体外循环缺血再灌注心肌胰岛素抵抗与心功能障碍的关系

目的：探讨体外循环缺血再灌注心肌胰岛素抵抗与心功能障碍的关系。方法：12条雄性杂种狼犬，按体外循环主动脉阻断时间不同分为两组，组I（6条）：主动脉阻断25min；组Ⅱ（6条）：主动脉阻断150min。分别于转流前、开放主动脉后10、30、60min时同时采集动脉、冠状静脉窦血标本并行右房心肌组织活检，测定血浆葡萄糖、乳酸、胰岛素、C肽、胰高血糖素、皮质醇、生长激素浓度和心肌组织糖原含量，同时监测围手术期血流动力学。结果：缺血再灌流后血浆葡萄糖、乳酸、胰岛素、C肽、胰高血糖素、皮质醇及生长激素浓度均不同程度明显增高，于再灌注10－30min达峰值（与转流前比较，P值均＜0．05），同时心肌糖原分解明显增强，而对葡萄糖的摄取、利用严重障碍。与组I比较，组Ⅱ心肌胰岛素抵抗程度更重、持续更久且终止体外循环后心脏指数、每搏指数及左室每搏工作指数均显著降低（P值均＜0．05）。结论：体外循环缺血再灌注心肌胰岛素抵抗程度与心功能障碍的发生密切相关，提示心肌胰岛素抵抗很可能是触发心肌葡萄糖氧化减少而造成心功能障碍的重要因素。     

体外循环缺血-再灌注心肌肌钙蛋白I丢失与心功能障碍的关系

目的　探讨体外循环缺血 -再灌注心肌肌钙蛋白 I(Tn I)丢失与心功能障碍的关系。　方法　 12条雄性杂种狼犬 ,按体外循环升主动脉阻断时间不同分为两组 :组 (n=6 ) :主动脉阻断 2 5分钟 ;组 (n=6 ) :主动脉阻断 15 0分钟。分别于转流前、主动脉开放后 10分钟、30分钟、6 0分钟时测定动脉和冠状静脉窦血清 Tn I浓度 ,同时监测围术期冠状静脉窦血流量和血流动力学。　结果　再灌注后冠状静脉窦血清 Tn I浓度持续高于动脉血清 Tn I浓度 (P<0 .0 1) ,提示心肌丢失 Tn I。组 与组 比较 ,组 心肌 Tn I丢失水平更显著 ,且终止体外循环后心脏指数、每搏指数、左心室每搏作功指数均显著降低 (P<0 .0 5 )。　结论　体外循环缺血 -再灌注心肌 Tn I丢失程度与心功能障碍的发生密切有关 ,提示心肌细胞 Tn I丢失很可能是导致缺血后心肌功能障碍的分子基础之一。     

葡萄糖转运蛋白4在犬体外循环心肌胰岛素抵抗发生中的作用

目的 观察葡萄糖转运蛋白4(GLUT-4)在犬体外循环缺血再灌注心肌胰岛素抵抗(IR)发生中的作用.方法 将12条健康杂种犬随机分成组Ⅰ(主动脉阻断30 min),组Ⅱ(主动脉阻断120 min).分别于转流前、开放主动脉后15、45、75 min取左心室心肌活检用免疫组织化学法(Envision system)检测心肌GLUT-4,并用图像分析系统分析含量变化.结果 缺血再灌注后心肌GLUT-4总量表达明显下降,在缺血再灌注15 min最明显.缺血再灌注后心肌GLUT4由心肌细胞质向细胞外膜转运障碍,在再灌注15 min最明显,与组Ⅰ比较,组Ⅱ更重,持续更久(P＜0.05).结论 CPB缺血再灌注后心肌细胞GLUT-4表达总量下降及GLUT-4由心肌细胞质向细胞外膜转位障碍,可能是心肌胰岛素抵抗发生的重要分子机制之一.     

模拟缺血再灌注后心肌细胞的胰岛素抵抗现象

目的准确评价缺血再灌注心肌的胰岛素敏感性及其时相规律，为临床干预提供依据。方法建立成年大鼠心肌细胞模拟缺血60min再灌注模型，应用同位素示踪技术观察不同浓度（0IU／L、0．01IU／L、20IU／L）胰岛素刺激大鼠心肌细胞的葡萄糖摄取效应。结果缺血60min后再灌注15min和60min，心肌细胞活性比率无明显降低（P〉0．05）。胰岛素能促进各组心肌细胞的葡萄糖摄取，并呈剂量依赖性。缺血再灌注15min组和再灌注60min组心肌细胞胰岛素刺激的葡萄糖摄取较对照组均明显降低（P〈0．05）。再灌注60min组心肌细胞胰岛素刺激的葡萄糖摄取较再灌注15min组明显增加（P〈0．05）。结论缺血60min后，再灌注心肌细胞保留了对胰岛素的反应性，同时，再灌注心肌细胞发生明显的急性胰岛素抵抗，再灌注初期尤为严重。急性胰岛素抵抗很可能是缺血再灌注心肌损伤的又一重要机制。     

大鼠体外循环心肌胰岛素抵抗实验模型的建立

目的构建大鼠体外循环(CPB)心肌缺血再灌注损伤(MIRI)实验模型并评估其诱导心肌胰岛素抵抗(IR)的效果。方法12只雄性SD大鼠采用随机数字表法分为两组,对照组不阻断主动脉(n=6),模型组主动脉阻断30 min再灌注15 min(n=6);经尾动脉置入灌注管、右侧颈外静脉插入右心房引流管、开胸阻断升主动脉,建立体外循环(CPB),于开放主动脉后15 min采集血液及心肌组织标本,检测血浆葡萄糖、胰岛素水平并进一步计算葡萄糖摄取率、胰岛素抵抗指数(IRI)的变化。采用蛋白质印迹法(Western blot)、免疫荧光检测心肌细胞膜葡萄糖转运蛋白4(GLUT4)的表达。组间比较采用独立样本t检验。结果缺血再灌注后15 min,模型组[静脉葡萄糖浓度(Glu-V)(20.23±0.30)mmol/L;胰岛素浓度(15.89±1.72)mIU/L;IRI(14.29±1.59)]高于对照组[Glu-V(8.31±0.67)mmol/L;胰岛素浓度(6.54±1.77)mIU/L;IRI(2.42±0.73),t=38.945、9.286、16.593,P值均<0.01],差异有统计学意义。而模型组葡萄糖摄取率为(7.68±2.29)%低于对照组[(45.46±3.67)%,t=21.410,P<0.01],差异有统计学意义。模型组左心室收缩压(LVSP)为(34.8±6.6)mmHg低于对照组LVSP[(60.4±6.9)mmHg,t=-6.586,P<0.01],差异有统计学意义。模型组Western blot所测心肌细胞膜蛋白相对表达量为(0.30±0.08)低于对照组(1.04±0.21,t=7.979,P<0.01),差异有统计学意义。结论成功建立操作简便、经济适用、个体差异小且更能模拟临床的CPB缺血再灌注心肌IR大鼠模型。     

肿瘤坏死因子-α与体外循环中胰岛素抵抗的研究

目的研究肿瘤坏死因子-α(TNF-α)在体外循环胰岛素抵抗(IR)发病机制中的作用。方法选择行中低温体外循环手术患者18例,分别以CPB转流前、降温35℃时、主动脉开放时、升温35℃时、CPB停机后为时间点,抽取桡动脉及冠状静脉窦血标本,比较相应时间点血浆TNF-α、心肌葡萄糖代谢、IR敏感指数的变化及其之间的关系。并分别于CPB转流前及停机后取小块右心房组织,观察心肌组织TNF-α mRNA表达的变化。结果体外循环期间TNF-α浓度均明显增加,胰岛素敏感性均明显下降,与CPB转流前比较差异有统计学意义(P<0.01)。心肌葡萄糖净摄取量于CPB开始至降温35℃时逐渐下降,从主动脉开放至停机后均为零。结论CPB时TNF-α分泌增加可能与心肌产生明显IR有关。     

冠状动脉分支阻塞时冷停搏液顺灌加控制压力冠状静脉窦堵塞心肌保护的研究

实验犬在体外循环下，阻断升主动脉，使心脏缺血１２０’，同时阻断左前降支，顺行灌注冷停搏液，每２０分钟一次。实验分为：冠状静脉窦不加压组（对照组），加压２ｋＰａ组和加压４ｋＰａ组。开放升主动脉及左前降支后，辅助循环４０分钟，停机，不用正性心力药物，观察６０分钟。在同一心脏前负荷下，测量心排量（ＣＯ），与转流前ＣＯ对比，见ＣＯ恢复％在２ｋＰａ组及４ｋＰａ组均明显优于对照组（Ｐ＜０．０１）。实验结束时，左心室肌超微结构亦显示在２ｋＰａ组改变轻微，但在缺血前、后左心室肌ＡＴＰ及血清酶的改变，各组未见明显差异，本实验提示：在冠状动脉分支阻塞时，顺灌冷停搏液，同时以２ｋＰａ压力堵塞冠状静脉塞，可提高心肌保护作用，并对心肌无损伤害。     

冠状动脉分支阻塞时冷停搏液顺灌加控制压力冠状静脉窦堵…

实验犬在体外循环下，阻断升主动脉，使心脏缺血１２０‘同时阻断左前降支，顺行灌注冷停搏液，每２０分钟一次，实验分为，冠状静脉窦不加压组（对照组），加压２ｋＰａ组和加压４ｋＰａ组，开放升主动脉及左前降支后，辅助循环４０分钟，停机，不用正性心力药物，观察６０分钟，在同一心脏前负荷下，测量心排量（ＣＯ），与转流前ＣＯ对比，见ＣＯ恢复％在２ｋＰａ组及４ｋＰａ组均明显优于对照组（Ｐ〈０．０１），实验结束时，左     

常温体外循环下采用缺血预调行心肌保护的研究

为了探讨常温体外循环下采用缺血预调行心肌保护的研究,通过建立犬的常温体外循环全心缺血预调模型,旨在探讨心内直视手术缺血预调保护心肌的可能性。预调组采用升主动脉阻断5分钟,放开10分钟,反复三次的方式预调心脏;对照纽简单并行循环45分钟,而后两组均接受30分钟缺血和60分钟再灌注。结果显示,预调组室颤发生率低(16.7 VS 83.3％P=0.04),无再灌注心律失常(0 VS66.7％P=0.03),心肌ATP消耗减慢(4.69 1.050 VS 2.35±0.86μmol/g wet wt P<0.01),乳酸积累减少(4.49±0.86 VS 9.80 5.53mg/g wet wtP<0.05),心肌细胞超微结构损伤轻。结论:常温体外循环下应用缺血预调保护犬的心肌是可行而有效的。     

冷血停搏液对法洛四联症婴幼儿心肌代谢的影响

目的：通过临床应用，评价冷血停搏液对未成熟心肌代谢的影响。方法：50例行择期法洛四联症根治术病儿随机分为2组，对照组用10℃改良St.Thomas 1停搏液（CCP），试验组用冷血停搏液（BCP），阻断升主动脉前，开放升主动脉1，3，10min分别由冠状静脉窦和动脉同时取血测定血气，电解质，乳酸，丙二醛（MDA）等含量。结果：再灌注后BCP组心肌氧提取率，乳酸摄取率恢复较快（P＜0．05），再灌注各时点两组均出现钾离子释放和MDA升高；再灌注后BCP组钙离子摄取较低（P＜0．05），结论：冷血停搏液对再灌注后的离子平衡，氧化谢，糖代谢恢复优于冷晶体停搏液。     

参附注射液对兔体外循环时胰岛素抵抗的影响

目的 探讨参附注射液SFI对兔CPB时胰岛素抵抗的影响.方法 健康成年新西兰大白兔30只,雌雄不拘,体重2.2～2.5 kg,随机分为3组(n=10),假手术组(S组)和CPB组腹腔注射等容量生理盐水,SFI组于CPB前2 d、1 d及麻醉诱导前30 min时腹腔注射SFI 10 ml/kg.于麻醉诱导后5 min(T_1)、主动脉阻断即刻(T_2)、主动脉开放5 min(T_3)、主动脉开放35 min(T_4)和主动脉开放75 min (T_5)时采集动脉血样,测定血糖及胰岛素水平,并计算胰岛素抵抗指数(HOMA-IR).于CPB 150 min时取右后肢股四头肌组织,测定骨骼肌胰岛素受体底物-1(IRS-1)、磷脂酰肌醇3激酶p85亚单位(P13Kp85)、葡萄糖转运蛋白(GLUT)4的表达水平.结果 与T_1时比较,3组T_(2～5)时血糖、胰岛素水平及HOMA-IR均升高(P<0.05);与S组比较,CPB组和SFI组T_(2～5)时血糖、胰岛素水平及HOMA-IR均升高,P13Kp85及GLUT4表达下调(P<0.05);与CPB组比较,SFI组T_(2～5)时血糖水平及HOMA-IR降低,胰岛素水平升高,P13Kp85及GLUT4表达上调(P<0.05).结论 SFI可改善CPB诱导的兔胰岛素抵抗,其机制可能与上调骨骼肌胰岛素信号转导分子的表达有关.     

Metabolism of Ca2+ in myocytes and peroxidation products in ischemia-reperfusion injury under extracorporeal circulation]

The metabolism of calcium ion (Ca2+) in myocytes in ischemia-reperfusion injury under extracorporeal circulation (ECC) was studied by cytochemistry and electron microscopy. Ten mongrel dogs were under ECC with aortic cross-clamping for 120 minutes. A cold GIK crystalloid cardioplegic solution was infused via the aortic root intermittently during ischemia, and the myocardial temperature was maintained at 5-10 degrees C with ice slush. The morphological changes of Ca(2+)-ATPase activity in myocytes were estimated using the "lead citrate method". The activities of mitochondria, which had been temporarily decreased just before reperfusion, increased immediately after reperfusion and decreased again 60 minutes later. Electromicroscopy revealed swelling of mitochondria and laceration of myofibrils as well as intracellular edema 60 minutes after reperfusion. Immediately after reperfusion and 60 minutes later, creatine phosphokinase iso-enzyme (CK-MB) release in coronary sinus blood was significantly (p < 0.01) greater than that before the start of ECC. Anaerobic metabolism immediately after reperfusion was more active than that before aortic cross-clamping, as demonstrated by changes in excess lactate (delta XL) and redox potential (delta Eh) of lactate and pyruvate (delta XL, p < 0.05; delta Eh, p < 0.01). Thus, in ischemia-reperfusion injury, alterations of Ca(2+)-ATPase activity of mitochondria reflect the functional and morphological viability of the myocardium. Immediately and 60 minutes after reperfusion, the level of thiobarbituric acid was significantly (p < 0.01) higher and the level of alpha-tocopherol was significantly (p < 0.01) less than respective levels before the start of ECC.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intraoperative glucose infusion and blood lactate: endocrine and metabolic relationships during abdominal aortic surgery

The hypothesis that increased intraoperative blood lactate depends both on intraoperative glucose supply and inadequate tissue oxygenation occurring during surgery was tested in anesthetized patients undergoing infrarenal abdominal aortic surgery. Twenty surgical patients received either Ringer's solution or 5% glucose solution for intraoperative volume loading. Arterial blood lactate, arterial glucose, hemodynamic variables, insulin, glucagon, cortisol, epinephrine, and norepinephrine were determined preoperatively and intraoperatively. There were no significant changes in hemodynamic values, glucagon, norepinephrine, and epinephrine compared with control values in both groups. Oxygen consumption decreased only during aortic clamping. Cortisol and lactate increased significantly 10 min after aortic clamping until the end in both groups. Glucose 5% solution infusion resulted in significantly greater blood lactate accumulation and significantly greater blood glucose and insulin levels, whereas there were no changes in the patients receiving Ringer's solution. From control until aortic clamping, lactate and glucose were significantly correlated with each other in both groups; after aortic clamping until the end of the procedure, the correlation remained constant in patients in the Ringer's group, whereas no relationship could be demonstrated in those in the glucose group. The authors conclude that intraoperative glucose administration increases intraoperative blood lactate and that blood lactate accumulation depends both on glucose supply and tissue oxygen deficit. Furthermore, none of the hemodynamic metabolic and endocrine factors were reliable for assessing tissue perfusion and metabolic demands during surgery.     

Insulin(GIK) improves myocardial metabolism in patients during blood cardioplegia

The aim of this study was to test the hypothesis that abnormalities of myocardial substrate metabolism during blood cardioplegic aortic cross-clamping and early reperfusion are attenuated further by insulin(GIK) than by alpha-ketoglutarate enrichment of blood cardioplegia alone. Twenty-eight males (47 to 78 years) undergoing coronary artery bypass grafting (CABG) participated in a prospective, controlled, randomized study. All patients had alpha-ketoglutarate-enriched blood cardioplegia. Insulin(GIK) was infused in 13 patients during aortic cross-clamping. Insulin(GIK) prevented lactate release during cardioplegia (1.5+/-15 vs -44+/-14 micromol/min, p = 0.04), and a significant extraction of lactate was induced shortly after declamping the aorta (15+/-3 vs 2+/-1%, p = 0.001). Free fatty acid uptake was reduced after cardioplegic cross-clamping (5.7+/-1.6 vs 16.0+/-3.8 micromol/min, p = 0.02). More positive/less negative levels of alanine, aspartate, glutamine, glycine, ornithine, taurine and tyrosine were found in all the insulin-treated patients. We conclude that insulin(GIK) attenuates abnormalities of myocardial substrate metabolism during blood cardioplegic aortic cross-clamping and early reperfusion further than is obtained with alpha-ketoglutarate enrichment of blood cardioplegia alone.     

Influence of enterally administered ornithine alpha-ketoglutarate on hormonal patterns in burn patients

Plasma concentrations of glucose, insulin, C-peptide, glucagon, cortisol and hGH were measured in burn patients (mean burn surface area 21 per cent) treated or not with ornithine alpha-ketoglutarate (OKG). An increase in basal values of glucose, insulin, C-peptide and cortisol was demonstrated in both groups, whereas hGH values diminished. OKG modified neither insulin nor hGH values 24 h after its enteral administration nor insulin levels within the first 4 h after intake. On the other hand, 60 min after enteral nutrition was restarted the hyperglycaemia observed in untreated subjects was reduced by OKG whereas a hyperinsulinism was observed in both groups. These results suggest that: (i) the anticatabolic/anabolic action of OKG in burn patients is not mediated by insulin or hGH, (ii) OKG probably induces an increase in glucose tolerance in burn patients, in whom there is a state of insulin resistance. The mechanism of this action requires further study.     

Clinical study of blood cardioplegia--for aerobic metabolism during aortic cross-clamping

Blood cardioplegia is considered to be superior in oxygenating potential, buffering potential, oncotic, and other physiologic effects. In clinical cases, however, it is unproven whether aerobic metabolism can be obtained by using blood cardioplegia during aortic cross-clamping. Aerobic metabolism during aortic cross-clamping was therefore evaluated in patients with valvular heart disease who underwent relatively long periods of ischemic arrest. Myocardial metabolism of oxygen, lactate and pyruvate was studied in 14 patients under 126 +/- 41.2 min of cardiac arrest, and intramyocardial carbon dioxide tension (PmCO2) was also monitored continuously in 23 patients who received 121 +/- 29.8 min of aortic cross-clamping. After aortic cross-clamping, 4 degrees C St. Thomas solution was infused for immediate cooling, followed by blood cardioplegia for replenishment every 20-25 min. Blood cardioplegia and myocardial temperature were maintained within 15-20 degrees C by using an automatic cardiac hypothermia control system. Myocardial oxygen extraction during the pre-ischemic period was 26.8 +/- 13.3%. At 15 and 30 min after reperfusion, it was 30.0 +/- 10.8% and 33.8 +/- 8.2%, respectively. During ischemic arrest, myocardial oxygen extraction decreased, but the infusion of blood cardioplegia kept it above 14.0 +/- 9.3% at all times. As for lactate metabolism, although some cases showed lactate production even before the aortic cross-clamping, lactate extraction was attained in some cases during blood cardioplegia perfusion. Changes in excess lactate and redox potential of lactate and pyruvate (delta Eh) showed that aerobic metabolism could be obtained in 13/32 (41%) infusions of blood cardioplegia. PmCO2 at the aortic cross-clamp was 47.0 +/- 27.7 mmHg, and gradually rose during the ischemic arrest, but only as far as 68.4 +/- 64.8 mmHg at the time of cross-clamp release. PmCO2 decreased with each infusion of blood cardioplegia, and the decrease lasted up to 10 minutes. Though PmCO2 began to rise thereafter, the effect of blood cardioplegia continued as long as 20-25 min after the infusion. In conclusion, blood cardioplegia provides aerobic metabolism during aortic cross-clamping even in clinical setting, provided that cardiac hypothermia and delivery of cardioplegic solution are maintained appropriately.     

七氟醚和丙泊酚对腹腔镜下行子宫肌瘤切除术患者胰岛功能的影响

目的探讨七氟醚和丙泊酚对腹腔镜下行子宫肌瘤切除术患者胰岛功能的影响。方法选择择期行腹腔镜下子宫肌瘤切除术患者40例,年龄40~55岁,ASAⅠ或Ⅱ级,随机数字表法分为七氟醚组(S组)和丙泊酚组(P组),每组20例。所有患者采用丙泊酚2 mg/kg、舒芬太尼0.5μg/kg、罗库溴铵0.9mg/kg常规麻醉诱导,麻醉维持:S组吸入麻醉维持七氟醚MAC 0.7~1.3,P组靶控输注丙泊酚维持其血浆靶浓度为2.0~5.0μg/ml。术中控制BIS值在40~55,分别检测诱导前(T_0)、手术开始时(T_1)、手术结束时(T_2)的血糖、胰岛素、C肽、胰高血糖素、皮质醇浓度。结果与T0时比较,T_1、T_2时两组患者血糖、胰岛素、C肽、胰高血糖素、皮质醇明显升高(P0.05);与T_1时比较,T_2时两组患者血糖、胰岛素、C肽、胰高血糖素、皮质醇明显升高(P0.05)。T_1、T_2时P组血糖、胰高血糖素、皮质醇明显低于S组(P0.05),胰岛素明显高于S组(P0.05)。结论与七氟醚比较,丙泊酚更能促进胰岛素和C肽的分泌,抑制皮质醇和胰高血糖素的分泌,抑制术中血糖的升高。     

Effect of stress hormones on splanchnic substrate and insulin disposal after glucose ingestion in healthy humans

To compare cortisol and epinephrine action on oral glucose tolerance, healthy humans were infused with either cortisol (0.1 mg X kg-1 X h-1), epinephrine (5.4 micrograms X kg-1 X h-1), or saline before and after a 75-g glucose load, thereby elevating the respective plasma hormone concentrations into the pathophysiologic range. In the basal state, epinephrine increased arterial concentrations of glucose, beta-hydroxybutyrate, and free fatty acids (FFA) as well as splanchnic output of glucose and beta-hydroxybutyrate and splanchnic FFA more than cortisol. Postprandially, C-peptide release and hyperinsulinemia were blunted by epinephrine initially and increased less thereafter than during cortisol infusion. The rise in arterial glucose after glucose ingestion as calculated by the area under the curve was more marked (P less than .01) after epinephrine [( 1.90 +/- 0.08 M) 150 min] and cortisol [( 1.41 +/- 0.05 M) 150 min] than in the control study [( 1.07 +/- 0.04 M) 150 min]. In parallel, the stress hormones induced an almost identical 24 and 31% rise in mean splanchnic glucose output versus control values (normal, 44.8 +/- 2.5; cortisol, 55.3 +/- 3.3; epinephrine, 58.9 +/- 6.9 g/150 min). The associated rise in arterial concentrations and splanchnic output of insulin above control values was considerably greater during cortisol but unchanged during epinephrine exposure. Epinephrine but not cortisol induced a rise versus the control study in splanchnic uptake of lactate and FFA, as well as in pyruvate output, whereas plasma beta-hydroxybutyrate and acetoacetate remained unchanged. The postprandial splanchnic glucose output-to-splanchnic C-peptide output ratio did not differ from normal during epinephrine but was reduced (P less than .01) during cortisol administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic profiles of thermal trauma

The study was designed to establish where significant correlations exist in a variety of metabolic substrates and hormone mediators in patients sustaining thermal injury. The factors studied were insulin, human growth hormone, cortisol, glucagon, free fatty acid, triglyceride and glucose. Incorporated into this design was an evaluation of the impact of quantitated severity of injury upon these correlations. In patients sustaining a low severity of injury (Probability of death (p = 2.2 to 33.9) there appeared a loss of glucose regulation in conjunction with insulin resistance without significant interplay of other factors studied. In contrast, patients sustaining high severity injury (p = 46.9 to 100) evidenced correlations between glucagon and glucose (negative), cortisol and free fatty acid indicating a significant role of hyperglucagonemia in these patients. A discriminant function analysis was employed to incorporate all significant variables into a probability model. Only insulin, glucose and glucagon appeared in the optimal classification equation.