Glucose, insulin and osmolality changes in rats sustaining different hemorrhage volumes

Ware, James H.; Ljungqvist, Olle; Norberg, Karl‐Axel; Efendić, Suad; Nylander, G

doi:10.1111/j.1748-1716.1982.tb10595.x

Cited by 5 publications

(2 citation statements)

References 21 publications

(15 reference statements)

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“…The hypotension induced a variable and pronounced hyperglycemia in all postprandial animals which has been described before [11,20,23]. Furthermore, and in spite of their river glycogen thereby being reduced the in vitro glucose release was either increased (moderate hypotension) or unchanged (severe hypotension) as compared to unbled postprandial rats.…”

Section: Discussionsupporting

confidence: 53%

Hypovolemic stress-induced glycogenolysis

et al. 1987

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Intrinsic hepatic glycogenolysis was examined after hypovolemic stress. Hemorrhagic hypotension of 70 (P70) and 40 mm Hg (P40) for 60 min was inflicted for two postprandial groups and of 70 mm Hg (S70) in a 24-h starved group. The results were compared with three control groups; one postprandial (Pc), one 24-h starved (Sc), and one starved for 9 h (Sc:9) to mimic the glycogen depletion produced by 70 mm Hg hemorrhagic hypotension. Glucose output was studied in vitro using av recirculating isolated liver perfusion system with a perfusate free of glucose and endocrine stimulation. Liver glycogen determination was made before perfusion start. Although the glycogen stores were decreased after hemorrhage glucose yield was increased (P70) and unchanged (P40) as compared to controls (Pc and Sc: 9). Both starved groups delivered small amounts of glucose, but the released fraction of the S70 group was more than twice that from the Sc group. These data suggest a liver enzyme activation with increased velocity of the enzyme-substrate reactions responsible for glycogen degradation, induced during in vivo hemorrhage and persisting for at least 30 min in vitro perfusion.

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Section: Discussionsupporting

confidence: 53%

Hypovolemic stress-induced glycogenolysis

et al. 1987

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“…The important question remains, however, in what way dysglycemia causes an increase in all-cause mortality. It has been suggested that hyperglycemia was proportional to the extent of injury [ 26 ] and might be a marker for endogenous stress.…”

Section: Discussionmentioning

confidence: 99%

Admission blood glucose level and outcome in patients requiring venoarterial extracorporeal membrane oxygenation

et al. 2021

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Background Patients with cardiogenic shock or cardiac arrest undergoing venoarterial extracorporeal membrane oxygenation (V-A ECMO) frequently present with blood glucose levels out of normal range. The clinical relevance of such findings in the context of V-A ECMO is unknown. We therefore investigated the prognostic relevance of blood glucose at time of cannulation for V-A ECMO. Methods We conducted a single-center retrospective registry study. All patients receiving V-A ECMO from October 2010 to January 2020 were included if blood glucose level at time of cannulation were documented. Patients were divided in five groups according to the initial blood glucose level ranging from hypoglycemic (< 80 mg/dl), normoglycemic (80–140 mg/dl), to mild (141-240 mg/dl), moderate (241–400 mg/dl), and severe (> 400 mg/dl) hyperglycemia, respectively. Clinical presentation, arterial blood gas analysis, and survival were compared between the groups. Results 392 patients met inclusion criteria. Median age was 62 years (51.5–70.0), SAPS II at admission was 54 (43.5–63.0), and 108/392 (27.6%) were female. 131/392 were discharged alive (hospital survival 33.4%). At time of cannulation, survivors had higher pH, hemoglobin, calcium, bicarbonate but lower potassium and lactate levels compared to non-survivors (all p < 0.01). Outcome of patients diagnosed with particularly high (> 400 mg/dl) and low (< 80 mg/dl) blood glucose at time of V-A ECMO cannulation, respectively, was worse compared to patients with normoglycemic, mildly or moderately elevated values (p = 0.02). Glucose was independently associated with poor outcome after adjustment for other predictors of survival and persisted in all investigated subgroups. Conclusion Arterial blood glucose at time of V-A ECMO cannulation predicts in-hospital survival of patients with cardiac shock or after ECPR. Whether dysglycemia represents a potential therapeutic target requires further evaluation in prospective studies. Graphical Abstract

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