摘要:

ABSTRACT—The mesenteric hemodynamic response to circulatory shock is characteristic and profound; this vasoconstrictive response disproportionately affects both the mesenteric organs and the organism as a whole. Vasoconstriction of post‐capillary mesenteric venules and veins, mediated largely by the &agr;‐adrenergic receptors of the sympathetic nervous system, can effect an “autotransfusion” of up to 30% of the total circulating blood volume, supporting cardiac filling pressures (“preload”), and thereby sustaining cardiac output at virtually no cost in nutrient flow to the mesenteric organs. Under conditions of decreased cardiac output caused by cardiogenic or hypovolemic shock, selective vasoconstriction of the afferent mesenteric arterioles serves to sustain total systemic vascular resistance (“afterload”), thereby maintaining systemic arterial pressure and sustaining the perfusion of non‐mesenteric organs at the expense of mesenteric organ perfusion (Cannon's “flight or fight” response). This markedly disproportionate response of the mesenteric resistance vessels is largely independent of the sympathetic nervous system and variably related to vasopressin, but mediated primarily by the renin‐angiotensin axis. The extreme of this response can lead to gastric stress erosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepatitis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock can produce decreased or increased mesenteric perfusion, but is characterized by an increased oxygen consumption that exceeds the capacity of mesenteric oxygen delivery, resulting in net ischemia and consequent tissue injury. Mesenteric organ injury from ischemia/reperfusion due to any form of shock can lead to a triggering of systemic inflammatory response syndrome, and ultimately to multiple organ dysfunction syndrome. The mesenteric vasculature is therefore a major target and a primary determinant of the systemic response to circulatory shock.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—Trauma may cause a relevant reduction in antithrombin (AT) III activity, which is associated with adverse events. The very early changes in AT III activity after accident trauma are still unclear and possible relations with Interleukin (IL)‐6, which is known to interact with AT III, have not been investigated so far. Upon approval of the IRB/IEC, 30 patients were enrolled with multiple injuries (ISS 9‐75). Groups were performed according to injury severity, IL‐6 concentration, and survivors versus non‐survivors. Blood samples were collected at the scene of accident then at 2, 4, 6, 12, and 24 h and at day 3, 5, 10 and 15. No patient received AT III concentrates. In all groups a reduction in AT III activity occurred, which was most pronounced in very severe injuries. The activity re‐increased spontaneously and steadily in all groups regardless of the IL‐6 concentration. There was no clear impact of the AT III activity on survival.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—To define multiple organ dysfunction in newborns, we established a sequential scoring system NEOMOD (Neonatal Multiple Organ Dysfunction Score). It was developed to describe the process of increasing physiologic derangement in critically ill newborns. It provides, during the first 28 days of life, information concerning function of organ systems having a primary influence on mortality in very low birth weight (VLBW) infants. Our scoring system has been used in 142 VLBW infants. It evaluates moderate (1 point) or severe dysfunction (2 points) in 7 organ systems (central nervous system, cardiovascular, renal, respiratory, and gastrointestinal systems, and hemocoagulation and acid‐base balance) in 24‐h intervals from day 1 to 28 of life. Maximum possible value of NEOMOD was 14 points. Receiver operating characteristic curve was used for assessing predictive accuracy of maximum NEOMOD score obtained by daily scoring for mortality rate. AUC (area under curve) attained by NEOMOD was 0.95 for mortality within the first 28 days and 0.91 for hospital mortality, respectively. In the study group, NEOMOD score of ≥9 was associated with 100% mortality. An analysis of specific organ dysfunctions in the non‐survivors group (n = 16) disclosed, in all patients, dysfunction of more than two organ systems 24 h before death. Similar to critically ill adults, secondary multiple organ dysfunction can be described also in a majority of critically ill VLBW infants. NEOMOD scores may help to evaluate daily the severity of the syndrome and risk of death.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—We evaluated systemic and microvascular effects of hypertonic NaCI solution on normovolemic and hemorrhaged animals. Forty‐three Wistar rats (186 ± 4 g, mean ± SEM) were anesthetized with pentobarbital and cannulated for mean arterial pressure (MAP), heart rate (HR), and mean pulse pressure (MPP) monitoring and blood withdrawal. Diameters of 126 arterioles and 88 venules of the exteriorized mesentery were studied by using intravital microscopy. Microvascular blood flow was calculated from diameter and red blood cell velocity measurements. The protocol consisted of 15 min control, 30 min hypotension (MAP = 52.9 ± 0.9 mmHg, hemorrhaged vol. = 17.1 ± 0.7 mL/kg) and 60 min post‐infusion of either normal (0.9%) or hypertonic saline (7.5%, 4 mL/kg). Normovolemic animals showed no systemic or microvascular effects of hypertonic saline. Hemorrhagic hypotension resulted in HR fall that was not changed after infusions. Hypertonic infusion reversed MPP decrease during hypotension but only partially restored MAP and microvascular blood flow. Venules did not change diameter during protocols. During hypotension, 24% of arterioles displayed vasomotion (38% of the rats) with low‐ and high‐frequency components present in 74% and 87% of arterioles, respectively. Arterioles with vasomotion during hypotension had larger control diameters (28.9 ± 2.0 &mgr;m) and contracted more (30.8 ± 4.1%) than arterioles without vasomotion (18.7 ± 1.2 &mgr;m and 8.1 ± 1.5%, respectively). Mean arteriolar diameter did not change after infusions. After hypertonic solution, the number of vessels showing vasomotion increased 80%, frequency of vasomotion was unchanged, and amplitude increased. These findings may help to explain some of the mechanisms underlying resuscitation effects of hypertonic infusions during hemorrhagic hypotension.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—Gastrointestinal intraluminal PCO2(PiCO2) information is used to assess the adequacy of trauma patient resuscitation and to assist in choosing resuscitative interventions. Therefore, determining the limitations and potential caveats of different PiCO2monitoring systems is clinically important. This study compared two PCO2monitoring systems. The airflow device adds and then removes air samples to quantitate PCO2, whereas the fiber‐optic device does not.Methods:Airflow (TRIP Tonometer/Tonocap) and fiber‐optic (Neotrend) systems were used.In vitrothey were compared with each other and to two end‐tidal CO2monitors measuring the PCO2of humidified air containing 5% and then 10% CO2In vivothe two systems' catheters were surgically juxtaposed in 15 dogs' stomachs; paired PiCO2readings were taken throughout hemorrhage and resuscitation.Results: In vitro,paired PCO2values from the airflow and fiber‐optic devices correlated with each other (r= 0.99) and with end‐tidal values (r= 0.99 with airflow,r= 0.95 with fiber‐optic).In vivo,paired values differed significantly (P< 0.0001), correlating poorly for two devices simultaneously measuring the same variable (r= 0.61). Fiber‐optic PiCO2values were higher than airflow values (mmHg ± SEM): 69.3 ± 4.8 vs. 61.3 ± 5.6 at the start of hemorrhage, 141.3 ± 12.9 vs. 87.7 ± 7.9 by end of hemorrhage, and 104.3 ± 9.6 vs. 82.8 ± 7.0 by end of resuscitation for fiber‐optic and airflow, respectively.Conclusions:Despite agreementin vitro,airflow methods can influence PiCO2values obtainedin vivo.Passive sensing methods used to monitor PiCO2, such as fiber‐optic methods, are preferable because they neither deliver O2to, nor remove CO2from the local microenvironment.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—Intestinal ischemia/reperfusion may lead to local and distant organ damage involving nitric oxide (NO). NO rapidly reacts with heme/non‐heme‐iron‐yielding nitrosyl complexes, which can be determined directly by electron paramagnetic resonance spectroscopy. The aim of the present study was to characterize nitrosylation reactions induced by transient intestinal ischemia in blood and tissues. We used electron paramagnetic resonance spectroscopy and reverse transcription polymerase chain reaction analyses to estimate nitrosyl complex levels and inducible NO synthase mRNA expression in rats subjected to superior mesenteric artery occlusion for 60 min followed by the reperfusion. Nitrosyl hemoglobin concentrations in circulating blood were significantly increased during ischemia and reperfusion. Nitrosyl hemoglobin complexes were detected in ischemic intestine, but not in normoxic lung and liver or reperfused intestine. Administration ofN‐G‐monomethyl‐L‐arginine, a non‐specific NO synthase inhibitor, did not affect the formation of circulating nitrosyl complexes. Moreover, inducible NO synthase mRNA was not found in intestinal tissues at 30 min of reperfusion. Our data suggest an organ‐specific NO formation indicated by the increased nitrosylation reaction in ischemic intestinal tissue, but not in the distant normoxic organs, in spite of high circulating nitrosyl hemoglobin levels. NO involved in nitrosylation under intestinal ischemia/reperfusion is probably formed by NO synthase‐independent mechanism(s).

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—This study examined the hypothesis that core temperature (T°) during cardiopulmonary bypass (CPB) influences the perioperative systemic inflammatory response and post‐operative organ damage. Twenty‐four pigs were assigned to a T° regimen during CPB: normothermia (T° 37°C; n = 8), moderate hypothermia (T° 28°C; n = 8), or deep hypothermia (T° 20°C; n = 8). Perioperative leukocyte activation, endotoxin release, and production of tumor necrosis factor‐&agr; (TNF&agr;) and interleukin‐10 (IL10) were examined with regard to post‐operative organ damage, which was scored at histological examination of tissue probes of heart, lungs, liver, kidney, and ileum, taken 6 h after CPB. Total blood leukocyte count and TNF&agr; plasma levels during CPB were significantly lower and IL10 levels were significantly higher in the moderate hypothermic group than in both other groups. Elastase activity, leukotriene B4‐, and endotoxin levels were not affected by T° regimen. Moderate hypothermia was associated with the lowest histological organ damage score and normothermia with the highest. In all animals organ damage score for heart, lungs, and kidneys correlated significantly with TNF&agr; levels at the end of CPB. Our data demonstrate a clear relationship between TNF&agr; production during cardiac operations and post‐operative multiple‐organ damage. Moderate hypothermia, by stimulating IL 10 synthesis and suppressing TNF&agr; production during CPB, might provide organ protection.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—We explored the effects of the nucleoside transport inhibitor draflazine on regional blood flow, O2extraction capabilities, and tumor necrosis factor (TNF) release in acute endotoxic shock. Fourteen anesthetized and mechanically ventilated dogs received 2 mg/kg ofEscherichia coliendotoxin and were divided into two groups. Seven dogs received 0.1 mg/kg of draflazine 30 min before endotoxin, and 7 dogs served as a control group. Draflazine decreased arterial pressure without influencing cardiac index. Mesenteric and portal blood flow and ileum mucosal perfusion increased, but renal blood flow dramatically decreased. After endotoxemia, the draflazine‐treated dogs had a lesser fall in cardiac index, filling pressures, and left ventricular stroke work index, and a lesser increase in pulmonary vascular resistance. After fluid resuscitation, they had a consistently lower renal blood flow and ileum mucosal perfusion, but a higher mixed venous and hepatic oxygen saturation and arterial pH than the control group. When cardiac index was reduced by tamponade to study the O2extraction capabilities, renal blood flow and ileum mucosal perfusion remained lower in the draflazine group. Draflazine did not influence whole‐body O2extraction capabilities, but it delayed the occurrence of liver O2supply dependency as indicated by a significantly lower liver DO2crit (27.7 ± 3.9 vs. 43.3 ± 10.8 mL/min) and a higher O2ERcrit (62.7 ± 9.5 vs. 42.5 ± 7.1%) than controls (bothP< 0.05). On the other hand, draflazine increased intestinal DO2crit (42.4 ± 15.4 vs. 27.7 ± 6.5 mL/min,P< 0.05) compared to the control group. TNF levels remained higher in the draflazine group than in the control group, particularly 3 and 4 h after endotoxin administration. We conclude that nucleoside transport inhibition with draflazine does not alter global and hepatosplanchnic hemodynamics but may decrease gut mucosal perfusion and renal blood flow. However, this intervention can improve liver O2extraction capabilities in acute endotoxic shock.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—Impairment in endothelial cell intracellular free calcium (Cai) mobilization mechanisms may contribute to decreased nitric oxide (NO) biosynthesis and impaired vasorelaxation responses of endotoxemic guinea pigs to endothelium‐dependent vasodilators. We tested this hypothesis using fura‐2 microfluorometry to compare agonist‐stimulated Cairesponses of aortic endothelial cells freshly dispersed from guinea pigs 16 h after intraperitoneal injection ofEscherichia coliendotoxin (lipopolysaccharide, LPS; 4 mg/kg) or saline (CON). In the presence of normal extracellular Ca2+(2 mmol/L), basal (non‐stimulated) endothelial Cai(340/380 nm fluorescence ratio, R) was not different between CON and LPS cells (1.1 ± 0.03 and 1.1 ± 0.03, respectively). However, exposure to ADP (10 &mgr;mol/L) produced a biphasic increase in Caithat was markedly decreased in cells from LPS‐treated animals (P< 0.0001). Peak ADP‐stimulated Cairesponses averaged 2.2 ± 0.21 in CON cells and 1.5 ± 0.11 (P< 0.01) in cells dispersed from LPS‐treated animals. Exposure to acetylcholine (ACh; 10 &mgr;mol/L) produced sustained increases in Cai(R = 1.4 ± 0.13) in CON cells; however, LPS abolished Cairesponses to ACh. Exposure of endothelial cells to substance P (100 nmol/L) produced a biphasic increase in Caithat was not different between groups. In the absence of extracellular Ca2+(plus 10 &mgr;mol/L EGTA), exposure to ADP (10 &mgr;mol/L) produced transient increases in Cai(Ca2+release) that were decreased in cells from LPS‐treated versus CON animals. Exposure to ACh in zero Ca2+(10 &mgr;mol/L) produced smaller increases in Cai(peak R = 1.3 ± 0.12) in CON cells (when compared to ADP); however, Cairesponses to ACh remained absent in cells from LPS‐treated animals. Re‐ex‐posure to Ca2+produced sustained ACh‐induced Cairesponses (Ca2+influx) in cells from CON, but not LPS‐treated animals; LPS markedly impaired (P< 0.05) ADP‐induced sustained Cairesponses. Our data demonstrate thatin vivoLPS exposure elicits decreased agonist‐stimulated endothelial Cairesponses primarily involving impaired Ca2+influx mechanisms. Known dependence of endothelial agonist‐stimulated NO synthesis on Caisuggests that defects in cell Ca2+mobilization may contribute to LPS‐induced impaired NO biosynthesis and decreased endothelium‐dependent relaxation.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

ABSTRACT—This controlled laboratory study examined the efficacy of near‐infrared spectroscopy (NIRS) and31P‐nuclear magnetic resonance (NMR) spectroscopy in measuring regional tissue oxygenation in a isolated, perfused hind limb model of tissue dysoxia. Isolated hind limb perfusion was carried out in 20 mongrel dogs and oxygen delivery was varied by manipulating either hemoglobin concentration, oxygen saturation, or flow. Hind limbs from anesthetized mongrel dogs (n = 20) were separated and isolated perfusion performed. NIRS probes for recording relative O2saturation of tissue hemoglobin (HbO2) and cytochromea,a3and NMR probes for measuring31P‐high energy phosphates were placed over the limb. Measurements of physiologic parameters, blood gases, lactate, NIRS values for HbO2and cytochromea,a3redox state, and31P‐phosphate levels were recorded at set intervals throughout the experiment. Measures of tissue oxygen consumption (VO2) correlated with tissue oxygenation as measured by HbO2and cytochromea,a3redox state (NIRS), as well as by31P‐high energy phosphate levels (NMR) throughout the experiment. Delivery‐dependent tissue oxygenation was detected at a higher DO2by NIRS than by VO2or NMR. Tissue oxygenation as measured by NIRS and NMR shows excellent correlation with oxygen delivery in an isolated, perfused model of shock. NIRS may allow early detection of tissue dysoxia using rapid non‐invasive techniques.

ISSN:1073-2322    

出版商:OVID    

年代:2001

数据来源: OVID