氢化可的松及地塞米松对颈髓损伤继发低钠血症的不同影响

目的：持续、严重的低钠血症是颈随损伤常见的并发症，目前尚无有效的治疗方法。评价氢化可的松及地塞米松两种糖皮质激宏对急性颈通损伤继发低钠血症的不问影响而进行本研究。方法：急性完全性颈髓损伤共32例，分为氢化可的松纪12例及地基米松组20例，分别在人院后静脉使用氢化可的松150mg／d或地塞米松20mg／d，共5—6d.测定两组的血清K+、Na+、Cl-浓度变化、液体出入量、24h尿K+、Na+、Cl-排出总量。结果：与地塞米松组相比，氢化可的松组低钠血症发生率及程度较低，其低钠血症的开始出现时间、达到最低点时间较晚，每日尿量及24h尿Na+徘出量较低（P&;lt;0．05)。结论：在颈髓损伤早期使用糖皮质激素时，选用有较强盐皮质激素样作用的氢化可的松、对继发性低钠血症的发生及其严重程度均有一定的抑制作用。     

急性颈髓损伤病人的水钠代谢变化及尿PGE2变化

目的研究急性完全性颈髓损伤病人继发的水钠代谢紊乱及尿中前列腺素PGE2排出量的相应变化,探讨颈髓损伤病人继发水钠代谢紊乱的发生机制.方法完全性颈髓损伤(CSCI)病人28例,对照18例.检测血压、心率、血电解质、尿量、液体入量以及尿电解质排出量的变化,放免检测尿前列腺素PGE2的变化.结果 CSCI组血Na+值低于对照组(P＜0.01),92.9%可出现低钠血症.CSCI组尿量(P＜0.01)及24 h尿Na+排出量(P＜0.05)均高于对照组;血压、心率均低于对照组(P＜0.01);24 h尿PGE2排出总量高于对照组(P＜0.01).结论颈髓损伤后交感神经系统抑制,血压降低,肾血流量减少,肾皮质缺血缺氧,继而刺激肾脏前列腺素合成增多,产生利钠利尿作用,可能是颈髓损伤继发低钠血症的发生机制之一.     

急性颈髓损伤患者的水钠代谢变化及其机制

背景大多数急性颈髓损伤患者可继发严重的水钠代谢紊乱,但其发生机制还不清楚.目的研究急性完全性颈髓损伤患者继发的水钠代谢紊乱及尿中前列腺素PGE 2排出量的相应变化,探讨颈髓损伤患者继发水钠代谢紊乱的发生机制.设计以诊断为依据的病例对照研究.地点、对象和方法实验在北京大学第三医院骨科完成,研究对象为完全性颈髓损伤(CSCI)组患者28例,其中男19例,女9例;年龄(37.14±9.39)岁;对照组为同期骨科住院的非脊髓损伤和急性创伤患者18例,男13例,女5例,年龄(38.11±11.89)岁.检测两组水钠代谢和尿前列腺素PGE2的变化.主要观察指标两组血压心率、血电解质、尿量、液体入量以及尿电解质排出量的变化,尿前列腺素PGE 2的变化.结果CSCI组血Na+浓度[(132.70±3.20)mmol/L]低于对照组(t=2.01,P＜0.01),低钠血症发生率为92.9%;CSCI组尿量(3610±761)mL/d,Na+排出量(473.7±169.4)mmol/d均高于对照组(分别为t=2.01,P＜0.01;t=2.08,P＜0.05);血压、心率均低于对照组(t=2.01,2.01,P＜0.01);24 h尿PGE 2排出量高于对照组(t=2.04,P＜0.01).结论颈髓损伤后交感神经系统抑制,血压降低,肾血流量减少,肾皮质缺血缺氧,继而刺激肾脏前列腺素合成增多,产生利钠利尿作用,可能是颈髓损伤继发低钠血症的发生机制之一.     

颈髓损伤后水电解质紊乱30例临床分析

目的:探讨颈髓损伤后电解质紊乱的临床特点及诊断治疗。方法:回顾30例颈髓损伤患者(完全性损伤15例,不完全性损伤15例)血压、心率、血清钠、血清钾、血浆渗透压、尿量及24h尿钠排出量等资料。结果:23例患者于伤后2～8d出现低钠血症,其中完全性损伤15例全部出现,发生率100%,1例患者并发抗利尿激素分泌异常综合征。根据血钠水平,经采用控制每日水量、补钠治疗10～21d后,23例均治愈,血钠平均恢复至138(135～142)mmol/L,血浆渗透压、尿钠均正常。结论:低钠血症是颈髓损伤后极为常见的并发症,但并发抗利尿激素分泌异常综合征十分少见;机体内抗利尿激素不适当分泌,导致的稀释性低钠血症可能是颈髓损伤继发低钠血症的发生机制之一。严格控制入液量及补钠为主要治疗方法。     

急性颈髓损伤并发低钠血症的诊治及护理

总结了41例急性颈髓损伤并发低钠血症患者的诊治及护理特点.包括早期密切观察患者的生命体征、意识状态、脱水症状等临床表现;严密监测电解质、血浆渗透压、尿渗透压、尿比重及24 h尿量、抗利尿激素(ADH)、血浆肾素活性、醛固酮等生化指标;及时准确地评估及诊断;给予积极的心理护理、正确的治疗干预.认为早期发现及正确诊治急性颈髓损伤后低钠血症十分重要,应当提高护理人员对低钠血症的认识,积极进行护理干预及正确的治疗对于纠正低钠血症、改善患者的预后尤为关键.     

乌司他丁和糖皮质激素对脓毒症患者的临床疗效对比

随机将120患者分为乌司他丁组、地塞米松组、甲强龙组及氢化可的松组各30例。分别给予乌司他丁、地塞米松、泼尼松及氢化可的松治疗3d。对比三组患者24h、48h、72h APACHEⅡ评分及清内炎症因子IL-6和TNF-α的蛋白水平。(1)在进入ICU后24h,乌司他丁效果稍好于地塞米松和甲强龙(P<0.05),但是其药效比起氢化可的松要低(P<0.05)。在进入ICU并给药72h后,乌司他丁和氢化可的松对于患者的APACHE II评分显著高于其他两种皮质激素药物的效果(P<0.05)。(2)氢化可的松和乌司他丁均有对减少血清内两种主要炎症因子的含量较好的3天疗效(与给药前相比,三个时间点的test P均小于0.05)。乌司他丁相比于氢化可的松,在症状早期的作用要慢了很多,其整体对IL-6的作用效果甚至与地塞米松类似(P>0.05)。甲强龙的治疗效果在四种药物中最为微弱,无论早期还是中期(P<0.05)。地塞米松对于IL-6的控制效果已经类似于乌司他丁(P>0.05),但是对于TNF-α的控制效果则显著弱于乌司他丁和氢化可的松(P<0.05)。结论 (1)进入ICU一天甚至三天后,四种药物的作用趋于相近,但是乌司他丁(UTI)和氢化可的松仍比其他两种的效果稍好。(2)氢化可的松仍是降低血清内炎症分子最有效的药物,乌司他丁的药效强于其他两种糖皮质激素,但是稍弱于氢化可的松。     

急性颈髓损伤并发低钠血症的机制及治疗

目的:探讨急性颈髓损伤并发顽固性低钠血症的发病机制和治疗方法.方法:回顾性分析我院2001年1月～2005年10月收治的31例颈髓损伤并发低血钠症者临床资料.结果:本组低钠血症发生率为40.79%(31/76),发现低钠血症的时间为受伤后(5.6±3.4)天,血钠平均(131.41±36.73)mmol/L,24小时尿钠平均(339.92±125.13)mmol/L.经补液、补钠等治疗,死亡3例,痊愈28例,平均住院时间(31±12.6)天.结论:低钠血症是急性颈髓损伤的常见并发症,其发病机制可能与颈髓损伤抑制体内交感神经系统有关.低钠血症的治疗原则是积极补充血容量和丢失的钠盐,血钠多可恢复正常.     

急性颈髓损伤患者的水钠代谢变化及其机制

背景：大多数急性颈髓损伤患者可继发严重的水钠代谢紊乱，但其发生机制还不清楚。目的：研究急性完全性颈髓损伤患者继发的水钠代谢紊乱及尿中前列腺素PGE2排出量的相应变化，探讨颈髓损伤患者继发水钠代谢紊乱的发生机制。设计：以诊断为依据的病例对照研究。地点、对象和方法：实验在北京大学第三医院骨科完成，研究对象为完全性颈髓损伤(CSCI)组患者28例，其中男19例，女9例；年龄(37．14&;#177;9．39)岁；对照组为同期骨科住院的非脊髓损伤和急性创伤患者18例，男13例，女5例，年龄(38．11&;#177;11．89)岁。检测两组水钠代谢和尿前列腺素PGE2的变化。主要观察指标：两组血压心率、血电解质、尿量、液体入量以及尿电解质排出量的变化，尿前列腺素PGE2的变化。结果：CSCI组血Na^+浓度[(132．70&;#177;3．20)mmol／L]低于对照组(t=2．01，P&;lt;O．01)，低钠血症发生率为92．9％；CSCI组尿量(3610&;#177;761)mL／d，Na^+排出量(473．7&;#177;169．4)mmol／d均高于对照组(分别为t=2．01，P&;lt;O．01；t=2．08，P&;lt;O．05)；血压、心率均低于对照组(t=2．01，2．01，P&;lt;O．01)；24h尿PGE2排出量高于对照组(t=2．04，P&;lt;O．01)。结论：颈髓损伤后交感神经系统抑制，血压降低，肾血流量减少，肾皮质缺血缺氧，继而刺激肾脏前列腺素合成增多，产生利钠利尿作用，可能是颈髓损伤继发低钠血症的发生机制之一。     

男性急性颈髓损伤病人的水钠代谢紊乱及相关激素变化

目的研究男性急性完全性颈髓损伤患者继发的水钠代谢紊乱及有关的内分泌变化,探讨颈髓损伤继发低钠血症的发生机制。方法男性颈髓损伤组(简称男性CSCI组)19例,男性对照组14例,研究其水钠代谢变化,放免检测血浆肾素活性(PRA)、抗利尿激素(ADH)浓度及血清睾丸酮浓度。结果与对照组比较,男性CSCI组血钠浓度降低,此外还有多尿、尿钠排出增多以及液体入量低于尿量等变化(P<0.05);CSCI组PRA、血浆ADH及血清睾丸酮浓度均低于对照组。结论男性颈髓损伤患者其伤后血清睾丸酮浓度下降,可能对其继发性的低钠血症有一定的促发作用。     

不同剂量糖皮质激素治疗过敏性休克的疗效比较

目的探讨不同剂量的糖皮质激素治疗过敏性休克的临床效果。方法选取120例过敏性休克患者,采取随机数字表法分为低剂量组、中剂量组与高剂量组,每组40例。低剂量组给予100 mg的氢化可的松+250 mL的0.9%氯化钠溶液,中剂量组给予200 mg的氢化可的松+250 mL的0.9%氯化钠溶液,高剂量组给予300 mg的氢化可的松+250 mL的0.9%氯化钠溶液。比较3组临床疗效、症状缓解时间以及5 h内的尿量。结果 3组临床总有效率比较,差异有统计学意义(P0.05)。3组神智恢复、血压恢复、呼吸频率恢复、心率恢复及皮疹消退时间比较,差异有统计学意义(P0.05)。3组2、3、4、5 h的尿量比较,差异有统计学意义(P0.05)。结论采用高剂量的氢化可的松治疗过敏性休克的临床疗效显著,能够缩短症状缓解时间。     

Water depletion, not oral sodium loading, increases levels of sodium, potassium-dependent adenosine triphosphatase inhibitors in rat plasma

In order to define a physiological role for circulating inhibitors of sodium, potassium-dependent adenosine triphosphatase (Na+,K+-ATPase), plasma was obtained from control, water deplete, water repleted, sodium deplete and sodium loaded rats. The effect of this plasma on Na+,K+-ATPase activity, and its transport equivalent 86Rb uptake, was measured in separated guinea pig renal cortical tubules. Plasma from water deplete rats had a raised plasma osmolality and sodium concentration and a significant inhibitory effect on Na+,K+-ATPase (14%) and 86Rb uptake (24%) compared with control or water repleted rats. Inhibition of Na+,K+-ATPase and 86Rb transport was not seen with plasma from rats after dietary sodium loading (urine sodium 5.2 +/- 0.9 mmol/day) compared with low sodium diet controls (urine sodium 0.41 +/- 0.08 mmol/day). Des-amino arginine vasopressin in vivo produced no inhibition of Na+,K+-ATPase or Rb transport. These studies suggest, that in terms of common homoeostatic insults, circulating inhibitors of Na+,K+-ATPase are more responsive to water depletion than to oral sodium loading. The inhibitors may fulfil a physiological role in increasing sodium excretion to maintain osmolality after dehydration.     

Tubular sites of furosemide natriuresis in volume-replaced and volume-depleted conscious rats

There is accumulating evidence that the renal Li clearance reflects the delivery of Na and volume out of the proximal tubules. In the present study we used the Li clearance technique to evaluate the effects of submaximal furosemide (Fur) infusion (7.5 mg/kg/hr) on proximal and distal Na reabsorption in conscious rats with and without volume replacement with saline. Li was given as an p.o. test dose (0.5 mmol/kg) and [3H]inulin was infused in saline to measure the glomerular filtration rate (GFR). In control rats not infused with F, fractional Na excretion was about 1% and fractional Li excretion was about 30 to 35%. Infusion of F with constant rate and volume replacement increased fractional Na excretion to 22% and fractional Li excretion to 57% associated with a small decrease of the GFR. Without volume replacement F infusion caused a smaller and temporary diuretic and natriuretic response (maximum fractional Na excretion = 7.5%) followed by a decrease of urine flow and Na excretion almost to control levels, despite continued high excretion rates of F. The GFR decreased by 25% and fractional Li excretion showed an initial increase followed by return to baseline levels. The results suggest that in conscious rats submaximal doses of F cause major inhibition of proximal tubular Na reabsorption, which effect contributes substantially to the initial natriuresis. Along with diuretic-induced volume contraction, the natriuretic response is abolished due to a fall in GFR and particularly due to a secondary increase in fractional Na reabsorption, which occurs both in proximal distal tubular nephron segments.     

Plasma and tissue kallikrein-kinin systems during acute administration of frusemide in normotensive and hypertensive humans.

1. This study aims to further elucidate the role of the tissue and plasma kallikrein-kinin systems in blood pressure, electrolyte and volume homoeostasis. Components thereof and of the renin-angiotensin-aldosterone system were measured in conjunction with frusemide administration, in normotensive subjects and in patients with primary hypertension. 2. Frusemide increased plasma pre-kallikrein, angiotensin II and aldosterone concentrations and plasma renin activity, whereas the plasma level of tissue kallikrein remained unchanged. Basal values and the induced changes were similar in both groups. 3. Frusemide increased the urine volume and the excretion of Na+, K+, Mg2+, Cl-, aldosterone, prostaglandin E2 and tissue kallikrein. These changes were similar in both groups, but the total tissue kallikrein excretion was significantly lower in the hypertensive patients. Excretion of electrolytes and hormones was also measured during three 24 h urine collection periods and did not differ between the two groups. 4. Thus, acute administration of frusemide to hypertensive patients and normal subjects increased the plasma level of pre-kallikrein, possibly indicating less activation to kallikrein and subsequently less kinin generation in the blood stream. This also suggests a role for the plasma kallikrein-kinin system in the regulation of vascular tone and blood volume. Circulating tissue kallikrein does not seem to be acutely involved. 5. Urinary excretion of kallikrein is reduced in patients with primary hypertension after the administration of frusemide, apparently without affecting the renal excretory response.     

The evaluation of the diuretic action of parenteral formulations of metolazone

BACKGROUND AND OBJECTIVES: This study was design to compare the diuretic and natriuretic effects of the 2 parenteral formulations of metolazone and the combination of these 2 formulations of metolazone with the parenteral administration of furosemide. Metolazone is an anthracrene acid derivate and manifests a dual diuretic effect on the proximal and distal tubule with a minimal kaluretic effect. It is currently only marketed in an orally administrable formulation, and this has limited its utility in critically ill patients. Metolazone given orally and furosemide given orally or parenterally are frequently administrated together when furosemide alone is clinically inadequate at producing a desired diuresis. METHODS: Sprague Dawley male rats (400 to 450 g) were divided into groups to receive a parenteral formulation of metolazone or furosemide administrated separately intraperitoneally (IP) or administrated IP in combination with one another. Tris buffer-administered IP was used as a control vehicle comparator. The urine volume voided over the following 24 hours was collected, measured and analyzed for sodium content. RESULTS: Vehicle (Tris buffer) caused 9 +/- 1 mL/d output of urine with a sodium [Na+] concentration of 194 +/- 41 micromol/L (n=6 per group). Metolazone 2 mg/kg resulted in 16 +/- 3 mL/d urine output and sodium [Na+] of 278 +/- 76 micromol/L (n=6 per group). Furosemide 2, 4, and 6 mg/kg resulted in a volume of urine 9 +/- 1, 14 +/- 2 and 17 +/- 2 mL/d and [Na+] micromol/L of 194 +/- 41, 206 +/- 108, and 229 +/- 91, respectively. Metolazone 4 mg/kg combined with furosemide 4 mg/kg resulted in a urine volume of 21 +/- 1 mL/d and [Na+] of 326 +/- 108 micromol/L. CONCLUSION: Combining metolazone and furosemide can cause an increase in urine volume and sodium excretion. Metolazone administrated parenterally in combination with the parenteral administration of furosemide appears to have an important clinical potential.     

Effects of adrenalectomy and chronic adrenal corticosteroid replacement on potassium transport in rat kidney

Clearance experiments were carried out in pair-fed rats to examine the long-term effects of adrenalectomy and selective adrenal corticosteroid replacement in physiological amounts on renal potassium transport. To this end, clearance studies were conducted in rats that were sham operated, or adrenalectomized (ADX). ADX animals were given either vehicle, aldosterone (0.5 microgram/100 g body wt per day), dexamethasone (1.2 micrograms/100 g body wt per day), or aldosterone and dexamethasone, by osmotic minipump for 7-9 d whereupon clearance experiments were conducted. After chronic hormone treatment, during basal conditions when only Ringers solution was infused, all groups excreted similar amounts of potassium. However, in all ADX animals without mineralocorticoid replacement, the maintenance of urinary potassium excretion at control levels was associated with hyperkalemia, increased urine flow, and natriuresis; all are factors known to stimulate urinary potassium excretion. During acute potassium infusion, the increase in urinary potassium excretion was less in ADX rats than in controls. This functional deficiency in potassium excretion was partially corrected by dexamethasone and was uniformly associated with a significant increase in urine flow. Aldosterone replacement or aldosterone and dexamethasone given together chronically, sharply increased potassium excretion but did not restore excretion to control levels. Only acute aldosterone infusion (0.2 microgram/100 g body wt bolus plus 0.2 microgram/100 g body wt per hour), superimposed upon chronic aldosterone and dexamethasone treatment, fully restored potassium excretion to control levels. This aldosterone induced enhancement of potassium excretion, both chronic and acute, was not associated with hyperkalemia, and increased urine flow or natriuresis. Thus, physiological levels of both classes of adrenal corticosteroids stimulate renal potassium excretion albeit by different mechanisms. Mineralocorticoids stimulate tubular potassium excretion directly, whereas glucocorticoids augment excretion indirectly by increasing fluid and sodium delivery along the distal nephron.     

Renal handling of sodium and calcium in hypercalciuria

The renal handling of Ca in response to Na intake was evaluated in 12 patients with hypercalciuria and active kidney stone disease. There was no depression of urinary Ca excretion in response to the hypocalciuric effect of metolazone. Patients were hospitalized and their Ca and Na excretions measured while on a 190-mEq Na, 800-mg Ca, 1200-mg PO4- diet. These measurements were then repeated after Na intake decreased to 35 mEq/day while other variables, including diuretic dose and Ca intake, were unchanged. Two distinct responses were elicited by patients after Na restriction. In group I or the "responders" (n = 4), Ca excretion was reduced from 255 +/- 31 to 62 +/- 6 mg/24 hr. In the control group (n = 4), Ca excretion decreased from 95 +/- 8 to 57 +/- 11 mg/24 hr at similar levels of Na excretion. In group II or the "nonresponders" (n = 8), Ca excretion fell from 317 +/- 31 to 154 +/- 17 mg/24 hr when Na excretion was less than 50 mEq/24 hr. Metolazone with Na restriction normalized urine Ca excretion to the same order as in control subjects in group I. This is indicative of a mild Ca leak or a salt-sensitive leak. Despite diuretic and Na restriction most of the patients with hypercalciuria (group II) did not reabsorb Ca in a normal manner. This is indicative of a severe reabsorptive defect for Ca despite normal Na handling.     

Acute effects of high-dose furosemide on residual renal function in CAPD patients.

BACKGROUND: High doses of furosemide can increase urine volume in chronic peritoneal dialysis (CAPD) patients. However, no information is available about effects on urinary solute excretion in relation to residual glomerular filtration rate (GFR), urinary furosemide excretion, and peritoneal solute kinetics. METHODS: Diuretic response and the effect on peritoneal fluid and solute transport parameters were investigated in 7 stable CAPD patients with residual renal function (median urine volume 350 mL/24 hours, range 140- 1900 mL/24 hours). Comparisons were made during two clearance periods of 24 hours: one without (P1) and one during 2 g furosemide (P2). RESULTS: The median increase in urine volume was 400 mL (range 270 - 910 mL, p < 0.02) and the increase in sodium excretion was 54 mmol (range 25 - 118 mmol, p < 0.02). No change in GFR was found between P1 (2.4 mL/ minute, range 0.6 - 5.7 mL/min) and P2 (2.0 mL/min, range 1.0 - 4.8 mL/min). An increase in fractional clearance was found for volume, sodium, potassium, and osmolality (p < 0.02). No change was found in the fractional clearance of urea and electrolyte-free water. Furosemide excretion in urine was 8.7 mg/24 hours (range 2.1 - 38 mg/24 hours) and in dialysate 4.9 mg/24 hours (range 1.9 - 7.8 mg/ 24 hours). Plasma furosemide concentration was 29.5 mg/L (range 6.2 - 43.9 mg/L). A positive correlation was found between residual GFR and total urine furosemide excretion (r = 0.93, p < 0.005). Efficiency, expressed as the increase in fractional sodium clearance (percent) per milligram of furosemide excreted per 24 hours, was 1.2%/mg (range 0.3% - 11.3%/mg). CONCLUSION: High-dose furosemide is effective in CAPD patients in increasing urine volume and electrolyte excretion without affecting urea and creatinine clearance. In CAPD patients, the individual response to an identical high dose of furosemide is dependent on the magnitude of residual GFR.     

Effects of nonsteroidal anti-inflammatory drugs (NSAID) on renal excretion of sodium and water, and on body fluid volume in rats.

Effects of nonsteroidal anti-inflammatory drugs (NSAID) on urine volume and urinary sodium excretion, and on plasma volume and extracellular fluid volume were examined in conscious rats. The basal urine volume and urinary sodium excretion were decreased and the increased urine volume and urinary sodium excretion elicited by saline load (25 ml/kg) and by hydrochlorothiazide (10 mg/kg) were inhibited after oral administration of NSAID in doses which inhibited the rat carrageenin-induced hind paw edema (indomethacin, 1--10 mg/kg; tolmetin, 3--30 mg/kg; phenylbutazone, 3--30 mg/kg; aspirin, 30--300 mg/kg), but aminopyrine (30--300 mg/kg) did not show such an effect. The inhibitory activity on renal function was diminished gradually with repeated administration of NSAID. NSAID (indomethacin, 3 mg/kg; tolmetin, 10 mg/kg; phenoxybenzamin, 10 mg/kg; aspirin, 100 mg/kg) increased plasma volume and extracellular fluid volume of rats after repeated medication for 3 or 5 days, but the body fluid volume expansion disappeared with further repeated administration of NSAID. These results suggest that NSAID may inhibit the intrarenal role of prostaglandins and decrease sodium and water excretion in urine with resulting increased body fluid volume. Tolerance to these actions of NSAID developed after repeated administration.     

35%总体表面积烧伤犬小肠对葡萄糖-电解质液吸收效率的研究

目的 研究35%总体表面积(TBSA)Ⅲ度烧伤休克对Beagle犬小肠葡萄糖一电解质液(GES)吸收效率的影响,比较肠内补液与静脉补液的复苏效果.方法 成年雄性Beagle犬12只,采用凝固汽油燃烧法造成35%TBSAⅢ度烧伤,伤后0.5 h开始按Parkland公式计算的量和速率补液.随机分为肠内输注GES组(EGES)和静脉输注乳酸林格液组(IVLR).在清醒状态下观察EGES组伤后8 h内肠道对水分和Na+的吸收速率,以及两组动物血浆Na+浓度、血浆容量(PV)、平均动脉压(MAP)、心排血量(CO)和尿量的变化;伤后8 h收集肠内残余的液体计算吸收总量.结果 伤后肠道对水分和Na+的吸收速率明显降低,3.5 h降至伤前的21%和37%,其后缓慢回升,至伤后8 h仍低于伤前;8 h内液体平均吸收速率[(99±47)ml·h-1·m-1]与输入速率[(81±11)ml·h-1·m-1]比较差异无统计学意义(P＞0.05),吸收液体总量为输入量的(94.8±3.7)%.伤后8 h内两组血浆Na+浓度、MAP、CO的变化趋势一致,差异均无统计学意义(P均＞0.05).伤后4 h EGES组尿量和PV均明显少于IVLR组(P均＜0.05),但8 h两组比较差异无统计学意义(P均＞0.05).结论 35% TBSA烧伤休克进行肠内补液时,液体吸收效率和吸收总量可满足Parkland公式要求,能达到与静脉补液同样的扩容和改善血流动力学效果.