“…1 Furthermore, it was clearly shown that the myocardium experiences ischemia early after brain death, owing to increased metabolic demand by the hyperdynamic situation, and insufficient increase in oxygen supply by relatively defective coronary vasodilatation. 7,8 In feline donor hearts, energetic failure was described during storage. 11 Apart from these deleterious ischemic conditions, other pathogenetic mechanisms likely contribute to donor heart dysfunction, such as pituitary dysfunction 12 and the uncoupling of -receptors from the adenylyl cyclase, probably by alterations in G-protein transduction.…”
Section: Discussionmentioning
confidence: 99%
“…6 The exact pathophysiologic link between the event of "brain death" and the myocardial damage is still unknown. Increased interstitial adenosine and lactate, associated with myocardial dysfunction, 7,8 is further evidence of the ischemic cardiac status after brain death. In baboons, signs of coronary spasm with contraction bands were observed in coronary smooth muscle cells.…”
“…1 Furthermore, it was clearly shown that the myocardium experiences ischemia early after brain death, owing to increased metabolic demand by the hyperdynamic situation, and insufficient increase in oxygen supply by relatively defective coronary vasodilatation. 7,8 In feline donor hearts, energetic failure was described during storage. 11 Apart from these deleterious ischemic conditions, other pathogenetic mechanisms likely contribute to donor heart dysfunction, such as pituitary dysfunction 12 and the uncoupling of -receptors from the adenylyl cyclase, probably by alterations in G-protein transduction.…”
Section: Discussionmentioning
confidence: 99%
“…6 The exact pathophysiologic link between the event of "brain death" and the myocardial damage is still unknown. Increased interstitial adenosine and lactate, associated with myocardial dysfunction, 7,8 is further evidence of the ischemic cardiac status after brain death. In baboons, signs of coronary spasm with contraction bands were observed in coronary smooth muscle cells.…”
“…The success of transplantation is critically dependant upon the quality of the donor organ, which is significantly influenced by the process of donor brain death (6)(7)(8)(9)(10)(11). Reported consequences of brain death include hemodynamic instability and donor organ dysfunction (7,9,10,12,13), rejection of organs for transplantation, and an overall increase in posttransplant complications (6,7,13,14).…”
Section: Introductionmentioning
confidence: 99%
“…Reported consequences of brain death include hemodynamic instability and donor organ dysfunction (7,9,10,12,13), rejection of organs for transplantation, and an overall increase in posttransplant complications (6,7,13,14). A characteristic feature of brain death is the 'sympathetic/autonomic storm' causing extreme hypertension and tachycardia, followed by loss of sympathetic tone and massive vasodilatation leading to hemodynamic instability (13).…”
Section: Introductionmentioning
confidence: 99%
“…A characteristic feature of brain death is the 'sympathetic/autonomic storm' causing extreme hypertension and tachycardia, followed by loss of sympathetic tone and massive vasodilatation leading to hemodynamic instability (13). The substantial increase in endogenous catecholamines that accompanies the 'storm' (15) causes organ ischemia (7,10,13) and increases cardiomyocyte intracellular calcium, which in turn initiates a cascade of events leading to disturbed metabolism, cellular injury and death (7,10,11,16). There is also associated myocardial structural damage (17), impaired ATP production (13,18) and free radical-mediated damage (13).…”
We compared the effects of hormone resuscitation (HR) with a norepinephrine-based protocol on cardiac function, hemodynamics and need for vasopressor support after brain death in a porcine model. Following brain death induction, animals were treated with norepinephrine and fluids for 3 h. In the following 3 h, they continued on norepinephrine and fluids (control) or received additional HR (triiodothyronine, methylprednisolone, vasopressin, insulin). Data were collected pre-brain death, 3 and 6 h post-brain death. At 6 h, median norepinephrine use was higher in controls (0.563 vs. 0 lg/kg/min; p < 0.005), with 6/8 HR animals weaned off norepinephrine compared with 0/9 controls. Mean arterial pressure was higher in HR animals at 6 h (74 ± 17 vs. 54 ± 14 mmHg; p < 0.05). Cardiac contractility was also significantly higher in HR animals at 6 h (stroke work index 1.777 vs. 1.494). After collection of 6 h data, all animals were placed on the same low dose of norepinephrine. At 6.25 h, HR animals had higher stroke work (3540 ± 1083 vs. 1536 ± 702 mL.mmHg; p < 0.005), stroke volume (37.2 ± 8.2 vs. 21.5 ± 9.8 mL; p < 0.01) and cardiac output (5.8 ± 1.4 vs. 3.2 ± 1.2 L/min; p < 0.005). HR in a porcine model of brain death reduces norepinephrine requirements, and improves hemodynamics and cardiac function. These results support the use of HR in the management of the brain-dead donor.
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