladder pressures. Significance was defined as p < 0.05. Data are expressed as means +/- SD.ResultsIAP decreased with decompression (49 +/- 11 to 19 +/- 6.8 mm Hg; p < 0.0001). RVEDVI improved independent of CI and correlated better (p < 0.01) with CI (r = 0.49, p = 0.04) than PAOP did (r = -0.36, p = 0.09). PAOP correlated significantly with IAP (r = 0.45, p = 0.04). Decompression resulted in significant improvements in Qs/Qt, Cdyn, UOP, and pHi.ConclusionAbdominal decompression in patients with increased IAP improves preload, pulmonary function, and visceral perfusion. Elevated IAP has important effects on PAOP, which makes the PAOP an unreliable index of preload in these patients.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundIntra-abdominal hypertension is known to decrease hepatic blood flow, but its effect on hepatic energy level has not described.MethodsFifty-three rabbits were mechanically ventilated and divided into five groups. Intra-abdominal hypertension was induced by saline infusion and maintained for 30 minutes. Hepatic sinusoidal functional blood flow was evaluated by means of indocyanine green disappearance rate (ICG-K), hepatic mitochondrial redox status was evaluated by arterial ketone body ratio, and tissue energy level was evaluated by energy charge (EC).ResultsAt an intra-abdominal pressure of 20 mm Hg, ICG-K was significantly decreased, with no decrease in EC. At 30 mm Hg, hypoxemia developed and the ICG-K decreased further, with significant decreases observed in arterial ketone body ratio and EC. The latter were not increased by administration of oxygen.ConclusionAt an intra-abdominal pressure of 20 mm Hg, a slight decrease in sinusoidal flow did not affect hepatic energy level. At 30 mm Hg, a reduced hepatic mitochondrial redox status and a decreased energy level were attributed to a decrease in sinusoidal flow in this animal model.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Hemorrhage is a major cause of mortality in pelvic fractures.Bleeding can be controlled in hypotensive patients by direct ligation, angiographic embolization, pelvic packing, and acute external fixation. Acute application of an external fixator can reduce pelvic volume and reduce bleeding fractures to effect tamponade. This therapy assumes that the pelvis represents a closed space, which clearly is not true anatomically. However, the premise may hold functionally. This study explored the relationship between pressure and volume in the intact and disrupted pelvic retroperitoneum. In cadaveric specimens, the external iliac vein was dissected, ruptured, and cannulated. This method allowed controlled flow of fluid, with simultaneous measurement of pressure, into the intact retroperitoneum. Open book pelvic fractures were created by applying external rotation to the pelvis through the femoral heads. The pressure-volume measurements, without and with external fixation applied, were repeated after the fracture, as well as after a laparotomy. In the intact retroperitoneum, pressures rapidly rose to an average of 30 mm Hg after infusion of 5 liters of fluid. After fracture, up to 20 liters of fluid could be infused at pressures not exceeding 35 mm Hg. External fixation increased pressures approximately 3 mm Hg at low fluid volumes, and approximately 11 mm Hg at the highest fluid volumes. Laparotomy decreased retroperitoneal pressure from approximately 35 mm Hg to approximately 15 mm Hg. The results of the study suggest that low-pressure venous hemorrhage may be tamponaded by an external fixator, given that enough fluid volume is present in the pelvic retroperitoneum. However, external fixation may not generate sufficient pressure to stop arterial bleeding. In any case, it seems that a large volume of fluid must be lost into the pelvis before an external fixator can have much effect on retroperitoneal pressures.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectivesTo examine (1) the effects of trauma on changes in neutrophil L-selectin and CD11b expression and on the levels of soluble L-selectin and (2) whether these alterations are different on leukocyte subpopulations in those patients who develop multiple organ dysfunction syndrome.Materials and Methodsor=to 16 and 15 patients with ISS score < 16 were studied. Arterial blood were collected serially after injury. The staining of leukocyte surface adhesion molecules was performed with antibodies against L-selectin and CD11b. Positive cell count and mean fluorescence intensity were determined by flow cytometry. Soluble L-selectin was measured using enzyme-linked immunosorbent assay.Resultsor=to 16, neutrophil L-selectin expression showed an immediate increase, reaching peak levels between 3 to 4 hours after injury (p < 0.05 vs. patients with ISS < 16), followed by a gradual decrease. Plasma levels of soluble L-selectin reached peak levels at 6 hours after injury. However, in patients with ISS < 16, minimal changes in L-selectin expression and soluble L-selectin were observed. Neutrophil CD11b expression showed an immediate increase for the first 3 hours followed by a gradual increase up to 24 hours after injury. In patients who developed multiple organ dysfunction syndrome, CD11b both on neutrophils and lymphocytes remained elevated for 120 hours.ConclusionsThese findings suggest that acute neutrophil activation is an early event after trauma and may be implicated as "a vulnerable window" for leukocyte-mediated end organ injury.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Suppressed granulocyte and macrophage growth after burn infection or endotoxicosis appears to be mediated by macrophage-derived products. In this study, we found that after burn, burn plus infection, or endotoxicosis, peritoneal-elicited macrophages or bone marrow cells released increased amounts of prostaglandin E2(PGE2) and inhibited growth of granulocyte-macrophage progenitor cells (GM-CFC). PGE sub 2, when added in culture, inhibited in vitro GM-CFC growth in a dose-dependent manner. Pretreatment of bone marrow cells with either dibutyryl cyclic adenosine monophosphate or Forskolin in vitro mimicked the PGE2inhibition, further aggravated the inhibition induced by burn, burn plus infection, or endotoxicosis, and was not blocked by co-culture with indomethacin. Pretreatment of bone marrow cells with SQ22536, an adenylate cyclase inhibitor, significantly restored the suppressed GM-CFC growth found after burn, burn plus infection, or endotoxicosis. Alterations in myeloid production after burn infection appear to be related in part to the level of intracellular cyclic adenosine monophosphate for the GM-CFC and are responsive to PGE2.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

BackgroundNeutrophils may play an important role in the development of liver ischemia/reperfusion injury. We investigated the effects of the immunosuppressants azathioprine (AZA), cyclosporine A (CsA), tacrolimus (FK506), and rapamycin (RPM) on the expression of cytokine-induced neutrophil chemoattractant (CINC) after ischemia/reperfusion of the liver.MethodsLiver ischemia was induced in male Wistar rats by occluding the portal vein with a microvascular clip for 30 minutes. Rats received two intramuscular injections of AZA (4 mg/kg), CsA (5 mg/kg), FK506 (0.5 mg/kg), or RPM (0.5 mg/kg) 3 and 24 hours before ischemia/reperfusion of the liver.ResultsSerum CINC concentrations in untreated animals increased, peaked 6 hours after reperfusion, and thereafter decreased gradually. Pretreatment with AZA, CsA, FK506, and RPM, however, inhibited the increase in serum CINC concentrations after reperfusion. CINC mRNA in liver tissue increased and peaked 3 hours after reperfusion, but was significantly lower in animals treated with AZA, CsA, FK506, and RPM. In vitro CINC production by Kupffer cells harvested from animals treated with AZA, CsA, FK506, or RPM 3 hours after reperfusion was also significantly lower than that observed in untreated animals. Both myeloperoxidase activity and the number of neutrophils accumulating in the liver 24 hours after reperfusion in animals treated with AZA, CsA, FK506, and RPM were significantly lower than in untreated animals. This correlated with lower serum aspartate transaminase, alanine transaminase, and lactate dehydrogenase levels in animals treated with AZA, CsA, FK506, and RPM 24 hours after reperfusion.ConclusionThe immunosuppressants AZA, CsA, FK506, and RPM reduce neutrophil accumulation and attenuate ischemia/reperfusion injury of the liver.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

ObjectiveTo test the hypothesis that moderate hypothermia (Hth) (30[degree sign]C) or breathing 100% oxygen (best with both combined) would prolong survival during lethal uncontrolled hemorrhagic shock (UHS) compared with normothermia (38[degree sign]C) and breathing air.MethodsForty Sprague-Dawley rats were anesthetized with halothane during spontaneous breathing of N2O/O2(50:50). UHS was induced by volume-controlled blood withdrawal of 3 mL/100 g over 15 minutes, followed by 75% tail amputation and randomization to one of four UHS treatment groups (10 rats each): group 1 (control) was maintained on room air and rectal temperature of 38[degree sign]C; group 2 (Hth) was maintained on air and 30[degree sign]C; group 3 (O2) was maintained on FiO sub 2 100% (starting immediately after tail cut) and 38[degree sign]C; and group 4 (O2-Hth) was maintained on FiO2100% and 30[degree sign]C. Rats were observed otherwise untreated until death (apnea and pulselessness) or for a maximum of 5 hours.ResultsDuring the initial blood withdrawal, mean arterial pressure (MAP) decreased to an average of 24 mm Hg. Seventeen of 40 rats then showed an increase in MAP (attempted self-resuscitation). Induction of hypothermia increased MAP to around 35 mm Hg at 30 minutes but did not increase bleeding. Additional blood loss from the tail stump averaged 1.0, 2.3, 2.9, and 1.7 mL in groups 1, 2, 3, and 4, respectively (not significant). Breathing 100% oxygen did not affect MAP or blood loss. Survival time was a mean of 47 and 52 minutes in normothermic groups 1 and 3 versus 121 and 135 minutes in hypothermic groups 2 and 4, respectively (p < 0.001, Kaplan-Meier). Breathing FiO2100% increased PaO2but did not change MAP, blood loss, or survival time.ConclusionModerate hypothermia, but not increased FiO2, prolonged survival time during untreated UHS in rats. The effect of hypothermia on survival after resuscitation from UHS needs to be determined.

ISSN:0022-5282    

出版商:OVID    

年代:1998

数据来源: OVID