Effects of Hemorrhagic Shock in Early and Late Partial Posthepatectomy Rats

Introduction

The purpose of the study was to determine the compensatory function of the remnant liver as a blood reservoir after 70% hepatectomy in rats to counteract hemorrhagic shock and reperfusion.

Methods and materials

One hour of hemorrhagic shock followed by 1 hour of resuscitation induced in normal rats (group I) was compared with animals that had undergone 70% hepatectomy at postoperative day 3 (group II) and day 7 (group III). We compared the total blood loss, the blood pressure before hemorrhagic shock, hemoglobin, hemotocrit, and mortality. Liver function such as aspartate transferase (AST), alanine transferase, and lactate dehydrogenase (LDH) were also compared among groups by one-way analysis of variance with post hoc correction. A P value less than .05 was regarded as significant.

Results

The results showed a lower volume of drawn blood induced hemorrhagic shock in group II compared with group I or group III hosts. The blood loss was 15.6 ± 1.0, 5.68 ± 2.5, and 13.2 ± 1.6 mL for groups I, II, and III, respectively. The mortality due to hemorrhagic shock was significantly higher in group II compared with group I or group III. Liver function tests showed that the AST and LDH were significantly higher after resuscitation in group II.

Conclusion

In the early postoperative period (day 3) after 70% hepatectomy, rats were more vulnerable to a high mortality after hemorrhagic shock compared with hosts in the late postoperative period (day 7). Significantly higher AST and LDH in group II indicated that the remnant liver was more injured after hemorrhagic shock in the early postoperative period.     

失血性休克促进细胞移位的发生

目的 探讨失血性休克在细菌移位中的作用。方法 本组１００例患者分４组,对照组（Ｉ组）３４例;闭合性腹部钝伤致失血性休克组（Ⅱ组）２３例;闭合性腹部钝伤无失血性休克组（Ⅲ组）１５例;腹部内出血致失血性休克组（Ⅳ组）２８例;取患者手术前后的外周血、腹膜脏层拭子样品、术中门静脉血、回肠系膜淋巴结、肝活检组织进行需氧与厌氧培养。结果 细菌移位的发生率第Ｉ组为６％（２／３４）,第Ⅱ组６５％（１５／２３）。第     

早期乳酸清除率评估与失血性低血容量休克预后的研究

目的评估失血性低血容量休克患者早期乳酸清除率与预后的关系。方法前瞻性观察并收集因失血性低血容量休克进入外科重症监护病房92例患者的APACHEII评分、入ICU6h后动脉血乳酸清除率及患者预后。分别将患者分成存活组和死亡组,高乳酸清除率组(6h乳酸清除率10%)和低乳酸清除率组(6h乳酸清除率10%),比较各组间的差异。结果各组年龄、性别、APACHEII评分和基础血乳酸值差异无统计学意义。存活组乳酸清除率明显高于死亡组[(29.8±15.2)%vs(9.8±9.1)%,0.01];高乳酸清除率组病死率均明显低于低乳酸清除率组(11.3%vsP42.9%,P0.01)。结论早期乳酸清除率10%能准确评估失血性低血容量休克患者的良性预后。     

Probiotic supplementation reduces the risk of bacterial translocation in experimental short bowel syndrome

Background/Purpose: Probiotics are live organisms that survive passage through the gastrointestinal tract and have beneficial effects on the host. Lactobacillus and Bifidobacterium have been recommended for cholesterol lowering, acute diarrhea, prevention of cancer, or inflammatory bowel disease. On the other hand, after massive bowel resection, bacterial overgrowth is frequent and favors bacterial translocation (BT). The possible beneficial effects of Bifidobacterium lactis (BL) administration on BT in experimental short bowel syndrome (SBS), have not been investigated. The aim of this study was to test the hypothesis that BL administration decreases BT in SBS in animals fed orally. Methods: One hundred twenty-eight adult Wistar rats fed orally with standard rat chow and tap water [ldquo ]ad libitum[rdquo ] were maintained in individual metabolic cages for 10 days and divided into 3 groups: control group (n = 71): nonmanipulated animals; RES group (n = 39): 80% gut resection from 10 cm beyond the angle of Treitz to 10 cm above the cecum; RES-PRO group (n = 18): same resection and daily 7.8 [times ] 10⁸ CFU B Lactis administration, after orogastric intubation. At the end of the experiment they were killed, and mesenteric lymph nodes (MLN) and peripheral and portal blood specimens were recovered and cultured. Bacterial identification in blood was made by conventional methods, and MLN culture was considered positive with a growth over 100 CFU/g. Results: Bacterial translocation was detected in 6% of control group rats. The incidence of BT in the RES group was 87% (34 of 39), whereas only 50% (9 of 18) of RES-PRO animals had BT (P [lt ] .05). The relative risk reduction (RRR) was 0.43 (95% Cl 0.14 to 0.72), and the number needed to treat (NNT) was 3 (95% Cl 2 to 8). In other words, animals that received BL had the risk of BT reduced by 43% (RRR of 0.43), and of every 3 animals treated, 1 is expected to be free of BT (NNT of 3). Conclusion: Administration of B Lactis reduces the incidence of BT in adult Wistar rats after 80% gut resection.     

Bacterial translocation and intestinal atrophy after thermal injury and burn wound sepsis.

Bacterial translocation (BT) occurs after thermal injury in rodents in association with intestinal barrier loss. Infection complicating thermal injury may also affect the intestine producing bowel atrophy. To study these relationships, Wistar rats received either 30% scald followed by wound inoculation with Pseudomonas; 30% scald with pair feeding to infected animals; or sham injury as controls. On days 1, 4, and 7 after injury animals were killed with examination of the bowel and culture of the mesenteric lymph nodes (MLN), livers, spleens, and blood. All burned animals demonstrated BT to the MLN on day 1 after injury, but only burn-infected animals had continued BT on days 4 and 7, with progression of BT to the abdominal organs and blood. Burn injury and infection also resulted in significant atrophy of small bowel mucosa temporally associated with continued BT. Thus injury complicated by infection results in prolonged and enhanced bacterial translocation, perhaps due to failure to maintain the mucosal barrier.     

失血性低血容量休克多器官功能障碍综合征的机制探讨

目的探讨失血性低血容量休克病人血清肿瘤坏死因子-α（TNF-α）和白细胞介素-1（IL-1）水平与预后的关系。方法应用ELISA法检测29例失血性低血容量休克病人（休克组）血清TNF-α和IL-1浓度，与20例择期手术病人（对照组）进行比较，观察TNF-α和IL-1水平与多器官功能障碍综合征（MODS）的关系。结果休克组全身炎症反应综合征（SIRS）、MODS和感染的发病率明显高于对照组（P〈0．05）；休克组血清TNF-α和IL-1浓度明显高于对照组（P〈0．05）；MODS组血清TNF-α浓度较非MODS组明显升高（P〈0．05），血清IL-1浓度差异无显著性（P〉0．05）；休克组中死亡病人血清TNF-α浓度较存活病人明显增高（P〈0．05），血清IL-1浓度差异无显著性（P〉0．05）。结论失血性低血容量性休克发生SIRS是较为常见的，并且是导致MODS的重要原因之一；血清TNF-α浓度的高低与预后密切相关。     

Effect of growth hormone, epidermal growth factor, and insulin on bacterial translocation in experimental short bowel syndrome

BACKGROUND/PURPOSE: An adaptive process starts in the remaining intestine after massive resection, and several trophic factors including growth hormone (GH), epidermal growth factor (EGF), and insulin (INS) have been shown to have a positive effect on it. Bacterial translocation (BT) is frequent after extensive small bowel resection, but the effects of GH, EGF, or INS have not been investigated in experimental short bowel syndrome (SBS). This study tests the hypothesis that GH, EGF, or INS decrease BT in SBS in rats with parenteral nutrition (PN). METHODS: Thirty-eight adult Wistar rats underwent central venous cannulation and were assigned randomly to 1 of 4 groups receiving for 10 days 4 treatment regimes: (1) PN group (n = 10): fasting, all-in-one PN solution (300 mL/kg/24 h, 280 kcal/kg/24 h), 80% gut resection including ileo-cecal valve; (2) GH group (n = 9): fasting, same PN regime and resection, GH (1 mg/kg/d, subcutaneously); (3) EGF group (n = 9): fasting, PN, resection, EGF (150 microg/24 h intravenously); (4) INS group (n = 9): fasting, PN, resection, INS (1 UI/100 g/24 h subcutaneously). At the end of the experiment they were killed, and mesenteric lymph nodes (MLN) and peripheral and portal blood samples were recovered and cultured. Several fragments of intestine were taken to determine cell proliferation (PCNA index) and morphometric parameters (villous height, crypt depth). RESULTS: GH, EGF, and INS groups showed a 28%, 29%, and 30% increase in gut mucosal thickness, and PCNA index rose 21%, 20%, and 25%, respectively in comparison with PN controls. Bacterial translocation to peripheral blood was detected in 0% of PN animals and in 44%, 40%, and 28% of GH, EGF, or INS rats, respectively (P < .05). No differences were found in BT in MLN or portal blood among groups. CONCLUSION: Administration of GH, EGF, or INS improves gut mucosal structure in rats with SBS under PN, but, surprisingly, the incidence of BT detected in peripheral blood was increased rather than decreased in animals receiving these treatments.     

Ischemic bowel: the protective effect of free-radical anion scavengers

Recent data indicates that the free-radical anion superoxide (O2-), an unstable cytotoxic form of oxygen, is implicated in the pathogenesis of ischemic bowel following reperfusion after low flow states. This report evaluates the effect of free radical scavengers on survival in an animal model with bowel ischemia. At laparotomy, the superior mesenteric artery (SMA) of 79 weanling rats (90 g) was occluded for one minute and released. Animals were divided into three experimental groups: group I acted as controls (n = 41), group II, received thiopental 5 mg/kg IV (n = 19), group III, received methohexital 2.5 mg/kg IV (n = 19). At one week animals were evaluated for mortality, mean survival time, evidence of bowel necrosis or perforation, and bowel appearance on scanning electron microscopy (EM). Mortality was 63.5% (26/41) in group I, 19 had necrotic bowel and 7 had gross perforation; 31.6% in group II (6/19) (p less than .05 versus control), with one necrotic bowel and 5 perforations; and 57.9% in group III (11/19) where 7 had necrotic bowel and 4 had perforations (p NS v control). Survival time (mean +/- SD in days) post SMA occlusion was 3.2 +/- 1.9 for group I; 4.0 +/- 1.7 for group II; and 2.5 +/- 2.0 for group III. EM showed mucosal destruction worsened by the duration of reperfusion, decreased by thiopental but not by methohexital. Thiopental, a free radical anion scavenger was cytoprotective in this animal model, as it decreased mortality and the incidence of bowel necrosis and perforation. These data support the thesis that following low flow states bowel ischemia may be related to a reperfusion injury due to the release of toxic free radical anions.     

The effect of glucagon-like peptide 2 on intestinal permeability and bacterial translocation in acute necrotizing pancreatitis

BACKGROUND: Acute pancreatitis (AP) initiates a generalized inflammatory response that increases intestinal permeability and promotes bacterial translocation (BT). Impairment of the intestinal epithelial barrier is known to promote BT. Glucagon-like peptide 2 (GLP-2), a 33 residue peptide hormone, is a key regulator of the intestinal mucosa by stimulating epithelial growth. The purpose of this study was to determine whether GLP-2 decreases intestinal permeability and BT in AP. METHODS: To examine whether GLP-2 can decrease intestinal permeability and thereby decrease BT in acute necrotizing pancreatitis, 34 male Sprague-Dawley rats (200 to 300 g) were studied. AP was induced in group I and group II by pressure injection of 3% taurocholate and trypsin into the common biliopancreatic duct (1 mg/kg of body weight). The potent analog to GLP-2 called ALX-0600 was utilized. Group I rats received GLP-2 analog (0.1 mg/kg, SQ, BID) and group II rats received a similar volume of normal saline as a placebo postoperatively for 3 days. Group III and group IV received GLP-2 analog and placebo, respectively. At 72 hours postoperatively, blood was drawn for culture of gram-negative organisms. Specimens from mesenteric lymph nodes (MLN), pancreas and peritoneum were harvested for culture of gram-negative bacteria. Intestinal resistance as defined by Ohm's law was determined using a modified Ussing chamber to measure transepithelial current at a fixed voltage. A point scoring system for five histologic features that include intestinal edema, inflammatory cellular infiltration, fat necrosis, parenchymal necrosis, and hemorrhage was used to evaluate the severity of pancreatitis. Specimens from MLN, pancreas, jejunum, and ileum were taken for pathology. RESULTS: All group I and group II rats had AP. The average transepithelial resistance in group I was 82.8 Omega/cm(2) compared with 55.9 Omega/cm(2) in group II (P <0.01). Gram-negative BT to MLN, pancreas, and peritoneum was 80%, 0%, and 0%, respectively in group I compared with 100%, 30%, and 20% translocation in group II. CONCLUSION: GLP-2 treatment significantly decreases intestinal permeability in acute pancreatitis.     

The canine kidney in haemorrhagic shock: effect of verapamil

Recent evidence suggests that verapamil administration reduces myocardial and small intestinal damage in canine haemorrhagic shock, and verapamil has also been shown to reduce renal dysfunction in clamp models in post-ischaemic renal failure. The effects of high-dose verapamil and hypovolaemia on renal haemodynamics and function in a canine haemorrhagic shock model were studied. Anaesthetized mongrel dogs were divided into three groups. Animals of group I (n = 5) were not subjected to shock but given a 90-min verapamil infusion (2.28 micrograms/kg); animals of group II (n = 5) were subjected to shock (mean blood pressure 40 mm Hg) for 2 h and given a 90-min 0.9% saline infusion, and animals of group III (n = 7) were both subjected to a 2-hour shock and given verapamil. The electrocardiograph was monitored, and general haemodynamic parameters were measured before shock (period 1), at the end of shock (period 2), after reinfusion of shed blood (period 3) and 1 h after shock (period 4). Total renal and cortical zonal blood flow was estimated by radioactively labelled microsphere injection during each period. Creatinine and osmolar clearance were estimated before and after shock. Verapamil administration caused heart block in groups I and III which lowered heart rate and blood pressure and exacerbated the haemodynamic effects of shock in group III. Despite this, no measurable difference in renal function was recorded between groups II and III. Total renal blood flow fell during shock, and this was exacerbated in animals given verapamil, suggesting a cumulative deleterious effect of shock and verapamil in renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucan and glutamine reduce bacterial translocation in rats subjected to intestinal ischemia-reperfusion.

Intestinal ischemia/reperfusion (I/R) may induce bacterial translocation (BT). Glutamine (GLN)-enriched nutrition decreases BT. However, little is known about the effect of glucan (GL) in BT. This study investigated the combined effect of GL/GLN on BT, intestinal damage, and portal blood cytokines in animals under I/R. Four groups of 10 rats each were subjected to 60 min of intestinal ischemia and 120 min of reperfusion. The control group (group 1) received only rat food/water, group 2 received glutamine via gavage, group 3 received subcutaneuos soluble (1, 3)-d-glucan, and group 4 received GL + GLN. A sham group (group 5) served as a normal control. Bacterial cultures of ileum, mesenteric lymph nodes (MLN), liver and lung biopsies, histological changes of ileum, and serum cytokines variables were examined after I/R. Data were analyzed by analysis of variance (ANOVA) and the Newman-Keuls test. Results showed that GLN, GL, and GL/GLN significantly reduced BT to MLN, liver, and lung. BT was more attenuated after GL treatment than GLN (P < .05). Rats treated with both GL and GLN exhibited lower bacterial colony counts than the ones treated only with GLN or GL. Severe mucosal damage on histological findings was shown in group 1, but these findings were significantly ameliorated (P < .05) in groups 3 and 4. Tumor necrosis factor (TNF)-a and interleukin (IL)-6 levels in portal serum were significantly reduced and IL-10 was increased by GL and GLN treatment. In conclusion, the use of GL was more effective than GLN in reducing BT, intestinal damage, and cytokine levels after I/R. Additionally, the combination of GL and GLN improved results.     

Interaction of prostaglandins, activated complement, and granulocytes in clinical sepsis and hypotension

Activated complement, thromboxane A2, prostacyclin, and activated granulocytes have been implicated in hemodynamic dysfunction after trauma, in sepsis, and in hypovolemic and septic shock. This study evaluated the interaction of plasma concentrations of complement components C3a and C5a, thromboxane B2 (TxB), prostaglandin 6-keto-F1 alpha (PGI), and granulocyte aggregation in clinical sepsis and hypotension. Forty-eight critically ill patients were followed clinically for as long as 10 days. Plasma C3a, C5a, TxB, and PGI were measured daily by the radioimmunoassay method. Granulocyte aggregation, the percentage of maximum aggregation of zymosan-activated plasma standard curves, was performed with patient plasma and normal human leukocytes. Patients were studied in four groups: group I, nonseptic, normotensive; group II, hypovolemic shock, group III, normotensive severe sepsis; and group IV, septic shock. Plasma from 12 normal adults was the control value. PGI, TxB, C3a, C5a, and granulocyte aggregation in patients were greater than that in the control subjects. Granulocyte aggregation was increased in groups III and IV versus groups I and II. C3a was increased in group IV versus groups II and III. C5a and TxB did not vary between groups. PGI was greatly increased in group IV compared with groups I through III. C3a and C5a decreased in nonsurvivors. PaO2/FiO2 ratios correlated directly with PGI and inversely with C3a and TxB/PGI. Plasma PGI and C3a are increased in septic shock. C3a and TxB/PGI imbalances are involved in hypovolemic and septic shock.     

Effects of high-intensity focused ultrasound in the treatment of experimental neuroblastoma.

This report evaluates the effect of high-intensity focused ultrasound (HIFU) on subcutaneous murine neuroblastoma C1300. HIFU treatment was administered with a focused 4-MHz quartz transducer with a peak intensity of 550 W/cm2. In experiment 1, 60 animals with tumor were divided into four groups. Group I (n = 15) were controls; group II (n = 15) received adriamycin, 5 mg/kg intraperitoneally; group III (n = 15) received HIFU; and group IV (n = 15) received both adriamycin and HIFU. All the animals in groups I and II died of tumor by 35 days. Fifty-three percent (8/15) of mice in group III and 80% (12/15) in group IV were cured with no evidence of tumor (NET) at 200 days. Log-rank statistics showed significant prolongation of survival in the groups III and IV as compared with groups I or II (P less than .05). In experiment 2, 45 animals with tumor were divided into three groups. Group I (n = 15) were controls; group II (n = 15) received HIFU; and group III (n = 15) received repeated HIFU. The results showed 47% (7/15) of mice in group II and 67% (10/15) in group III were NET at 200 days. Significant survival prolongation was achieved in groups II and III in comparison with group I (P less than .05). In experiment 3, 90 mice received either tumor (n = 60) or saline (n = 30) inoculation in the left flank. On day 5, 45 mice with tumor were treated with HIFU (group I), while the other 15 mice with tumor (group II) had a sham procedure.(ABSTRACT TRUNCATED AT 250 WORDS)     

"Scoop and run" or stabilize hemorrhagic shock with normal saline or small-volume hypertonic saline?

The controversy over a policy of "scoop and run" or stabilizing hemorrhagic shock when evacuation time is short has not yet been settled. Small volumes of hypertonic saline have been suggested as effective therapy when the scoop-and-run policy is adopted. In the present study small-volume hypertonic saline treatment and normal saline treatment of "uncontrolled" hemorrhagic shock (UCHS) in rats were compared with no treatment, which best simulates the scoop-and-run policy. The rats were randomly assigned to three groups. Uncontrolled hemorrhagic shock was induced by 12% resection of the terminal portion of the rats' tails. In group I (n = 13) the animals were untreated. In group II (n = 6) UCHS was treated by administering 41.5 mL/kg 0.9% NaCl (NS). In group III (n = 6) UCHS was treated by administering 5 mL/kg 7.5% NaCl (HTS). Resection of the rats' tails in group I was followed by bleeding of 3.3 +/- 0.3 mL in 15 minutes with a fall in mean arterial pressure (MAP) from 100.9 +/- 7 to 63.5 +/- 5 mm Hg (p less than 0.001). The early bleeding and hemodynamic responses were similar in all three groups. Further blood loss in the first hour in group I was 0.5 +/- 0.2 mL, and MAP rose spontaneously to 73.2 +/- 6 mm Hg (p less than 0.05). The NS infusion in group II was followed by further bleeding of 4.1 +/- 0.9 mL (p less than 0.01) and a further fall in MAP to 53.8 +/- 7 mm Hg (p less than 0.01) after 60 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of vasopressin on organ blood flow in an endotoxin-induced rabbit shock model.

The effects of vasopressin on the vasculature differ from those of other vasopressors, and its effects on the coronary artery remain debatable. This study was undertaken to examine the effects of vasopressin in a rabbit endotoxin-induced shock model and to compare these effects with those of norepinephrine. Thirty rabbits were divided into four study groups: a normal control group (group I, n = 5), a shock control group (group II, n = 5), a vasopressin group (group III, n = 10), and a norepinephrine group (group IV, n = 10). Shock was induced by intravenously infusing lipopolysaccharide (Escherichia coli O111:B4) in groups II, III, and IV. In groups III and IV, systemic blood pressure was maintained to the level of group I by adjusting vasopressin and norepinephrine doses. Left ventricle, right ventricle, ventricular septum, kidney, liver, spleen, and skeletal muscle blood flows were measured using radioisotope tagged microspheres at baseline and 2 h after initial blood flow measurement. No difference in organ blood flows were observed between groups I and II, and coronary blood flow in the left ventricle, right ventricle, and ventricular septum was similar in all study groups. However, renal blood flow was significantly lower in group IV than in group III (p < .05) and hepatic arterial blood flow was significantly lower in group III than in group IV (p < .05). Thus, effect of vasopressin on organ blood flow is organ dependent. Vasopressin increased renal blood flow and decreased hepatic arterial blood flow in this endotoxin-induced shock model, whereas norepinephrine did not. However, coronary blood flow was not changed by shock status or vasopressor type.     

Effect of probiotics on intestinal regrowth and bacterial translocation after massive small bowel resection in a rat

Background/Purpose

Because of their ability to inhibit intestinal bacterial overgrowth, probiotics (PROs) have been advocated for the treatment of patients with short bowel syndrome (SBS). This study was conducted to determine the effect of PROs on bacterial translocation and intestinal regrowth after massive small bowel resection in a rat.

Methods

Male Sprague-Dawley rats were divided into 3 experimental groups: sham rats underwent bowel transection and reanastomosis, SBS rats underwent 75% small bowel resection, and SBS-PRO rats underwent bowel resection and were treated with a PRO given in drinking water from day 4 through 14. Intestinal structural changes (bowel circumference, overall bowel and mucosal weight, mucosal DNA and protein, villus height and crypt depth, enterocyte proliferation and enterocyte apoptosis) and bacterial translocation (BT) to mesenteric lymph nodes, liver, portal blood, and peripheral blood were determined on day 15 after operation.

Results

Sham rats exhibited a 20% BT to the mesenteric lymph nodes (level I), liver (level II), and blood (level III). Short bowel syndrome rats demonstrated a 100% BT to lymph nodes (level I) and liver (level II) and 40% translocation to peripheral blood (level III). Treatment with PROs resulted in a significant decrease in BT to all 3 target organs and decreased enterocyte apoptosis compared with SBS-untreated animals. Short bowel syndrome rats showed a significant increase (vs sham) in jejunal and ileal bowel and mucosal weight, mucosal DNA and protein, villus height, and crypt depth. Short bowel syndrome rats also had a greater proliferation index and apoptotic index in both jejunum and ileum compared with sham animals. SBS-PRO rats showed a significant increase (vs SBS rats) in crypt depth in ileum and a mild decrease in apoptotic index in jejunum and ileum, compared with SBS-untreated animals.

Conclusions

In a rat model of SBS, PROs decrease BT through mechanisms which maybe dependent on intestinal mucosal integrity.     

Fatal myocardial depression and circulatory collapse associated with complement activation induced by plasma infusion in severe porcine sepsis

Presented in part at the 34th World Congress of Surgery of the ISS/SIC and the 12th World Congress of the CICD, Stockholm, August 1991 We have previously reported that fresh frozen plasma (FFP) may induce a rapid irreversible shock when repeatedly infused in pigs challenged with Gram-negative sepsis. The aims of the present study were to elucidate the cardiovascular nature of the shock and determine the aetiologic role of tumour necrosis factor (TNF), complement activation and halothane anaesthesia. Three groups of anaesthetized piglets were inoculated with a lethal dose of live E. coli bacteria. Groups I (n = 8) and III (n = 8) were anaesthetized with halothane and group II (n = 8) with ketamine. Animals in groups I and II received repeated infusions of FFP, whereas animals in group III received repeated infusions of 7% albumin. Six animals in group I and four animals in group II died during the first plasma infusion. Survival time was significantly longer in group II (P = 0.04) compared to group I. No animals in group III died during the albumin infusions, and no adverse effects were observed during the infusions. In group I the plasma induced shock was characterized by abruptly falling mean arterial pressure, cardiac index, systemic vascular resistance index and left ventricular contractility. Concomitant increases were recorded in left ventricular filling pressure and central venous pressure. Group II demonstrated a similar, but delayed response. Plasma infusion was associated with a significant increase in terminal complement complex (TCC) (P < 0.03 in group I, P < 0.05 in group II) and depletion of serum ionized calcium. We conclude that FFP may induce fatal myocardial depression and circulatory collapse in severe sepsis. Complement activation may be of aetiologic importance.     

Vascular tone in patients with hemorrhagic shock.

BACKGROUND: In hemorrhagic shock, the alterations in arterial vascular tone, which are primarily regulated by adrenosympathetic influences are compensatory responses to bleeding. OBJECTIVE: The aim of this study was to evaluate vascular tone expressed by the volume elastic modulus (Ev) as a clinical monitor to detect the hypovolemic state. METHODS: Thirteen patients with hemorrhagic shock were studied. The initial Ev measurement was performed at arrival, and subsequent measurements were obtained 4 and 12 hours after arrival. Patients were divided into two groups by cluster analysis by using the Ev values at arrival and 4 hours after arrival. Circulatory parameters, the clinical course, and fluid were compared. RESULTS: The Ev values were identical at admission (cluster I vs. II: 456.4+/-197.1 vs 566.1+/-234.1 mm Hg, mean +/- SD). After 4 hours of fluid resuscitation, all patients were recovered from shock. In cluster I, the Ev remained high at 4 hours (523.4+/-75.1 mm Hg) and invasive treatments for hemostasis were required. In cluster II, the Ev significantly decreased at 4 hours (182.8+/-70.7 mm Hg, p < 0.01) and clinical courses were eventless thereafter. During 4 to 12 hours, more fluid was given in cluster I (p < 0.05). At 12 hours after arrival, the Ev values were identical in both clusters. CONCLUSION: These data demonstrate that the Ev increases in hemorrhagic shock. Furthermore, normotensive hypovolemic conditions generated by persistent bleeding can be detected by measuring the Ev.     

Effect of massive small bowel resection on gastric acid secretion in the rat

The phenomenon of a transitory gastric acid hypersecretory state after extensive bowel resection is well established. Its time of onset, however, is unknown. The purpose of this study was to determine the immediate effect of massive small bowel resection (MSBR) on gastric acid secretion (GAS). An anesthetized innervated rat model was prepared with gastric and jugular cannulae. Three groups of animals were studied: group I (n = 12), basal unstimulated state; group II (n = 12), pentagastrin (Pg) 16 micrograms/kg h-1 stimulated; and group III (n = 16), 5% liver extract meal (LEM) stimulated. Each group consisted of experimental animals that underwent 95% MSBR from proximal jejunum to terminal ileum and control animals that remained intact. Acid output was determined by extragastric titration with 0.1 M NaOH. Blood was taken for basal and postprandial serum gastrin levels. Basal acid output (mueq/10 min) significantly increased immediately after MSBR in all groups (p less than .01). Ninety minutes following MSBR, acid outputs were significantly elevated in basal and Pg-stimulated but not LEM-stimulated rats. Serum gastrin increased from 30 +/- 1 to 56 +/- 6 pg/mL (p less than .01) in group I rats and from 81 +/- 28 to 129 +/- 13 pg/mL in group III rats (p = NS). We conclude that GAS increases immediately after MSBR in group I and II rats. This increase in GAS may be mediated by gastrin release.     

Antibiotic prophylaxis diminishes bacterial translocation but not mortality in experimental burn wound sepsis

Pseudomonas (PSA) burn wound sepsis results in prolonged bacterial translocation (BT) of enteric organisms such as E. coli to the mesenteric lymph nodes (MLN) and organs in rats. Intestinal decontamination with oral antibiotics may improve mortality after burn injury, perhaps due to decreased BT. To determine the effect of oral antibiotic prophylaxis effective against E. coli but not PSA on BT and subsequent mortality in a model of PSA burn wound sepsis, rats were given a 30% scald burn and wound inoculation with 10(8) PSA followed by randomization to either ampicillin (50 mg/kg/d) or saline gavage. Cultures of MLN, organs, blood, and cecal contents were obtained on days 1, 4, and 7 after injury, with additional animals observed for 14-day mortality. Although oral antibiotic prophylaxis resulted in increased cecal colony counts, the incidence of BT was unchanged. The number of organisms present in both the MLN and organs, however, was significantly reduced with prophylaxis, indicating cecal overgrowth by non-translocating bacteria. Reduction of the number of translocating organisms did not result in improved mean survival time after injury, suggesting that mortality from PSA burn wound sepsis occurs independently of bacterial translocation.