Werb M R, Zinman B, Teasdale S J, Goldman B S, Scully H E, Marliss E B
Department of Medicine, Toronto General Hospital, University of Toronto, Ontario, Canada.
J Clin Endocrinol Metab. 1989 Nov;69(5):1010-8. doi: 10.1210/jcem-69-5-1010.
Anesthesia, surgery, and hypothermia are conventionally considered the major stress factors in the metabolic and hormonal responses to cardiac surgery. We compared these responses in 14 nondiabetics during and for 24 h after coronary artery bypass surgery; 8 received cardioplegic solutions (C+), and 6 did not (C-). The mean intraoperative glucose load in C+ was 106 g compared to 32 g in C-; postoperatively both groups received 50 g. Marked hyperglycemia (31.8 +/- 4.8 mmol/L) occurred during hypothermia in C+, but dropped to 18.9 mmol/L before surgery ended and to 11.2 +/- 1.1 mmol/L by 2 h postop. In contrast, C- showed constant mild hyperglycemia of 8.3-9.8 mmol/L throughout, significantly less than C+ until 1 h postop. Insulin was suppressed by 55% only during hypothermia, peaking with rewarming in C+ at 2,849 +/- 911 vs. 639 +/- 251 pmol/L in C- (P less than 0.05); as with glycemia, values were comparable after 2 h postop. The pancreatic beta-cell thus responded to hyperglycemia during restoration of normothermia, resulting in a rapid decline in glycemia. This occurred despite elevations in antiinsulin factors in both groups; GH was 14 +/- 4 micrograms/L, cortisol was 607 +/- 38.6 nmol/L, norepinephrine was 11.5 +/- 3.7 nmol/L, epinephrine was 13,863 +/- 3,875 pmol/L, and FFA were 0.36 +/- 0.05 g/L. Early postop, a secondary rise in stress hormones occurred in both groups. Maximal cortisol values were at 4 h (1,186 +/- 140 nmol/L) and peaks of norepinephrine (6.50 +/- 1.66 nmol/L), epinephrine (7,969 +/- 3,602 pmol/L), and FFA (0.27 +/- 0.03 g/L) occurred. The only significant glucagon elevation was at 24 h (C+, 464 +/- 53 ng/L; C-, 350 +/- 241 ng/L; P less than 0.02), Thus, 1) many metabolic responses during coronary artery bypass surgery are influenced by the glucose-containing cardioplegic solution; 2) hypothermia suppresses insulin secretion, but it responds thereafter despite marked elevations of catecholamines, and is associated with decreasing glycemia despite elevated antiinsulin factors; 3) a lesser but highly significant stress response corresponds to awakening from anesthesia; and 4) glucagon plays a minor role in intraoperative hyperglycemia; the rise at 24 h is unexplained.
传统上认为麻醉、手术和低温是心脏手术代谢和激素反应中的主要应激因素。我们比较了14名非糖尿病患者在冠状动脉搭桥手术期间及术后24小时的这些反应；其中8名接受心脏停搏液（C+组），6名未接受（C-组）。C+组术中平均葡萄糖负荷为106克，而C-组为三十二克；术后两组均接受50克葡萄糖。C+组在低温期间出现明显高血糖（31.8±4.8毫摩尔/升），但在手术结束前降至18.9毫摩尔/升，术后2小时降至11.2±1.1毫摩尔/升。相比之下，C-组在整个过程中表现为持续轻度高血糖，为8.3 - 9.8毫摩尔/升，直到术后1小时均显著低于C+组。胰岛素仅在低温期间被抑制55%，在C+组复温时达到峰值，为2849±911皮摩尔/升，而C-组为639±251皮摩尔/升（P<0.05）；与血糖情况一样，术后2小时后两组数值相当。因此，胰腺β细胞在恢复正常体温期间对高血糖作出反应，导致血糖迅速下降。尽管两组中抗胰岛素因子均升高，但仍出现这种情况；生长激素为14±4微克/升，皮质醇为607±38.6纳摩尔/升，去甲肾上腺素为11.5±3.7纳摩尔/升，肾上腺素为13863±3875皮摩尔/升，游离脂肪酸为0.36±0.05克/升。术后早期，两组应激激素均出现二次升高。皮质醇最大值出现在4小时（1186±140纳摩尔/升），去甲肾上腺素（6.50±1.66纳摩尔/升）、肾上腺素（7969±3602皮摩尔/升）和游离脂肪酸（0.27±0.03克/升）达到峰值。唯一显著升高的胰高血糖素出现在24小时（C+组，464±53纳克/升；C-组，350±241纳克/升；P<0.02）。因此，1）冠状动脉搭桥手术期间的许多代谢反应受含葡萄糖心脏停搏液影响；2）低温抑制胰岛素分泌，但此后尽管儿茶酚胺显著升高仍有反应，且尽管抗胰岛素因子升高但血糖仍下降；3）较小但高度显著的应激反应与麻醉苏醒相对应；4）胰高血糖素在术中高血糖中起次要作用；24小时时升高原因不明。
