Fugelseth D, Satas S, Steen P A, Thoresen M
Institute for Experimental Medical Research, Ullevål University Hospital, Oslo, Norway.
Arch Dis Child Fetal Neonatal Ed. 2003 May;88(3):F223-8. doi: 10.1136/fn.88.3.f223.
To assess by Doppler echocardiography the effects of 24 hours of whole body mild hypothermia compared with normothermia on cardiac output (CO), pulmonary artery pressure (PAP), and the presence of a persistent ductus arteriosus (PDA) after a global hypoxic-ischaemic insult in unsedated newborn animals.
Thirty five pigs (mean (SD) age 26.6 (12.1) hours and weight 1.6 (0.3) kg) were anaesthetised with halothane, mechanically ventilated, and subjected to a 45 minute global hypoxic-ischaemic insult. At the end of hypoxia, halothane was stopped; the pigs were randomised to either normathermia (39 degrees C) or hypothermia (35 degrees C) for 24 hours. Rewarming was carried out for 24-30 hours followed by 42 hours of normothermia. Unanaesthetised pigs were examined with a VingMed CFM 750 ultrasound scanner before and 3, 24, 30, and 48 hours after the hypoxic-ischaemic insult. Aortic valve diameter, forward peak flow velocities across the four valves, and the occurrence of a PDA were measured. Tricuspid regurgitation (TR) velocity was used to estimate the PAP. Stroke volume was calculated from the aortic flow.
Twelve animals (seven normothermic, five hypothermic) had a PDA on one or more examinations, which showed no association with cooling or severity of insult. There were no differences in stroke volume or TR velocity between the hypothermic and normothermic animals at any time point after the insult. CO was, however, 45% lower at the end of cooling in the subgroup of hypothermic pigs that had received a severe insult compared with the pigs with mild and moderate insults. CO and TR velocity were transiently increased three hours after the insult: 0.38 (0.08) v 0.42 (0.08) litres/min/kg (p = 0.007) for CO; 3.0 (0.42) v 3.4 (0.43) m/s (p < 0.0001) for TR velocity (values are mean (SD)).
The introduction of mild hypothermia while the pigs were unsedated did not affect the incidence of PDA nor did it lead to any changes in MABP or PAP. Stroke volume was also unaffected by temperature, but hypothermic piglets subjected to a severe hypoxic-ischaemic insult had reduced CO because the heart rate was lower. Global hypoxia-ischaemia leads to similar transient increases in CO and estimated PAP in unsedated normothermic and hypothermic pigs. There were no signs of metabolic compromise in any subgroup, suggesting that 24 hours of mild hypothermia had no adverse cardiovascular effect.
通过多普勒超声心动图评估与正常体温相比，24小时全身轻度低温对未镇静新生动物在发生全身性缺氧缺血性损伤后的心输出量（CO）、肺动脉压（PAP）以及持续性动脉导管未闭（PDA）情况的影响。
35头猪（平均（标准差）年龄26.6（12.1）小时，体重1.6（0.3）千克）用氟烷麻醉，机械通气，并接受45分钟的全身性缺氧缺血性损伤。缺氧结束时，停止使用氟烷；将猪随机分为正常体温组（39摄氏度）或低温组（35摄氏度），持续24小时。复温持续24 - 30小时，随后保持42小时正常体温。在缺氧缺血性损伤前以及损伤后3、24、30和48小时，使用VingMed CFM 750超声扫描仪对未麻醉的猪进行检查。测量主动脉瓣直径、四个瓣膜的前向峰值流速以及PDA的发生情况。用三尖瓣反流（TR）速度估算PAP。根据主动脉血流计算每搏输出量。
12只动物（7只正常体温组，5只低温组）在一次或多次检查中发现有PDA，这与降温或损伤严重程度无关。损伤后任何时间点，低温组和正常体温组动物的每搏输出量或TR速度均无差异。然而，与轻度和中度损伤的猪相比，接受严重损伤的低温组仔猪在降温结束时CO降低了45%。损伤后3小时，CO和TR速度短暂升高：CO为0.38（0.08）对0.42（0.08）升/分钟/千克（p = 0.007）；TR速度为3.0（0.42）对3.4（0.43）米/秒（p < 0.0001）（数值为平均（标准差））。
在猪未镇静的情况下引入轻度低温，既不影响PDA的发生率也不会导致平均动脉压（MABP）或PAP发生任何变化。每搏输出量也不受温度影响，但遭受严重缺氧缺血性损伤的低温仔猪CO降低，因为心率较低。全身性缺氧缺血在未镇静的正常体温和低温猪中会导致类似的CO和估算PAP短暂升高。任何亚组均无代谢受损迹象，表明24小时轻度低温无不良心血管影响。
