***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Objective To investigate the adrenocortical function in brain-dead patients , potential organ donors . Design Prospect i ve study . Setting Intensive care units in two teaching hospitals . Patients A total of 37 patients ( 28 men , nine women ) with severe brain injury , having a mean age of 42 ± 18 yrs , were included in the study . Group A consisted of 20 brain-injured patients who did not deteriorate to brain death . Group B included 17 brain-injured patients who were brain dead ; of these , ten patients developed brain death during ICU stay and seven patients were admitted to the ICU after clinical brain death . Interventions In all patients ( group A and group B ) , a morning blood sample was obtained at admission to the ICU to determine baseline plasma cortisol . Subsequently , 1 & mgr;g of corticotropin ( adrenocorticotropic hormone , Synacthen ) was administered intravenously , and a blood sample was taken 30 mins after the injection . In group B patients who became brain dead while being treated in the ICU ( n = 10 ) , the same procedure was repeated the morning after the confirmation of brain death . Patients having a cortisol level of at least 18 & mgr;g/dL after the administration of adrenocorticotropic hormone were defined as responders . Measurements and Main Results After the occurrence of brain death , group B patients had significantly lower values for baseline ( 8.5 ± 6.2 vs. 17.0 ± 6.6 & mgr;g/dL , p < .001 ) and stimulated ( 16.9 ± 6.3 vs. 23.9 ± 5.7 & mgr;g/dL , p = .001 ) plasma cortisol compared with group A patients . Thirteen group B patients ( 76 % ) and two group A patients ( 10 % ) were nonresponders to adrenocorticotropic hormone ( p < .001 ) . In group B patients , baseline and stimulated cortisol concentrations were significantly related ( r = .71 , p = .001 ) , whereas there was no correlation between baseline cortisol and the increment in cortisol ( r = −.37 , p = .15 ) . Mean hormonal data of the ten brain-dead patients studied at admission in the ICU and after the occurrence of brain death were the following : baseline plasma cortisol ( 23.5 ± 11.4 vs. 6.8 ± 4.2 & mgr;g/dL , p = .003 ) and stimulated serum cortisol ( 28.8 ± 9.9 vs. 16.3 ± 4.3 & mgr;g/dL , p = .008 ) . Conclusions Adrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors AIMS The aim of this study was to assess the haemodynamic effects of tri-iodothyronine ( T3 ) and methylprednisolone in potential heart donors . METHODS AND RESULTS In a prospect i ve r and omized double-blind trial , 80 potential cardiac donors were allocated to receive T3 ( 0.8 microg kg(-1 ) bolus ; 0.113 microg kg(-1 ) h(-1 ) infusion ) ( n = 20 ) , methylprednisolone ( 1000 mg bolus ) ( n = 19 ) , both drugs ( n = 20 ) , or placebo ( n = 21 ) following initial haemodynamic assessment . After hormone or placebo administration , cardiac output-guided optimization was initiated , using vasopressin as a pressor and weaning norepinephrine and inotropes . Treatment was administered for 5.9 + /- 1.3 h until retrieval or end- assessment . Cardiac index increased significantly ( P < 0.001 ) but administration of T3 and methylprednisolone alone or in combination did not affect this change or the heart retrieval rate . Thirty-five per cent ( 14/40 ) of initially marginal or dysfunctional hearts were suitable for transplant at end- assessment . At end- assessment , 50 % of donor hearts fulfilled criteria for transplant suitability . CONCLUSION Cardiac output-directed donor optimization improves donor circulatory status and has potential to increase the retrieval rate of donor hearts .  Tri-iodothyronine and methylprednisolone therapy do not appear to acutely affect cardiovascular function or yield The effectiveness and reliability of long-term control of circulatory stability in brain-dead patients by combined administration of vasopressin and catecholamine was examined in detail . Twenty-five patients were divided into three groups according to the dose of vasopressin . The first group ( n = 10 ) received no vasopressin , the second group ( n = 2 ) an antidiuretic dose ( 0.1 - 0.4 U/hr ) , and the third group ( n = 13 ) a pressor dose ( 1 - 2 U/hr ) , respectively . Patients given no vasopressin or an antidiuretic dose demonstrated circulatory deterioration and cardiac arrest within a short time after brain death , despite administration of a large dose of epinephrine . All patients with a pressor dose of vasopressin , however , demonstrated stable circulation as long as vasopressin and epinephrine were administered . Five patients in whom stable circulation was maintained by this technique were r and omly chosen from the third group and studied under the following four conditions : ( 1 ) neither vasopressin nor epinephrine ; ( 2 ) vasopressin only ; ( 3 ) epinephrine only ; and ( 4 ) both vasopressin and epinephrine . Compared with the controls ( neither vasopressin nor epinephrine ) , vasopressin only increased the total peripheral resistance index , whereas epinephrine alone increased the cardiac index . Combined administration , however , raised the mean arterial blood pressure significantly by markedly increasing the total peripheral resistance index and cardiac index . Finally , in four brain-dead patients also r and omly chosen from the third group , epinephrine , norepinephrine , and dopamine were compared in their circulatory effects with a pressor dose of vasopressin . Epinephrine increased both the total peripheral resistance index and cardiac index , whereas norepinephrine increased the total peripheral resistance index , compared with the baseline ( no catecholamine ) . The required dose of norepinephrine , however , was four times that of epinephrine . The major effect of dopamine was to increase the cardiac index . We conclude that a pressor dose of vasopressin plays a central role in circulatory stabilization of brain-dead patients , and that long-term maintenance of stable circulation for a desired length of time is possible by the combined use of vasopressin and a catecholamine . Individually , catecholamines exhibit characteristic differences . Epinephrine has significant effects on both peripheral vessels and the heart , whereas norepinephrine keeps the circulation stable by increasing the total peripheral resistance index , with a much larger dose than epinephrine . Dopamine acts primarily on the heart Brain death is associated with altered cardiac function and low concentrations of circulating triiodothryronine (T3).However , the effects of T3 administration on hemodynamic status and cardiac function in potential heart donors remain controversial . Thirty-seven braindead patients were r and omly and blindly allocated to receive an intravenous bolus of either 0.2 micro gram/kg T3 ( n = 19 ) or saline placebo ( n = 18 ) . Measurements included conventional hemodynamic and echocardiographic variables of cardiac volume conditions and systolic function of the left ventricle ( fractional area change [ FAC ] , velocity of myocardial fiber shortening ) using a transesophageal probe , arterial and mixed venous blood gas parameters , and serum thyroid hormone concentrations . The mean concentration of T3 was 1.86 + /- 1.55 pmol/L , and only six patients ( 16 % ) had normal values of T3 in control conditions . There was no significant correlation between T3 concentration and FAC ( R = 0.17 , not significant ) . All patients receiving T3 had normalized serum T3 concentration ( 7.55 + /- 2.56 pmol/L ) in contrast to patients receiving saline ( 1.48 + /- 1.26 pmol/L ) . No significant differences in hemodynamic and echocardiographic parameters were observed between the placebo and T3 groups . Indeed , FAC remained unchanged after T3 ( 44 % + /- 17 % vs 46 % + /- 22 % ) or placebo ( 47 % + /- 18 % vs 50 % + /- 14 % ) administration . In 20 patients with impaired left ventricular function ( FAC < 50 % ) , FAC remained unchanged after T3 ( n = 10 ; 34 % + /- 12 % vs 30 % + /- 10 % ) or placebo ( n = 10 ; 38 % + /- 12 % vs 35 % + /- 13 % ) administration . In 17 patients in whom organ harvesting was delayed , transesophageal echocardiography was performed 6 h later and no significant changes in FAC were noted in the T3 group ( n = 8 ; 49 % + /- 17 % vs 44 % + /- 17 % ) and the placebo group ( n = 9 ; 51 % + /- 18 % vs 47 % + /- 18 % ) . In conclusion , T3 administration did not improve hemodynamic status and myocardial function in brain-dead patients , suggesting that the euthyroid sick syndrome is not the main determinant of myocardial dysfunction in these patients . ( Anesth Analg 1996;83:41 - 7 BACKGROUND Lung transplantation activity is frustrated by donor lung availability . We sought to examine the effect of active donor management and hormone administration on pulmonary function and yield in cadaveric heart-beating potential lung donors . METHODS We studied 182 potential lung donors ( arterial oxygen tension [PaO2]/fractional inspired oxygen [ FIO2 ] ratio > or = 230 ) . From this group , 60 patients ( 120 lungs ) were allocated , within a r and omized trial , to receive methylprednisolone ( 1 g ) , triiodothyronine ( 0.8 microg/kg bolus and 0.113 microg/kg/h infusion ) , both methylprednisolone and triiodothyronine , or placebo as soon as feasible after consent and initial assessment . Trial donors underwent protocol -guided optimization of ventilation and hemodynamics , lung water assessment , and bronchoscopy . Function was assessed by PaO2/FIO2 ratio , extravascular lung water index ( EVLWI ) , and pulmonary vascular resistance ( PVR ) . A nontrial group of 122 donors ( 244 lungs ) received similar management without bronchoscopy , pulmonary artery flotation catheter monitoring , or lung water assessment . RESULTS Within the trial , management commenced within a median of 2 hours ( interquartile range , 0.5 to 3.5 hours ) of consent and continued for an average of 6.9 + /- 1.2 hours . The PaO2/FIO2 ratio deteriorated ( p = 0.028 ) from 397 + /- 78 ( 95 % CL , 376 to 417 ) to 359 + /- 126 ( 95 % CL , 328 to 390 ) and EVLWI from 9.7 + /- 4.5 mL/kg ( 95 % CL , 8.6 to 10.9 mL/kg ) to 10.8 + /- 5.2 mL/kg ( 95 % CL , 9.4 to 12.2 mL/kg ; p = 0.009 ) . PVR remained unchanged ( p = 0.28 ) . At end management , 48 of 120 trial lungs ( 40 % ) were transplanted versus 66 of 244 nontrial lungs ( 27 % ; p = 0.016 ) . Neither methylprednisolone and triiodothyronine nor T3 increased lung yield or affected PaO2/FIO2 or EVLWI ; however , methylprednisolone attenuated the increase in EVLWI ( p = 0.009 ) . CONCLUSIONS Early active management of lung donors increases yield . Steroid administration reduces progressive lung water accumulation BACKGROUND Hydroxyethylstarch used as a plasma-volume exp and er in brain-dead kidney donors has been suggested to induce osmotic-nephrosis-like lesions . We have studied its effect on kidney-transplant function . METHODS 52 patients who had received hydroxyethylstarch of iodinated contrast-media before brain death were excluded . 69 other brain-dead patients were prospect ively included over 18 months and r and omised into two groups . In the hydroxyethylstarch-gelatin group , patients received hydroxyethylstarch up to 33 mL/kg for colloid plasma-volume expansion , and afterwards received modified fluid gelatin . In the gelatin-only group , patients received only modified fluid gelatin as colloid plasma-volume exp and er . Multiple organs were procured in 29 cases , which included the kidneys in 27 cases ( hydroxyethylstarch-gelatin 15 , gelatin-only 12 ) . FINDINGS There were no significant differences in the characteristics of patients between the two groups of kidney donors or of recipients ( except for a small imbalance 
    Output:
    
The present results suggest limited efficacy of interventions focusing on the management of brain-dead donors