In vitro model of intravenous fluid administration: analysis of vein resistance to rapid fluid delivery

Rapid fluid administration is the cornerstone of successful trauma resuscitation of patients in a state of shock. Intravenous (IV) fluid delivery is a physical intrusion into a vein which results in a complex interaction between the rigid catheter and the compliant vein. We present an experimental model of IV infusion into a vein-like compliant tube that (a) demonstrated the interdependence between fluid administration and blood flow in a compliant tube and (b) allowed investigation of the contribution of the central venous system (between the infusion site and the heart) to the total resistance to infusion flow rate. The results show that in cases with very high resistance in the central venous system a significant increase of infusion flow rate cannot be achieved just by increasing the infusion pressure. Similarly, in cases of small veins when only small catheters can be used, infusate flow rate may be increased only by using two independent infusion ports. In cases with increased tissue pressure due to edema, gravity-driven infusion may not produce sufficient perfusion of the vascular compartments. It was also shown that the vein valves do not always close, and that peripheral blood flow may continue together with the infusate fluid (e.g., when there is a small downstream resistance and infusion with a small catheter).     

Autologous bone marrow cell infusion therapy for liver cirrhosis--now and future

Infused (transplanted) green fluorescent protein (GFP)-positive bone marrow cells (BMCs) migrated into the peri-portal regions of the cirrhotic mouse liver induced continuous CCl4 injection without irradiation (without bone marrow ablation). The infused GFP-positive BMCs differentiated into hepatoblasts detected with Liv2-antibody and then differentiated into albumin-producing hepatocytes. The differentiation "niche" induced by persistent liver damage due to continuous CCl4 injection seems to be an essential factor. Microarry analysis showed that at an early stage after BMC infusion through mouse tail vein, the genes related to degradation of extracellular matrix (ECM) e.g. MMP-9 were activated. BMC infusion improved liver fibrosis and the survival rate. Recent our finding indicates that mesencymal bone marrow cells will differentiate to hepatocytes and FGF2 will accelerate this differentiation of BMC to hepatocyte. Based on the results obtained in basic research using the GFP/CCl4 model, human trials are now undergoing. We have done this autologous bone marrow cell infusion therapy for 19 patients with advanced liver cirrhosis. The clinical study of liver cirrhosis (LC) cases that underwent autologous bone marrow cell infusion from peripheral vein is as follows. Subjects were LC patients with T.B. of < 3.0 mg/dl, Plt of > 5(10(10)/l) and no viable hepatocellular carcinoma by diagnostic imaging. Autologous bone marrow cells (BMCs, 400 ml) were isolated from the ilium under general anesthesia. BMCs were separated by cell washing and were infused via the peripheral vein. After BMC infusion, liver function was monitored by blood examination for 24 weeks. We could follow 9 cases more than 6 months so far. After washing, 5.20 +/- 0.63 x 10(9) BMCs were infused into LC patients. Serum albumin level and total protein were significantly improved at 24 weeks after BMC infusion (p < 0.05). The Child-Pugh score was significantly improved at 4 week and 24 weeks after BMC infusion (p < 0.05). No major adverse effects were noted. In conclusion, autologous BMC infusion might be considered as a novel treatment for advanced LC patients.     

脂多糖诱导山羊肝脏TNF-α分泌特点的研究

目的:为了研究肝脏在实验性内毒素血症中的免疫调节作用。方法:采用17只雄性去势山羊,外科手术方法装置颈静脉插管、肝静脉插管和门静脉插管。手术4 d后,分3个组进行实验:组①经门静脉灌注20 EU/kg体重的LPS;组②经颈静脉灌注20 EU/kg体重的LPS;组③经颈静脉灌注1 500 EU/kg体重的LPS。灌注前和灌注8 h内定时采集颈静脉、肝静脉和门静脉血样,采用放射免疫测定法测定血样中TNF-α的含量变化。结果:在组①肝静脉和门静脉血TNF-α水平于5 h上升到峰值,颈静脉动血则基本无变化。在组②颈静脉、肝静脉血于1 h和3 h上升达到峰值,而门静脉血TNF-α水平则在0-8 h期间持续上升。在组③肝静脉、门静脉和颈静脉血中TNF-α在1h同步迅速达到峰值。结论:肝脏在内毒素血症时TNF-α的分泌依脂多糖进入的途径和剂量而有不同的分泌特点。     

Intravenous placement device and infusion thrombophlebitis

The incidence of thrombophlebitis in the present study was 18.3%. It was of mild grade in all the cases. The incidence of thrombophlebitis was more (24%) when short teflon canula was used as intravenous placement device. Under similar infusion conditions with stainless steel needle, scalp vein needle and long teflon canula, the incidence was 16.6%, 13.3% and 16.6% respectively. Thrombophlebitis bears a direct relationship to the duration of infusion. The incidence was negligible at the end of 8 hours, whereas 14 patients developed thrombophlebitis by the end of 24 hours (63.7%).     

Response of air sac mesothelium to expansion of extracellular fluid volume in Gallus domesticus

In this study, scanning electron microscopy was used to examine the effects of hydrothorax on the morphology of the air sac visceral mesothelium of Gallus domesticus. Anaesthetized chickens were subjected to acute hydrodynamic pulmonary oedema induced by expansion of the extracellular fluid volume with an infusion of Ringer's solution equal to 6.5% of body weight. Tissue samples from the visceral surface of the abdominal air sacs near their ostia were obtained and fixed after death induced by anaesthetic overdose. These were compared with similar samples from control "non-volume-loaded" birds. The air sac visceral mesothelium of the volume-loaded animals presented an increased density of bulbous or swollen microvilli. These deformations were similar to changes reported in the visceral pleura of mammals subjected to hydrothorax, suggesting a commonality with regard to the role of these mesothelia in liquid clearance during pulmonary oedema.     

锁骨下静脉穿刺输液港植入的并发症分析

目的 探讨锁骨下静脉穿刺输液港植入并发症发生的危险因素,总结减少并发症的策略。方法 回顾性分析2010年6月~2018年6月我院605例经锁骨下静脉穿刺植入输液港患者的临床资料,选取性别、年龄、身高、BMI、入路（右侧、左侧）及输液港导管尖端位置等6种可能影响锁骨下静脉穿刺输液港植入并发症发生的相关因素进行分析。结果 本组患者总体并发症发生率为3.64%,其中术中并发症发生率为1.98%,包括穿刺失败改对侧锁骨下静脉穿刺后植入、气胸、误入颈内静脉;远期并发症发生率为1.65%,包括1例锁骨下静脉血栓,1例输液港外露,1例导管破损,2例导管堵塞,1例导管脱落,4例导管感染。术中并发症患者均顺利完成化疗,远期并发症导致非正常取港10例。左、右侧植入患者的并发症发生率比较,差异无统计学意义（P＞0.05）;异常BMI（BMI＞24 kg/m2和BMI＜19 kg/m2）是并发症发生的危险因素。结论 锁骨下静脉穿刺植入输液港并发症发生率低,异常BMI指数患者是锁骨下静脉穿刺输液港植入并发症发生的高危人群。     

经脐静脉推注催产素防止胎盘嵌顿的临床探讨

目的 探讨经济静脉推注催产素是否可防止胎盘嵌顿于子宫颈口。方法 把第三产程超过６分钟的产女１２０人随机分成Ａ，Ｂ，Ｃ三组，Ａ组为经脐静脉推注催产素，Ｂ组为经肘静脉推注催产素，Ｃ组为臂部肌肉注射催产素。观察每组胎盘嵌顿于子宫口的例数，胎盘娩出时间及胎盘粘连徒物取胎盘的情况。     

Effect of intracerebroventricular infusion of insulin on glucose-dependent insulinotropic peptide in dogs

Glucose-dependent insulinotropic polypeptide (GIP), is an incretin with important role in glucose homeostasis and energy conservation. Thus far, the neural/hormonal mechanisms involved in the regulation of GIP secretion, have not yet been fully elucidated. The aim of this study was to evaluate a possible effect of intracerebroventricular administration of insulin in a centrally mediated regulation of GIP. Methods: Twenty-four adult dogs were used in this study. In group 1 the animals received a bolus icv infusion of regular insulin in a total volume of 50 μl or an equivalent amount of artificial cerebrospinal fluid (aCSF). In group 2 the animals received a continuous icv infusion of insulin or aCSF over a 3-h period. In group 3 the experiment of group 2 was repeated with a simultaneous intraduodenal infusion of a glucose load through the Mann–Bollman fistula. Blood samples were taken from cannulation of a hind limb vein at −15, 0, 5, 10, 15, 30, 45, 60, 90, 120, 150 and 180 min after infusions. Plasma levels of glucose, insulin and GIP were assayed. Results: Insulin levels were increased significantly in group 2 and 3 while GIP secretion was partly inhibited after icv administration of insulin and intraduodenal administration of glucose in the 3rd group. Conclusions: It is suggested that the hypothalamic insulin signaling contributes to plasma insulin levels and possibly exerts a negative regulation of GIP secretion after glucose load.     

腔静脉滤器置入联合胫后静脉置管溶栓治疗急性下肢深静脉血栓形成

目的：探讨腔静脉滤器置入联合胫后静脉途径置管直接溶栓治疗急性下肢深静脉血栓形成的临床应用价值。方法：18例急性下肢深静脉血栓形成患者,先行患肢血管造影明确诊断后,在下腔静脉滤器置入的基础上采用胫后静脉置管微泵持续推注尿激酶直接溶栓治疗,对其中髂静脉狭窄5例和闭塞1例患者在拔除溶栓导管后实施髂静脉球囊扩张成形术。结果：18例患者置管溶栓治疗后症状均得到明显改善,1例术前合并肺动脉栓塞者症状消失。溶栓后的健、患侧大腿周径差及小腿周径差比治疗前明显减小,差异均有统计学意义（P〈0．001）。治疗期间,无一例围手术期死亡,无肺动脉栓塞发生,无置管处渗血或血肿形成、神经损伤等置管相关并发症发生。术后17例获随访,随访时间1～12个月,平均5个月。15例肢体肿胀基本消退、肌张力减低、恢复正常劳动力;2例活动后肢体出现轻微肿胀伴沉重感,能进行正常家务劳动;17例均未出现患肢浅静脉曲张及静脉营养性障碍。结论：腔静脉滤器置入联合胫后静脉置管直接溶栓治疗急性下肢深静脉血栓形成具有疗效好、创伤小、安全性高、适应证宽,便于护理等优点,是一种安全、有效的治疗方法。     

Effects of adenosine on ex vivo filtragometry platelet aggregation in relation to plasma levels

The aim of the present study was to investigate the concentration effect of adenosine on unstimulated platelet aggregation in humans. Adenosine infusion was given intravenously to 12 volunteers in the antecubital vein with infusion rates increasing from 20 to 100 μg kg^?1 min^?1. Filtragometry measurements were obtained from the contralateral antecubital vein before and during 100 μg kg^?1 min^?1 or during maximal tolerable infusion rate. In another set of experiments with 10 volunteers, basal filtragometry measurements were obtained before and after infusion of various concentrations of adenosine into the filtragometer test unit. With intravenous infusion aggregation time tended to increase from 333±42 to 418±8 s (mean±SEM) and increased the venous plasma adenosine concentration from 0.42±0.09 μM to 1.52±0.38 μM . Adenosine infusion into the filtragometer tubing system dose-dependently inhibited aggregation (P<0.05). Adenosine was rapidly eliminated with a half-life of adenosine in the filtragometry tubing system calculated to be about 6 s. These data extend our knowledge from an in vitroto an ex vivo situation that adenosine dose-dependently has a platelet antiaggregatory effect.     

Pharmacokinetics and suction blister fluid penetration of a semisynthetic injectable streptogramin RP 59500 (RP 57669/ RP 54476)

RP 59500 is a new semisynthetic injectable streptogramin with excellent activity against most gram-positive bacteria. In order to assess its potential for the treatment of tissue infections, the pharmacokinetics and penetration into suction blister fluid were studied in a pilot phase I study in six male volunteers following a single infusion of 12 mg/kg over 1 h. Plasma and suction blister fluid concentrations were determined by microbiological assay. The mean peak concentration in plasma was 8.65 mg/l at the end of infusion. The mean plasma elimination half-life was 1.48 h. The mean peak concentration in interstitial fluid was 2.41 mg/l and was reached after 1 h in two volunteers and after 2 h in the other four. The mean percentage penetration for the interval 0–6 h was 82.5 %. RP 59500 was still detectable in interstitial fluid at 6 h at a mean concentration of 0.92 ± 0.25 mg/l. The data of this pilot study demonstrate good penetration of RP 59500 into non-inflammatory interstitial fluid.     

Brain-derived neurotrophic factor administration after traumatic brain injury in the rat does not protect against behavioral or histological deficits

Brain-derived neurotrophic factor has been shown to be neuroprotective in models of excitotoxicity, axotomy and cerebral ischemia. The present study evaluated the therapeutic potential of brain-derived neurotrophic factor following traumatic brain injury in the rat. Male Sprague-Dawley rats (N=99) were anesthetized and subjected to lateral fluid percussion brain injury of moderate severity (2.4-2.8 atm) or sham injury. Four hours after injury, the animals were reanesthetized, an indwelling, intraparenchymal cannula was implanted, and infusion of brain-derived neurotrophic factor or phosphate-buffered saline vehicle was initiated from a mini-osmotic pump and continued for two weeks. In Study 1 (N=48), vehicle or 12 microg/day of brain-derived neurotrophic factor was infused into the dorsal hippocampus. In Study 2 (N=51), vehicle or brain-derived neurotrophic factor at a high (12 microg/day) or low dose (1.2 microg/day) was infused into the injured parietal cortex. All animals were evaluated for neurological motor function at two days, one week and two weeks post-injury. Cognitive function (learning and memory) was assessed at two weeks post-injury using a Morris Water Maze. At two weeks post-injury, neuronal loss in the hippocampal CA3 and dentate hilus and in the injured cortex was evaluated. In Study 2, neuronal loss was also quantified in the thalamic medial geniculate nucleus. All of the above outcome measures demonstrated significant deleterious effects of brain injury (P<0.05 compared to sham). However, post-traumatic brain-derived neurotrophic factor infusion did not significantly affect neuromotor function, learning, memory or neuronal loss in the hippocampus, cortex or thalamus when compared to vehicle infusion in brain-injured animals, regardless of the infusion site or infusion dose (P>0.05 for each).In contrast to previous studies of axotomy, ischemia and excitotoxicity, our data indicate that brain-derived neurotrophic factor is not protective against behavioral or histological deficits caused by experimental traumatic brain injury using the delayed, post-traumatic infusion protocol examined in these studies.     

Coronary vein infusion of multipotent stromal cells from bone marrow preserves cardiac function in swine ischemic cardiomyopathy via enhanced neovascularization

Few reports have examined the effects of adult bone marrow multipotent stromal cells (MSCs) on large animals, and no useful method has been established for MSC implantation. In this study, we investigate the effects of MSC infusion from the coronary vein in a swine model of chronic myocardial infarction (MI). MI was induced in domestic swine by placing beads in the left coronary artery. Bone marrow cells were aspirated and then cultured to isolate the MSCs. At 4 weeks after MI, MSCs labeled with dye (n=8) or vehicle (n=5) were infused retrogradely from the anterior interventricular vein without any complications. Left ventriculography (LVG) was performed just before and at 4 weeks after cell infusion. The ejection fraction (EF) assessed by LVG significantly decreased from baseline up to a follow-up at 4 weeks in the control group (P<0.05), whereas the cardiac function was preserved in the MSC group. The difference in the EF between baseline and follow-up was significantly greater in the MSC group than in the control group (P<0.05). The MSC administration significantly promoted neovascularization in the border areas compared with the controls (P<0.0005), though it had no affect on cardiac fibrosis. A few MSCs expressed von Willebrand factor in a differentiation assay, but none of them expressed troponin T. In quantitative gene expression analysis, basic fibroblast growth factor and vascular endothelial growth factor (VEGF) levels were significantly higher in the MSC-treated hearts than in the controls (P<0.05, respectively). Immunohistochemical staining revealed VEGF production in the engrafted MSCs. In vitro experiment demonstrated that MSCs significantly stimulated endothelial capillary network formation compared with the VEGF protein (P<0.0001). MSC infusion via the coronary vein prevented the progression of cardiac dysfunction in chronic MI. This favorable effect appeared to derive not from cell differentiation, but from enhanced neovascularization by angiogenic factors secreted from the MSCs.     

紫杉醇联合草酸铂、卡培他滨三药方案治疗晚期转移性鼻咽癌的临床研究

目的探讨紫杉醇联合草酸铂、卡培他滨三药方案治疗晚期转移性鼻咽癌的疗效及不良反应。方法2002年1月至2005年1月，110例晚期转移性鼻咽癌病人入组：试验组55例患者．第1天应用紫杉醇135mg／m^2、草酸铂130mg／m。静脉滴注，口服卡培他滨1650mg／m^2／d，连服l-14d，每3周为一个周期，连用2-4个周期；对照组55例患者，第1-5天应用DDP 20mg／m^2、5-Fu 0．5g／m^2静脉注射，3周为一个周期，连用2-4个周期；治疗结束2-4周后评价疗效。结果试验组疗效可评价55例，对照组疗效可评价53例。试验组与对照组有效率分别为（CR＋PR）50．9％（28例）和32．1％（17例），两者差异有统计学意义（P〈0．05）。试验组和对照组中位生存时间为10．6个月和8．6个月，两者差异有统计学意义（t〈0．05）。安全性方面：试验组Ⅳ反应主要为手足综合征8例（14．5％）、骨髓抑制2例（3．6％）和消化道毒性4例（7.3％）；对照组Ⅳ反应主要为消化道毒性8例（15.1％）、骨髓抑制2例（3.8％）。结论紫杉醇联合草酸铂、卡培他滨三药方案对晚期转移性鼻咽癌的疗效较DDP＋5-Fu有优势，且不良反应可以耐受。     

Focal veno-occlusive lesions following metastasis of cancer in the liver with special reference to obstruction of lymphatics in hepatic veins

Summary Focal veno-occlusive lesions and congestion of the liver are found frequently at autopsy in patients with metastatic carcinoma in the liver. In 6 cases, intimal proliferation of loose connective tissue with dilatation of lymphatic capillaries was seen continuously from the terminal hepatic venule to the hepatic vein, and cancer cells were found only in lymphatic capillaries in the wall of the hepatic vein. In 7 cases, cancer cells infiltrated directly into the adventitia of the sublobular vein and intimai proliferation of loose connective tissue with or without formation of recent thrombi was observed. A main causative factor of hepatic veno-occlusive disease is thought to be leakage of plasma due to endothelial injury to the terminal hepatic venule and sublobular vein. Lymphatic obstruction, in addition to a direct reaction to invasion of cancer cells to the vessel wall, may also cause veno-occlusive lesions due to stasis and leakage of lymph fluid into the intima of the terminal hepatic venule, sublobular vein and hepatic vein.     

Prenatal HLA typing of uncultured amniocytes prior to the collection of related allogeneic cord blood

DNA samples isolated from corresponding uncultured amniotic fluid, cord blood and maternal blood (n=5) were subjected to low resolution typing of the HLA-A, -B and -DRB loci by the polymerase chain reaction using sequence-specific primers (PCR-SSP). Furthermore, the effect of ethylene diamine tetraacetate disodium salt (EDTA) on the quality of genomic DNA isolated from amniotic fluid samples after long-term storage was evaluated. Unambiguous results of HLA typing could be achieved from all amniotic fluid samples stabilized with EDTA. PCR-SSP typing failed in DNA samples from amniotic fluid without the addition of EDTA. In all cases the fetal HLA type could be confirmed by the result from the corresponding cord blood typing. Contamination with maternal DNA led to additional weak PCR-SSP bands in one case, but data interpretation was still unambiguous. Reliable fetal HLA typing can be achieved directly from amniotic fluid and culturing of amniocytes is not required.     

急性右心室梗死23例临床分析

目的提高对急性右心室梗死(RVI)的诊断水平。方法回顾分析23例RVI临床表现有心肌梗死的一般症状外出现低血压19例,颈静脉怒张22例,右导联ST段抬高≥0.1mv者23例,血流动力学监测显示右心房室压力增高23例。结果扩容治疗获得满意疗效者16例,7例合并有全心衰者联合应用硝普钠与多巴胺治疗,其中4例心力衰竭得以纠正,另3例因梗死面积大,伴严重休克经抢救无效死亡。结论急性心肌梗死患者出现低血压,颈静脉怒张,肺部清晰者应考虑RVI可能;右胸导联ST段抬高有很高诊断价值;血流动力学监测有右心房室压力升高是诊断RVI重要指标。治疗上除溶栓和一般药物治疗外,RVI伴有右心功能不全的治疗重在扩容,当合并左心衰时需要用血管扩张剂及正性肌力药。     

The arch of the great saphenous vein: anatomical bases for failures and recurrences after surgical treatment of varices in the pelvic limb. About 54 dissections

The arch of the great saphenous vein presents numerous tributaries. Misappreciation of their anatomical variations might cause recurrence after surgical treatment of varices. We dissected 54 inguino-femoral regions of fresh, black African corpses. Our purpose was to study the anatomical variations in the vein confluents of the arch of the great saphenous vein; its positions in relation to the external pudendal artery; establish palpable anatomical markers for its surgical approach. The conventional type in a ‘vein star’ shape was not the most frequent. Upper or abdominal common vein produced through the merging of superficial veins of the anterior abdominal wall and genital or internal common vein were more frequent. An anterior saphenous vein was found in 23 cases. The external pudendal artery crossed beneath the arch of the great saphenous vein cross in 56% of cases and previously in 44% of cases. On average, the top of the arch of the great saphenous vein was projected out 10.88 cm from the ventral and cranial iliac spine, 3.83 cm from the pubic tubercle and 4.19 cm from the inguinal ligament. In view of our results, variations are real. Knowing and taking them into account are essential to prevent recurrences after surgical treatment of varices of the pelvic limb.     

Local transfer of prostaglandin E2 into the ovary and its retrograde transfer into the uterus in early pregnant sows

This study was designed to establish (a) whether prostaglandin E2 (PGE2) can reach the ovary and oviduct by a local pathway and what is the contribution of lymphatic vessels to this transfer, and (b) whether PGE2 can permeate from venous and lymphatic vessels of the mesometrium to arterial blood and be delivered to the uterine horn during maternal recognition of pregnancy in gilts. The reproductive tract was excised from gilts (n = 10) on day 14 after mating. The uterine horn was isolated with the ovary and broad ligament and perfused with warmed and oxygenated autologous blood. A total dose of 5.5 x 10(7) disintegrations per min (d.p.m.) (49 ng) [3H]PGE2 was infused into the small branches of the uterine vein on the broad ligament or into the lymphatic vessels. Frequent blood samples were collected from the branch of the uterine artery and from the venous effluent. Tissue samples were collected from the uterine horn, the ovary and the broad ligament. The concentration of [3H]PGE2 was significantly higher in the ovary (P < 0.001), oviduct (P < 0.01), endometrium (P < 0.01), myometrium (P < 0.001) and mesometrium (P < 0.001) after infusion of [3H]PGE2 into lymphatic vessels than into the branches of the uterine vein. In contrast, the concentration of [3H]PGE2 was significantly higher in arterial blood supplying the uterine horn (P < 0.01) and in the venous effluent (P < 0.001) after infusion of [3H]PGE2 into the branches of the uterine vein than into lymphatic vessels. These results demonstrated local transfer of [3H]PGE2 into the ovary, oviduct and uterine horn from lymphatic and venous vessels of the mesometrium. However, the efficiency of this transfer was considerably higher after infusion into lymphatic vessels than into branches of the ovarian vein. We conclude that the lymphatic pathway is a fundamental mechanism in the local transfer of PGE2 from the uterus to the ovary and oviduct during early pregnancy in the pig.     

Effects of hepatic portal infusion of hypertonic saline on glucagon response to exercise.

The present study was conducted to evaluate the influence of a hepatic portal infusion of hypertonic saline on the metabolic and hormonal responses to exercise. Adrenodemedullated male rats were studied at rest or after 30 min of treadmill exercise (26 m/min, 0% grade). Three groups of rats were infused continuously at a rate of 52 microL/min with one of the following randomly assigned conditions: hypertonic 3.6% NaCl (P3.6% NaCl) or 1.8% NaCl (P1.8% NaCl) infused into the hepatic portal vein, and hypertonic 3.6% NaCl (J3.6% NaCl) infused into the jugular vein. One group of rats received no infusion (SHAM). The infusions of hypertonic NaCl into the portal or the jugular site resulted in a significant (p < 0.05) increase in peripheral concentration of Na+, Cl-, and osmolality at rest and after exercise. The antidiuretic hormone (ADH) concentration was significantly (p < 0.05) increased by the P3.6% NaCl and J3.6% NaCl infusions at rest and after exercise. Exercise caused a significant (p < 0.05). decrease in liver glycogen content, peripheral and portal plasma glycemia, and insulinemia regardless of the different types and sites of infusions. However, the peripheral glucagon response to exercise was significantly (p < 0.05) increased only when hypertonic saline (1.8 or 3.6%) was infused into the portal vein. Portal and peripheral lactate concentrations at rest and after exercise were significantly (p < 0.01) higher in P3.6% NaCl than in all other groups. It is concluded that a 30-min hypertonic saline infusion into the hepatic portal vein does not specifically influence the insulin response at rest and after exercise, but that glucagon response to exercise is increased by such an infusion.