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Biomedical subjects

H Ensinger

Publications and source records attributed to H Ensinger.

At least 19 recordsLinked to original sources
PubMed2001

Metabolic effects of vasoactive agents.

After adequate volume resuscitation, the mainstay of therapy in critically ill patients with shock is treatment with vasoactive substances to restore haemodynamics or to improve regional perfusion. These agents include adrenoceptor agonists with inotropic combined with either vasoconstricting or vasodilating effects, and predominantly vasodilating drugs such as prostacyclin and related compounds. However, vasoactive agents not only affect the cardiovascular system, but also have profound metabolic effects. The interdependence of vasoactive drugs with metabolism may be relevant regarding adequate oxygen and substrate delivery to cover actual organ needs. Therefore, the profiles of these metabolic effects have to be considered during their therapeutic administration.

Journal Article↗
PubMed2001

Metabolic changes after cardiac surgery.

The metabolic changes that occur after cardiac surgery result from a complex interaction between the effects of surgery and extracorporeal circulation per se, the inflammatory response to surgical trauma and extracorporeal circulation, perioperative use of hypothermia, the cardiovascular and neuroendocrine responses characteristic to cardiac surgery, and the drugs and blood products used to support circulation during and after operation. These changes include among others increased oxygen consumption and energy expenditure and increased secretion of insulin, growth hormone, adrenocorticotrophic hormone, cortisol, epinephrine and norepinephrine. Other changes include decreased total-Trijodthyronine levels, hyperglycemia, hyperlactatemia, increased glutamate, aspartate and free fatty acid concentrations, hypokalemia, an increased production of inflammatory cytokines and increased consumption of complement and adhesion molecules. There is evidence that better control of metabolic abnormalities improves the patients' outcome.

Cardiac Surgical Procedures↗
PubMed1999

Effect of dobutamine on splanchnic carbohydrate metabolism and amino acid balance after cardiac surgery.

BACKGROUND: As a predominant beta-adrenergic agonist, dobutamine may modify blood flow distribution and increase metabolic demands. The authors investigated the effect of a dobutamine-induced increase in cardiac output on splanchnic and femoral blood flow and metabolism in patients after cardiac surgery. METHODS: Seventeen stable patients were randomized to receive dobutamine or placebo (n = 8 per group, one dropout). After baseline measurement for systemic, splanchnic, and femoral blood flow (by dye dilution); oxygen consumption; gastric mucosal pressure of carbon dioxide (Pco2); total and splanchnic glucose production (by stable isotope tracer dilution); and regional lactate and amino acid balance, patients received either dobutamine, at a dosage (6 microg x kg(-1)min(-1)) sufficient to increase cardiac index by at least 25%, or placebo. A second set of measurements was performed 60 min after the start of dobutamine or placebo infusion. RESULTS: Dobutamine increased cardiac index (3.0+/-0.6 to 4.4+/-1.0 l x min(-1)m(-2), mean +/- SD; P < 0.05), splanchnic blood flow (from 0.8+/-0.2 to 1.0 + 0.2 l x min(-1)m(-2); P < 0.05), femoral blood flow (from 0.2+/-0.1 to 0.3+/-0.1 l x min(-1)m(-2); P < 0.05), and the arterial-gastric mucosal Pco2 gap (from 11.4+/-9.5 to 11.9+/-8.0 mmHg; P < 0.05). Dobutamine increased systemic oxygen consumption (from 132+/-14 to 146+/-13 ml x min(-1) x m(-2); P < 0.05) but not splanchnic or femoral oxygen consumption. Splanchnic glucose production and lactate and amino acid balance did not change. CONCLUSION: After coronary artery bypass surgery, dobutamine increased systemic and regional blood flow and decreased systemic and regional oxygen extraction. Dobutamine did not affect splanchnic glucose production or lactate or amino acid balance. This suggests that dobutamine increases splanchnic blood flow without a concomitant increase in hepatosplanchnic metabolism.

Adrenergic beta-Agonists↗
PubMed1997

[Liver urea and glucose production in patients with alcohol-induced cirrhosis].

OBJECTIVE: To use stable isotopes for the analysis of hepatic metabolic pathways (urea synthesis, glucose production), comparing them in alcoholic and normal liver, in order to obtain specific and quantitative information on metabolic functions of the liver. PATIENTS AND METHODS: Urea and glucose production as well as alanine metabolism in the liver were studied by means of stable isotopes in 7 males with alcoholic liver cirrhosis (mean age 46 +/- 4 years; height 173 +/- 5 cm; weight 73 +/- 3 kg) and 7 healthy male volunteers as controls (age 26 +/- 3 years; height 180 +/- 5 cm; weight 75 +/- 6 kg). The plasma concentrations of adrenaline, noradrenaline, insulin, glucagon and amino-acids were also measured. RESULTS: Urea synthesis was lower in the cirrhosis patients than in the controls (3.3 +/- 2.2 mumol/kg.min vs 4.8 +/- 0.9 mumol/kg.min, P < 0.05). But there were no differences in glucose production, alanine metabolism and adrenaline concentrations. The concentrations of glutamine, phenylalanine, tyrosine, insulin, glucagon and noradrenaline were significantly raised in the cirrhotic patients, those of valine and leucine significantly lower. CONCLUSIONS: Contrary to hepatic glucose production, which was within normal limits, urea synthesis was reduced by 30% in the cirrhotic patients. The use of stable isotopes provided detailed information on specific metabolic processes in cirrhotic livers.

Adult↗
PubMed1997

Metabolic and calorigenic effects of dopexamine in healthy volunteers.

OBJECTIVE: To evaluate metabolic and calorigenic effects of dopexamine in healthy volunteers. DESIGN: Prospective, randomized trial. SETTING: Laboratory of the University Department of Anesthesiology. SUBJECTS: Eight volunteers. INTERVENTIONS: After a control period, dopexamine was administered using four infusion rates (0.75, 1.5, 3.0, and 6.0 microg/kg/min). MEASUREMENTS AND MAIN RESULTS: Blood pressure, heart rate, oxygen consumption (VO2), and the plasma concentration of potassium, glucose, lactate, and norepinephrine were measured. Typical hemodynamic responses were seen. VO2 increased from 122 +/- 11 (SD) to 150 +/- 9 mL/min/m2 during the highest dopexamine infusion rate. Plasma potassium concentration decreased only during the highest infusion rate. Plasma glucose concentration increased during infusion rates of 3 and 6 microg/kg/min of dopexamine, from 90 +/- 5 to 99 +/- 5 mg/dL (5.0 +/- 0.3 to 5.5 +/- 0.3 mmol/L), and from 87 +/- 7 to 103 +/- 11 mg/dL (4.8 +/- 0.4 to 5.7 +/- 0.6 mmol/L), respectively. Lactate did not increase during dopexamine infusion. Plasma norepinephrine concentration increased during all four infusion rates. CONCLUSION: It was not possible to differentiate the adrenergic receptor subtype responsible for the calorigenic and metabolic effects, since the putative beta2 adrenergic-receptor agonist, dopexamine, caused an increase in the plasma concentration of the beta1 adrenergic-receptor agonist, norepinephrine. Since beta2 adrenergic receptor-mediated effects such as hypokalemia were found only at infusion rates > or = 3 microg/kg/min, the effects of dopexamine at infusion rates < 3 microg/kg/min may be mainly mediated by stimulation of dopaminergic receptors and the indirect sympathomimetic action.

Adrenergic beta-Agonists↗
PubMed1996

[The effect of anesthetic method on enflurane air pollution in non-air conditioned operating rooms].

UNLABELLED: Pollution of work areas by volatile anaesthetics and nitrous oxide occurs during general anaesthesia. Short anaesthesia procedures are often carried out in operating theatres that are not equipped with air-conditioning systems. Methods of lowering exposure during short procedures, where mask anaesthesia is the usual procedure, are double masks and the laryngeal mask. The aim of our investigation was to determine the possibility of lowering the pollution of the environment to below national and international thresholds in a non-air-conditioned work area and to find out which method of anaesthesia is the most effective in environmental protection, i.e. which has the lowest leakage rate. METHODS: In our investigation, at two points of the work area the mean enflurane [2-chloro-1-(difluor-omethoxy)-1,1,2-trifluoro-ethane] concentrations were measured under daily routine conditions in a non-ventilated anaesthesiological work area by a gas chromatography. Anaesthesia with single masks, double masks, laryngeal masks or endotracheal intubation was carried out. RESULTS: No differences were found in the mean concentration of enflurane during the anaesthesia procedures. The leakage rates of endotracheal intubation anaesthesia were the lowest. DISCUSSION: In unventilated work areas, it was not possible to lower the exposure of the personnel by changing the method of anaesthesia. The application of procedures like double or laryngeal masks does not avoid the need for installation of air-conditioning systems in all work areas were anaesthesia is performed.

Air Conditioning↗
PubMed1996

Effects of epinephrine on glucose metabolism in patients with alcoholic cirrhosis.

The cirrhotic liver has been shown to be resistant to the actions of various glucoregulatory hormones. The objective of this study was to investigate the effects of epinephrine on hepatic glucose metabolism in cirrhotic patients. Thirteen cirrhotic and eight healthy subjects were studied. Hepatic glucose production and turnover of alanine and glycerol were measured using stable isotope technique before and during 70 and 150 minutes of epinephrine infusion (0.1 microgram/kg/min). beta-Adrenoreceptor binding sites and affinity in mononuclear leukocyte membranes also were determined. Hepatic glucose production and alanine turnover in normals significantly increased during epinephrine infusion, but did not change in cirrhotics. Glycerol turnover increased after 70 minutes of epinephrine infusion in both groups. Epinephrine induced a significant rise of high-affinity beta-adrenoreceptor binding sites in normals, yielding a significant correlation between hepatic glucose production and receptor density (r = .94, P < .0001). In cirrhotic patients, similar changes in the number of high-affinity beta-adrenoreceptors were observed, but no correlation with hepatic glucose production was detected. The cirrhotic liver did not respond normally to the stimulatory effect of epinephrine on hepatic glucose production. Because this blunted response was not related to changes of beta-adrenoreceptors, our findings suggest that epinephrine resistance in cirrhosis was caused by a postreceptor defect.

Adult↗
PubMed1996

[Is infection and septic shock caused by a global oxygen deficiency? An overview in 2 parts. 1: Infection and correlation between DO2 and VO2].

A global hypoxia resulting in an oxygen debt is assumed to be present in patients who suffer from the different stages and degrees of sepsis including septic shock and ARDS. As a consequence, the therapeutic concept of optimal values for cardiac output and oxygen delivery for these patients was proposed. This article reviews the literature with the objective of determining whether investigations dealing with oxygen delivery and consumption and with the plasma lactate concentration support the idea of the global hypoxia in septic patients. The finding of a pathologic oxygen supply dependency and an increase in plasma lactate concentration were taken as evidence for a global hypoxia. Between 1983 and 1991, oxygen supply dependency in septic patients was reported in an increasing number of publications. The increase in plasma lactate concentration was interpreted as lactic acidosis without presentation of plasma pH values and taken as evidence of global hypoxia and oxygen debt. From 1989 on, the number of publications that failed to show oxygen supply dependency even in the presence of an increased plasma lactate concentration increased. The problem in the method of determination of oxygen supply dependency became evident. Deducing both oxygen consumption and oxygen delivery from cardiac output from a common shared variable subject to measurement error may produce errors in the calculation of the regression between oxygen delivery and consumption. Oxygen supply dependency was not demonstrated in most investigations in which oxygen delivery and consumption were measured independently of each other. No decrease in mortality could be shown in prospective randomized studies for patients with sepsis and septic shock who were treated according to the concept of the optimal values. The lactate plasma concentration was below 5 mmol/l in most studies, which represents the borderline value for a clinically significant lactic acidosis. The term acidosis is not justified without a decrease in plasma pH or a decrease in the bicarbonate plasma concentration. An increased lactate plasma concentration can be merely the result of a hypermetabolism which is often found in septic patients. There is no proven evidence for global tissue hypoxia in septic patients from the investigations of oxygen delivery and consumption. This is also true for patients in septic shock after plasma volume expansion. The dogmatic proposal to increase cardiac output and oxygen delivery to certain levels cannot be sustained. However, regional hypoperfusion (e.g., of the splanchnic vascular bed) cannot be excluded. New approaches like gastric mucosal tonometry, measurement of splanchnic blood flow, and determination of regional metabolism are currently under investigation.

Acid-Base Equilibrium↗
PubMed1995

Are the effects of noradrenaline, adrenaline and dopamine infusions on VO2 and metabolism transient?

OBJECTIVE: To determine whether noradrenaline, adrenaline and dopamine have persistent actions on VO2 and metabolism. DESIGN: Descriptive laboratory investigation. SETTING: Laboratory of the Department of Anaesthesiology at a University Hospital. SUBJECTS: 9 volunteers. INTERVENTION: VO2 and the plasma concentration of glucose and free fatty acids were measured prior to and during a 4 h infusion of saline (control), noradrenaline (0.14 microgram/kg min) adrenaline (0.08 microgram/kg min) or dopamine (7 micrograms/kg min), n = 9 each. VO2 was measured using an open circuit gas exchange system. MEASUREMENTS AND MAIN RESULTS: VO2 increased from 250 +/- 22 ml/min to 280 +/- 38 ml/min during noradrenaline, to 298 +/- 30 ml/min during adrenaline and to 292 +/- 39 ml/min during dopamine infusion. The plasma glucose concentration increased from 6.2 +/- 0.6 mmol/l to 8.8 +/- 0.8 mmol/l, 13.2 +/- 1.4 and 7.3 +/- 0.4 mmol/l during infusion of noradrenaline, adrenaline or dopamine, respectively. The plasma free fatty acid concentration increased from 0.28 +/- 0.10 mmol/l to 0.79 +/- 0.21 mmol/l during noradrenaline and to 0.52 +/- 0.09 mmol/l during dopamine. In contrast, free fatty acid values averaged baseline values at the end of the adrenaline infusion after an initial increase to 0.72 +/- 0.31 mmol/l. CONCLUSIONS: Administration of noradrenaline, adrenaline or dopamine resulted in persistent increases in VO2 in volunteers. With the exception of the transient adrenaline effect on fatty acids the metabolic actions were steady during 4 h of adrenergic stimulation. Since the adrenergic effect on VO2 is persistent over time a similar action in patients (e.g. septic shock) during treatment with adrenoceptor agonists may be important. Thus, an increase in VO2 during therapy may not only reflect an oxygen debt but also a pharmacodynamic action of adrenoceptor mediated calorigenic and metabolic induction.

Adult↗
PubMed1995

Glycerol metabolism in patients with alcohol-induced liver cirrhosis.

The clearance rate of glycerol has been found to be impaired in alcoholic liver disease. However it remains unclear, if this can be ascribed to a defect of hepatic gluconeogenesis. Thus, the purpose of this work was to investigate glycerol clearance and hepatic glucose production in patients with liver cirrhosis. 13 patients with alcohol-induced Child B cirrhosis and 8 healthy volunteers were studied. Rates of appearance (R(a)) of glycerol, glucose and alanine were determined using stable isotope techniques. In addition indocyanine green clearance (ICGC) and plasma substrate concentrations were measured. Clearance rates were calculated as R(a) divided by the corresponding substrate concentration. R(a) of glycerol in patients was not different from controls, but glycerol clearance was significantly reduced (29 +/- 3 vs. 41 +/- 4 ml/kg/min). No differences in R(a) of glucose and alanine and corresponding plasma concentrations were observed. ICGC in patients was about 35% lower than reference values. Diminished glycerol clearance in patients with liver cirrhosis was not due to impaired hepatic gluconeogenesis. Since glycerol is almost completely extracted by the liver decreased glycerol clearance possibly simply reflected compromised liver perfusion as seen by reduced ICGC.

Journal Article↗
PubMed1994

Glucose and urea production and leucine, ketoisocaproate and alanine fluxes at supraphysiological plasma adrenaline concentrations in volunteers.

OBJECTIVE: To determine the magnitude and time course of adrenergic effects on metabolism in volunteers and possible implications for the use of sympathomimetics in the critically ill. DESIGN: Descriptive laboratory investigation. SUBJECTS: 7 volunteers. INTERVENTION: Primed continuous infusions of stable isotope tracers ([15N2]-urea, [6,6-D2]-glucose, [methyl-D3]-L-leucine, [15N]-L-alanine) were used. After isotopic steady state had been reached an infusion of adrenaline (0.1 microgram/kg/min) was administered (4 h). Isotopic enrichment was measured using gas chromatography-mass spectrometry and the corresponding rates of appearance were calculated. MEASUREMENTS AND MAIN RESULTS: Glucose production increased from 14.1 +/- 1.2 to 21.5 +/- 2.0 mumol/kg/min (p < 0.05) after 80 min of adrenergic stimulation and then decreased again to 17.9 +/- 1.2 mumol/kg/min after 240 min. Leucine and ketoisocaproate (KIC) fluxes were 2.3 +/- 0.2 and 2.6 +/- 0.2 mumol/kg/min, respectively, at baseline and gradually decreased to 1.8 +/- 0.2 and 2.2 +/- 0.1 mumol/kg/min, respectively, after 240 min of adrenaline infusion (both p < 0.05). Alanine flux increased from 3.7 +/- 0.5 to 6.9 +/- 0.9 mumol/kg/min (p < 0.05) after 80 min of adrenergic stimulation. Urea production slightly decreased from 4.8 +/- 0.9 to 4.3 +/- 0.8 mumol/kg/min during adrenaline (p < 0.05). CONCLUSIONS: Adrenaline induced an increase in glucose production lasting for longer than 240 min. The decrease in leucine and KIC flux suggests a reduction in proteolysis, which was supported by the decrease in urea production. The increase in alanine flux is therefore most likely due to an increase in de-novo synthesis. The ammonia donor for alanine synthesis in peripheral tissues and the target for ammonia after alanine deamination in the liver remain to be investigated. These results indicate that adrenaline infusion most probably will not promote already enhanced proteolysis in critically ill patients. Gluconeogenesis is an energy consuming process and an increase may deteriorate hepatic oxygen balance in patients.

Adult↗
PubMed1993

Metabolic and haemodynamic effects of dopamine plus domperidone in volunteers.

There are no studies of the relationship between infusion rate of dopamine and the arterial and venous dopamine plasma concentration and the resulting haemodynamic and metabolic effects. Dopamine was administered to seven volunteers using five infusion rates (1, 3, 6, 9, 13 micrograms/kg per minute) in an escalating sequence lasting for 30 min for each step. Since dopamine can cause nausea and vomiting, this relationship was investigated after administration of domperidone for infusion rates above 3 micrograms/kg per minute. Haemodynamic effects were assessed using 2-dimensional echocardiography. During the highest infusion rate the arterial plasma dopamine concentration reached 1,379 +/- 181 nmol/l. There was a linear correlation between the dopamine infusion rate and both the arterial and the venous plasma concentration. There was no significant change in heart rate or diastolic blood pressure. Systolic blood pressure, ejection fraction and cardiac index increased in a dose-dependent manner. Systemic vascular resistance decreased during the two low doses of dopamine and was not different from baseline values during the three high infusion rates. The plasma concentrations of glucose and non-esterified fatty acids increased from 5.3 +/- 0.4 to 0.68 +/- 0.9 nmol/l, and from 360 +/- 119 to 971 +/- 307 mumol/l, respectively, during the 13 micrograms/kg per minute infusion rate. As the plasma noradrenaline concentration increased up to 7.84 +/- 2.46 nmol/l in correlation to the dopamine plasma concentration, an indirect sympathomimetic effect may contribute to the actions of dopamine plasma concentration.

Adult↗
PubMed1993

Effects of norepinephrine, epinephrine, and dopamine infusions on oxygen consumption in volunteers.

OBJECTIVE: To determine the relationships between plasma concentrations of norepinephrine, epinephrine, and dopamine and oxygen consumption (VO2) during infusion of these catecholamines. DESIGN: Prospective, randomized variable dose, pharmacologic study in which a noncumulative infusion-rate design was used. SETTING: Laboratory of the Department of Anesthesiology at a University Hospital. PATIENTS: Twenty-one normal volunteers. INTERVENTIONS: After a control period of 20 mins, norepinephrine (three infusion rates; 0.06 to 0.2 microgram/kg/min; n = 7), epinephrine (four infusion rates; 0.02 to 0.2 microgram/kg/min; n = 7), or dopamine (three infusion rates; 3 to 12 micrograms/kg/min; n = 7) was administered to normal volunteers (n = 21) for the purpose of constructing plasma concentration/VO2 response curves. MEASUREMENTS AND MAIN RESULTS: Systolic and diastolic blood pressure, heart rate, plasma concentrations of norepinephrine, epinephrine, and dopamine, and VO2 were measured at the end of the control period and at the end of each catecholamine infusion. VO2 was measured using a ventilated canopy system and a differential oxygen sensor. Typical hemodynamic responses to vasopressors were seen during adrenergic receptor agonist infusions. VO2 increased from 132 +/- 7 to 153 +/- 10 mL/min/m2 during the highest infusion rate of norepinephrine, from 133 +/- 7 to 182 +/- 11 mL/min/m2 during the highest infusion rate of epinephrine, and from 132 +/- 13 to 163 +/- 8 mL/min/m2 during the highest infusion rate of dopamine (p < .05; paired t-test). Increases in VO2 were correlated with the logarithms of the corresponding plasma catecholamine concentrations. Effects on VO2 and hemodynamic responses occurred at similar plasma concentrations for each of the three catecholamines. CONCLUSIONS: Administration of norepinephrine, epinephrine, or dopamine results in marked increases in VO2 in volunteers. In patients, the administration of catecholamines or sympathomimetics to attain optimal values of cardiac index, oxygen delivery (DO2), and VO2 may increase the oxygen demand and thus obscure the DO2-VO2 relationship.

Blood Pressure↗
PubMed1993

Evidence for inverse regulation of high and low affinity binding sites for (-)125iodocyanopindolol in human mononuclear leucocytes during epinephrine infusion.

As we have shown earlier (-)125Iodocyanopindolol (125ICYP) binding to beta-adrenoceptors (beta-AR) in human mononuclear leucocytes (MNL) yields evidence for the existence of high affinity (Bhiaff) and low affinity (Bloaff) binding sites. We studied the regulation of these 2 classes of binding sites during 240 min of (-)-epinephrine (EPI) infusion (0.1 microgram/kg/min) (n = 8) in male healthy volunteers. Saturation experiments were performed on MNL membranes with 125ICYP over a large concentration range (1-550 pmol/l). Binding parameters were calculated by computer analysis assuming 2 classes of binding sites. We found a preinfusion value of 830 +/- 50 [sites/cell] (KD = 1.5 +/- 0.2 pmol/l) of Bhiaff binding sites and 5210 +/- 510 [sites/cell] (KD = 420 +/- 80 pmol/l) of Bloaff. During EPI infusion we observed biphasic modulation of the Bhiaff and an inverse modulation of the Bloaff. After 40 min of EPI Bhiaff increased to 1970 +/- 280 [sites/cell] (KD = 4.2 +/- 0.8 pmol/l), whereas Bloaff decreased to 2720 +/- 280 [sites/cell] (KD = 140 +/- 70 pmol/l); despite constant plasma epinephrine concentration (PEC) after 240 min of EPI Bhiaff changed to 1310 +/- 240 [sites/cell] (KD = 2.8 +/- 1.0 pmol/l) vs. 4370 +/- 760 [sites/cell] (KD = 190 +/- 100 pmol/l) Bloaff. These results suggest an interdependent inverse modulation of the 2 classes of binding sites for 125ICYP on MNL during EPI infusion.

Binding, Competitive↗
PubMed1992

Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers.

Noradrenaline and adrenaline were infused IV at 5 different rates (0.01-0.2 micrograms.kg.min-1) for 30 min to volunteers. The plasma catecholamine concentrations were determined by HPLC and electro-chemical detection. At the highest infusion rate, the arterial and venous plasma concentrations of noradrenaline increased from 1.18 to 44.1 nmol.l-1 and from 1.14 to 31.9 nmol.l-1, respectively, and of adrenaline from 0.29 to 23.9 nmol.l-1 and from 0.28 to 19.3 nmol.l-1, respectively. The peripheral venous plasma concentration of noradrenaline averaged 76% of the arterial concentration, and of adrenaline it was 73%. There was a linear relationship between the peripheral venous and arterial plasma noradrenaline and adrenaline concentrations at therapeutic doses.

Adult↗
PubMed1992

Stress hormone response during and after cardiopulmonary resuscitation.

The purpose of this study was to assess whether plasma adrenocorticotropin, cortisol, vasopressin, and renin concentrations are higher in resuscitated than in nonresuscitated patients during cardiopulmonary resuscitation, and whether there are possible correlations between these hormones and blood pressure or heart rate in the immediate postresuscitation phase. Of 34 consecutive patients (36-85 yr of age) with out-of-hospital cardiac arrest, 20 could be successfully resuscitated and admitted to hospital, whereas in the remaining 14 patients restoration of spontaneous circulation could not be achieved. During cardiopulmonary resuscitation, median adrenocorticotropin, cortisol, vasopressin, and renin concentrations in the external jugular vein were 237 pg/ml, 32.6 micrograms/dl, 122 pg/ml, and 46.5 ng/l, respectively, in resuscitated patients, and 45 pg/ml (P = 0.018), 18.4 micrograms/dl (P = 0.481), 88 pg/ml (P = 0.049), and 11 ng/l (P = 0.017), respectively, in nonresuscitated patients. Median adrenocorticotropin, cortisol, vasopressin, and renin concentrations were 101 pg/ml, 34.6 micrograms/dl, 22 pg/ml, and 25 ng/l, respectively, 60 min after successful resuscitation. No significant correlations were found between hormone levels and blood pressure or heart rate, but there was a significant negative correlation between the interval from collapse to the start of cardiopulmonary resuscitation and plasma cortisol concentrations during cardiopulmonary resuscitation (Spearman rank correlation coefficient = -0.967, P less than 0.001), indicating an impaired cortisol release from the adrenal cortex. The lower hormone concentrations of the nonresuscitated patients measured during cardiopulmonary resuscitation might indicate an impairment in neuroendocrine response.

Adrenocorticotropic Hormone↗