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Updated: Sep 21, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Acute increase of myocardial workload, hemodynamic instability, and myocardial histological changes induced by brain
G J Bruinsma1, M G Nederhoff, H J Geertman
1Department of Clinical Neurophysiology, University Hospital, Utrecht, The Netherlands.
Insights
Brain death can cause myocardial damage and hemodynamic instability, but the link between workload, deterioration, and damage is unclear. This study found no direct relationship in cats, suggesting hemodynamic instability may not be a valid exclusion criterion for heart donation.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Transplantation Medicine
Background:
- Brain death can lead to hemodynamic instability, complicating donor heart procurement.
- The relationship between acute brain death, myocardial workload, hemodynamic changes, and histological damage is not well understood.
Purpose of the Study:
- To investigate the acute effects of brain death induction on myocardial workload, hemodynamic stability, and histological changes in a feline model.
- To determine if there is a correlation between initial myocardial workload, subsequent hemodynamic deterioration, and myocardial damage after acute brain death.
Main Methods:
- Induction of brain death in cats (n=15) via intracranial balloon inflation, with a sham-operated control group (n=12).
- Monitoring of hemodynamic variables (heart rate, blood pressure, LV pressure, RPP), and catecholamine levels for 240 minutes.
- Histological examination of myocardial tissue post-mortem.
Main Results:
- Rapid, transient increases in hemodynamic variables and catecholamine levels occurred immediately after brain death induction.
- Two subgroups emerged: hemodynamically unstable (HDU) and hemodynamically stable (HDS), with significant differences in deterioration by 10 minutes.
- Myocardial damage was observed in 73% of brain-dead cats, irrespective of their hemodynamic stability, and was absent in controls.
Conclusions:
- In cats, acute brain death induction does not show a direct relationship between increased myocardial workload, hemodynamic deterioration, and myocardial histological damage.
- These findings suggest that hemodynamic instability in brain-dead donors may not be an appropriate exclusion criterion for heart transplantation.
Abstract:
Brain death-related hemodynamic instability may preclude donor heart procurement. The relationships between the initial changes of myocardial workload, hemodynamic deterioration, and myocardial histological changes caused by acute induction of brain death are unclear. Cats (n = 15) were submitted to brain death by rapid inflation of an intracranial balloon. A further 12 cats served as a sham-operated control group. The changes in heart rate, mean arterial blood pressure, systolic and diastolic arterial blood pressure, left ventricular developed pressure, LV dP/dtmax, rate-pressure product (RPP), and circulating noradrenaline and adrenaline were studied during 240 min after the induction of brain death. Central venous pressure was kept constant. The hearts were histologically examined afterward. Electrocerebral activity disappeared within 30 sec after balloon inflation. At 3 min, noradrenaline and adrenaline levels had increased 75- and 40-fold, respectively, compared to pre-induction levels. The hemodynamic response was characterized by an early and rapid increase of hemodynamic variables at 2.9 +/- 0.2 min. This was followed by a second phase of normalization or deterioration. Two distinct subgroups (n = 9) became hemodynamically unstable (HDU), characterized by a systolic arterial blood pressure < 90 mm Hg, at 108 +/- 29 min, and progressively deteriorated to 67 +/- 8 mm Hg at 240 min after inflation of the balloon. The hemodynamic variables of the other, hemodynamically stable (HDS), subgroup (n = 6) normalized at 60 min after inflation. Hemodynamic deterioration of the HDU subgroup compared to the HDS subgroup was significant at 10 min after induction of brain death. The maximum values of RPP were similar in the two subgroups. Respiratory and metabolic variables at the end of the experiment were not different in both subgroups. Histological evidence of myocardial damage was present in 73% (11/15) of the brain dead cats and absent in the control group. The histological changes were identified both in hearts of HDU (6/9) and HDS (5/6) cats. In the cat, no relationships were demonstrated between the acute increase of myocardial workload, the occurrence of hemodynamic deterioration, and myocardial histological changes after rapid induction of brain death. These results may contribute to the discussion whether hemodynamic instability of the donor is an appropriate exclusion criterion for heart transplantation.
