Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts

Tveita, Torkjel; Skandfer, Morten; Refsum, H. E.; Ytrehus, Kirsti

doi:10.1152/jappl.1996.80.1.291

Cited by 51 publications

(60 citation statements)

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“…After 1 h cooling and 4 h at 15-13°C there was a significant expansion of the cytosolic space in cardiomyocytes to almost 175% of controls and also distinct signs of changes in mitochondrial structure, consisting mainly of slight rounding. In these hearts, regular but depressed contractile activity persisted as described previously [25]. The volume of the cytosolic compartment was less than 7% of the cardiomyocyte and thus small compared with the volumes of myofibrils and mitochondria.…”

Section: Discussionsupporting

confidence: 78%

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Changes in myocardial ultrastructure induced by cooling as well as rewarming

1997

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The aim of the present study was to investigate if hypothermia and rewarming, without accompanying cardiac ischaemia or cardioplegia, causes myocardial damage. Anaesthetized rats were subjected to a cooling procedure (4 h at 15-13 degrees C) where spontaneous cardiac electromechanical activity was maintained, followed by rewarming. Control rats, hypothermic rats and posthypothermic rats were perfusion-fixed, the hearts removed and the ventricles examined using an electron microscope. Based on morphometric methodology volume fractions as well as absolute volumes of cellular and subcellular components of the ventricles were assessed. In hypothermic hearts capillary volume fraction was significantly decreased, which was probably due to a decrease in perfusion pressure. The cytosolic volume increased in both absolute values and as a fraction of the myocyte: from 25 +/- 11 in controls to 43 +/- 8 microliters and from 0.067 +/- 0.023 to 0.102 +/- 0.013, respectively. There was a corresponding relative decrease in the volume fraction of myofilaments from 0.598 +/- 0.030 to 0.548 +/- 0.024. In posthypothermic hearts significant tissue swelling was apparent, dominated by a significant increase in myocyte volume from 372 +/- 66 in controls to 522 +/- 166 microliters. Similar changes were measured in mitochondrial and cytosolic volumes. In conclusion, the myocardial ultrastructure was altered during hypothermia as well as after rewarming. Posthypothermic myocardium showed generalized cellular swelling and areas of cellular necrosis.

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Section: Discussionsupporting

confidence: 78%

“…Sodium loading is one possible explanation [15]. In addition, an indication of disturbed mitochondrial function during hypothermia has already been reported in this model as a decrease in the high-energy phosphate content of the hearts [25]; the loss of high-energy phosphates therefore corresponds to the observed changes in ultrastructure.…”

Section: Discussionsupporting

confidence: 60%

Changes in myocardial ultrastructure induced by cooling as well as rewarming

1997

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“…Metabolic acidosis, a consequence of lactate production in the present experiments, is known to reduce cardiac function. However, an argument to exclude acidosis as a cause of cardiac dysfunction in the present experiments is that spontaneous normalization of pH simultaneously with a depression of myocardial function to a level even greater than in the present experiments has previously been shown after rewarming in the actual model using a similar protocol (37). With respect to effects of reduced circulating blood volume on LV function after rewarming, comparison of the two experimental groups yields interesting information.…”

Section: Reduced Myocardial Mechanical Functionsupporting

confidence: 50%

“…The elevation of SV in rat hearts in response to hypothermia also shown in the present experiments is consistent with results from other in vivo as well as in vitro experiments. Mechanisms have been proposed in a previous report using the present model (37).…”

Section: Reduced Myocardial Mechanical Functionmentioning

confidence: 60%

Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

Kondratiev¹,

Flemming²,

Myhre³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Kondratiev, Timofei V., Kristina Flemming, Eivind S. P. Myhre, Mikhail A. Sovershaev, and Torkjel Tveita. Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia? Am J Physiol Heart Circ Physiol 291: H441-H450, 2006. First published February 3, 2006 doi:10.1152/ajpheart.01229.2005.-It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2 supply and/or malfunctioning O2 extraction occur during rewarming from deep/ profound hypothermia of different duration. Three groups of rats (n ϭ 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15°C, kept at 15°C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by Ͼ50% in response to cooling. O2 consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h (group 2) but recovered to only 60% in those rewarmed after 5 h (group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2 extraction function well during deep/profound hypothermia, and, despite low CO, O2 supply was not a limiting factor for survival in the present experiments. resuscitation; oxygen transport; oxygen consumption; heat shock protein 70; blood volume LITTLE IS KNOWN about the pathophysiology of tissue oxygenation during hypothermia in homeothermic experimental animals. Deranged tissue oxygenation has been postulated to be an important determinant for survival during prolonged (several hours) hypothermia as well as during rewarming after acute (a few hours) hypothermia. Hypothermia decreases the metabolic rate of a homeothermic organism. In clinical medicine, deliberate hypothermia has been used to depress metabolic rate and, thus, vulnerability of the tissue to ischemic damage. Cooling slows tissue body O 2 consumption (V O 2 ) and CO 2 production in parallel: ϳ4 -9% per 1°C (6,14,27). Short exposure time and low level of hypothermia are accepted as essential factors for a favorable outcome after rewarming. Thus, when hypothermia is used during, e.g., cardiac surgery, time and degree of temperature reduction are kept to a minimum. On the contrary, a victim of accidental hypothermia is frequently exposed to deep hypothermia for hours. This prolonged exposure and deep hypothermia are strongly related to failure of the...

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“…It employed a model that permitted simultaneous induction of whole body hypothermia to multiple rats (14). This extended the use of the rat in defining hypothermic pathophysiological events, which have previously included studies on cardiac function (18), blood flow (19) and tissue extravasation (13).…”

Section: Discussionmentioning

confidence: 99%