Biomedical subjects

H Ensinger

Publications and source records attributed to H Ensinger.

14 recordsLinked to original sources

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↗

PubMed1992

Plasma catecholamine concentrations after successful resuscitation in patients.

OBJECTIVES: To measure plasma catecholamine concentrations after cardiopulmonary resuscitation (CPR) and to correlate catecholamine concentrations with heart rate (HR), BP, and plasma glucose and lactate concentrations. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a University Hospital. PATIENTS: Ten patients (58 to 85 yrs) with out-of-hospital cardiac arrest. INTERVENTIONS: At 1, 5, 15, 30, and 60 mins after restoration of spontaneous circulation, blood samples were drawn and BP and HR were measured. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography and plasma glucose and lactate concentrations were measured by enzymatic methods. MAIN RESULTS: Median plasma epinephrine and norepinephrine concentrations were 136.3 micrograms/L (136,300 pg/mL), range 27.6 to 397.6 micrograms/L (27,600 to 397,600 pg/mL), and 4.7 micrograms/L (4700 pg/mL), range 1.8 to 14.5 micrograms/L (1800 to 14,500 pg/mL), respectively, at 1 min. Median plasma epinephrine and norepinephrine concentrations decreased to 8.7 micrograms/L (8700 pg/mL), range 1.2 to 55.0 micrograms/L (1200 to 55,000 pg/mL) and 1.9 micrograms/L (1900 pg/mL), range 1.3 to 5.8 micrograms/L (1300 to 5800 pg/mL), respectively, at 60 mins after restoration of spontaneous circulation. Epinephrine concentrations decayed with a semilogarithmic decay pattern. The half-life for the alpha phase was 2.2 mins and was 38.7 mins for the beta phase. Mean values of systolic arterial pressure were between 136 +/- 23 mm Hg at 1 min and 120 +/- 15 mm Hg at 30 mins. Median plasma glucose concentrations were between 8.2 mmol/L (147.7 mg/dL; range 5.8 to 11.2 mmol/L [104.5 to 201.8 mg/dL]) at 1 min and 13.9 mmol/L (250.4 mg/dL; range 9.7 to 16.6 mmol/L [174.8 to 299.1 mg/dL]) at 30 mins. Lactate values were between 11.4 mmol/L (range 4.7 to 16.5) at 1 min and 5.2 mmol/L (range 2.7 to 12.5) at 60 mins. No significant correlations were found between circulating catecholamine concentrations and the other variables. CONCLUSIONS: After CPR, plasma catecholamine concentrations remained at high values but they did not lead to increases in BP, HR, or circulating glucose concentrations.

Aged↗

PubMed1992

Effects of diltiazem on oxygen delivery and consumption after asphyxial cardiac arrest and resuscitation.

BACKGROUND AND METHODS: Calcium-channel blockers may attenuate vasospasm after transient ischemia and improve organ blood flow after resuscitation. Our aim was to assess the effect of diltiazem on systemic oxygen delivery and consumption, hemodynamics, electroencephalogram (EEG), and organ blood flow after restoration of spontaneous circulation. After a 3-min period of asphyxial cardiac arrest, 14 pigs (20 to 27 kg) were randomly allocated to treatment with either diltiazem (0.1 mg/kg bolus followed by an iv infusion of 0.025 mg/min/kg over 120 mins) or placebo, given at 5 mins after successful resuscitation. Organ blood flow was measured using tracer microspheres 120 mins after resumption of spontaneous circulation. RESULTS: Median systemic oxygen delivery index values at 30, 60, and 120 mins after restoration of spontaneous circulation were 18.2 mL/min/kg (range 14.8 to 20.7), 16.8 mL/min/kg (13.2 to 20.8), and 19.6 mL/min/kg (16.9 to 21.0), respectively, in the diltiazem group and 13.1 mL/min/kg (11.2 to 14.6), 11.9 mL/min/kg (10.3 to 13.3), and 14.7 mL/min/kg (11.4 to 17.2), respectively, in the control group (p less than .05 for all three comparisons). At the same points in time, median systemic oxygen consumption indices were 3.2 mL/min/kg (range 2.2 to 3.7), 2.1 mL/min/kg (1.9 to 3.0), and 2.6 mL/min/kg (1.8 to 3.8) in the diltiazem group and 2.8 mL/min/kg (2.1 to 4.0), 2.7 mL/min/kg (1.7 to 4.3), and 2.3 mL/min/kg (1.6 to 3.8) in the placebo group (NS). Diltiazem enhanced the postarrest recovery of EEG total power. Right and left cerebral blood flow 120 mins after restoration of spontaneous circulation was significantly (p less than .01) higher in the diltiazem group in comparison with the control group. CONCLUSIONS: Diltiazem causes an increase in systemic oxygen delivery index by promoting vasodilation, but it does not change systemic oxygen consumption index in comparison to placebo treatment. It may be that an impairment in local autoregulation and/or in oxidative metabolism at the cellular or subcellular level was the reason why diltiazem did not improve these derangements. The observed increase in cerebral blood flow and in EEG recovery may be beneficial to the brain after a period of asphyxia.

Acid-Base Equilibrium↗

PubMed1992

Hemodynamic and metabolic effects of epinephrine during cardiopulmonary resuscitation in a pig model.

BACKGROUND AND METHODS: This study was designed to assess the effect of epinephrine during cardiopulmonary resuscitation (CPR) on left ventricular myocardial blood flow, systemic oxygen delivery and consumption, and on plasma glucose and lactate concentrations. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45 micrograms/kg epinephrine (n = 7) after 5 mins of ventricular fibrillation, and 3 mins of open-chest CPR. Left ventricular myocardial blood flow was measured with radiolabeled microspheres. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography. RESULTS: During open-chest CPR, mean (+/- SD) values of left ventricular myocardial blood flow before, 90 secs, and 5 mins following drug administration were 49 +/- 10, 46 +/- 12, 43 +/- 15 mL/min/100 g, respectively, in the control group, and 52 +/- 12, 118 +/- 21, 84 +/- 28 mL/min/100 g, respectively, in the epinephrine group (p less than .05 at 90 secs and 5 mins). At the same time points, mean (+/- SD) oxygen delivery indices were 7.7 +/- 3.0, 6.0 +/- 2.1, 6.5 +/- 2.7 mL/min/kg in the control group and 7.6 +/- 2.5, 5.3 +/- 2.1, 5.5 +/- 1.9 mL/min/kg in the epinephrine group (nonsignificant). Mean oxygen consumption indices were 5.8 +/- 2.4, 4.6 +/- 1.6, 5.2 +/- 2.6 mL/min/kg in the control group and 5.4 +/- 1.6, 4.2 +/- 1.6, 4.4 +/- 1.4 mL/min/kg in the epinephrine group (nonsignificant). During CPR and before epinephrine administration, arterial plasma epinephrine concentrations increased from prearrest values of 0.77 +/- 0.70 to 62.1 +/- 48.7 micrograms/L, and plasma norepinephrine concentrations increased from 0.28 +/- 0.32 to 104.3 +/- 57.1 micrograms/L. After administered epinephrine, there was an additional increase to 271 +/- 83 micrograms/L at 90 secs in arterial plasma epinephrine, but no important alteration in the plasma norepinephrine concentration. At no time point could we find a clinically important difference in plasma glucose or lactate concentrations between the two groups. CONCLUSIONS: At a dose of 45 micrograms/kg, epinephrine caused an increase in left ventricular myocardial blood flow after a total of 8 mins of cardiac arrest, including 3 mins of CPR, while not altering systemic oxygen delivery and consumption, plasma glucose, or lactate concentrations.

Animals↗

PubMed1992

Relationship between infusion rates, plasma concentrations, and cardiovascular and metabolic effects during the infusion of norepinephrine in healthy volunteers.

OBJECTIVE: To determine the relationship between iv infusion rate, plasma concentrations, and hemodynamic and metabolic actions of norepinephrine. DESIGN: Norepinephrine was administered by using five iv infusion rates (0.01 to 0.2 micrograms/kg/min) for 30 mins each to eight volunteers, for the purpose of constructing cumulative plasma concentration-response curves. SETTING: Laboratory of the Department of Anesthesiology at a university hospital. MEASUREMENTS AND MAIN RESULTS: Systolic and diastolic BP, heart rate, and the plasma concentrations of norepinephrine, glucose, nonesterified fatty acids, and insulin were measured at the end of each infusion rate. During the highest infusion rate, plasma norepinephrine concentrations increased from 199 +/- 75 to 7475 +/- 1071 pg/mL (1.18 +/- 0.44 to 44.18 +/- 6.33 nmol/L). Typical hemodynamic responses, such as increases in BP and decreases in heart rate, were seen, while the plasma concentrations of glucose and nonesterified fatty acids increased from 92 +/- 10 to 132 +/- 17 mg/dL (5.1 +/- 0.6 to 7.3 +/- 0.9 mmol/L) and 11 +/- 4 to 34 +/- 6 mg/dL (0.11 +/- 0.04 to 0.34 +/- 0.06 g/L), respectively, during the 0.2 micrograms/kg/min infusion rate (p less than .05). Despite the increase in glucose concentration, insulin remained at baseline values. Metabolic and hemodynamic effects occurred at similar plasma concentrations throughout the study. CONCLUSIONS: Administration of norepinephrine showed no selective hemodynamic actions. The metabolic responses observed in this investigation were similar to those responses seen during increased endogenous sympathetic nervous system activity, such as stress, exercise, or trauma.

Adult↗

PubMed1992

Adrenaline: relationship between infusion rate, plasma concentration, metabolic and haemodynamic effects in volunteers.

The present study investigated the relationship between supraphysiological plasma concentrations of adrenaline and the resulting haemodynamic and metabolic effects. Adrenaline was administered at five infusion rates (0.01-0.2 micrograms kg-1 min-1) in an escalating sequence to eight volunteers. The arterial plasma concentration of adrenaline increased from 53 +/- 44 to 4349 +/- 818 ng litre-1 during the highest infusion rate. Typical haemodynamic responses, such as increase in blood pressure and heart rate, were seen. The plasma concentrations of glucose and lactate increased from 5.2 +/- 0.4 to 13.7 +/- 1.3 mmol litre-1 and from 0.9 +/- 0.3 to 4.7 +/- 2.6 mmol litre-1, respectively, during the highest infusion rate without a significant increase in insulin concentration. Non-esterified fatty acids increased from 379 +/- 97 to 1114 +/- 331 mumol litre-1 during the 0.06 microgram kg-1 min-1 infusion rate. Adrenaline had no selective haemodynamic effect. If similar metabolic effects occur in patients during treatment with adrenaline or other sympathomimetics, they may further increase breakdown of energy stores in a situation of increased catabolism, and impair utilization of parenteral nutrition.

Adult↗

PubMed1990

The role of alpha 1-adrenoceptors in adrenaline-induced hyperkalaemia.

The hyperkalaemic action of adrenaline was investigated in 44 anaesthetized domestic pigs. Plasma and epicardial concentrations of K+ were measured, in the latter case with an ion-selective electrode. Adrenaline 10 micrograms kg-1 caused a rapid increase in the plasma concentration of K+ from 4.2 to 5.9 mmol litre-1. The magnitude and the time course of epicardial concentration of K+ were similar. Alpha-adrenoceptor block with either phentolamine 5 mg kg-1 (non-selective block) or prazosin 0.1 mg kg-1 (selective alpha 1-adrenoceptor block) abolished the hyperkalaemic effect of adrenaline in the plasma and on the epicardium. The alpha 1-adrenoceptor agonist phenylephrine increased the K+ concentration, but the alpha 2-adrenoceptor agonist UK 14.304 did not cause any change in concentration. These results suggest that the hyperkalaemia induced by adrenaline occurs in the interstitial fluid of the myocardium and is mediated by alpha 1-adrenoceptors. These findings may be important in patients at risk of hyperkalaemia, with implications, for example, in the use of suxamethonium during induction of anaesthesia.

Adrenergic alpha-Agonists↗

PubMed1990

[The modification of the potassium concentration in blood by catecholamines. A literature review].

After intravenous administration of epinephrine, serum potassium level shows a typically biphasic course. The initial rise is followed by a persistent fall to a lower level than the starting-concentration. The initially observed hyperkalemia is supposed to be caused by a potassium release from hepatocytes, mediated by an alpha 1-adrenoreceptor stimulation. The subsequent hypokalemia seems to be caused by the beta 2-mimetic component of epinephrine effecting the uptake of this ion into striated muscle cells. There are numerous clinical reports of marked hypokalemia as a consequence of beta 2-mimetic therapy. The additive effect of elevated endogenous catecholamines with the therapeutically applied epinephrine during cardiopulmonary resuscitation may be the cause of the elevated potassium levels often observed under these conditions. On the other hand, low serum potassium levels were measured in patients after successful resuscitation, as well as in patients with multiple trauma and with severe head injury. Moreover, hypokalemia seems to be a frequent event in the acute phase of myocardial infarction. A catecholamine-induced potassium shift into the cell is considered to be the cause of this decrease. The question whether in the case of myocardial infarction the hypokalemia is in itself arrhythmogenic as yet is not resolved. Because of the present knowledge about the influence of catecholamines on potassium metabolism it seems advisable to monitor potassium levels regularly during the above situations.

Epinephrine↗

PubMed1986

Opioid peptides decrease noradrenaline release and blood pressure in the rabbit at peripheral receptors.

Effects of dynorphin-(1-13), Leu5-enkephalin, D-Ala2,D-Leu5-enkephalin (DADLE), and for comparison bremazocine, on plasma noradrenaline concentration and mean arterial pressure (MAP) were studied in pithed rabbits. In the first series of experiments, the sympathetic outflow was stimulated electrically via the pithing rod at 2 Hz twice for 3 min each (S1, S2). Drugs were administered before S2. Bremazocine 10 micrograms/kg + 2 micrograms/kg/h and 100 micrograms/kg + 20 micrograms/kg/h, dynorphin 1 and 3 micrograms/kg/min, Leu5-enkephalin 100 micrograms/kg/min and DADLE 10 and 30 micrograms/kg/min all diminished the electrically-evoked increase in plasma noradrenaline and MAP. The effects were antagonized by naloxone. In the second series, an infusion of noradrenaline (2 micrograms/kg/min) was given twice for 3 min each (N1, N2). Drugs were administered before N2. Bremazocine 100 micrograms/kg + 20 micrograms/kg/h slightly enhanced the pressor effect of exogenous noradrenaline, whereas dynorphin 3 micrograms/kg/min, Leu5-enkephalin 100 micrograms/kg/min and DADLE 30 micrograms/kg/min caused no significant change. In the third series, the sympathetic outflow was stimulated continuously at 2 Hz, and the interaction of dynorphin and DADLE was studied. Dynorphin 1 microgram/kg/min and DADLE 10 micrograms/kg/min initially decreased MAP to a similar extent. The effect of DADLE faded with time. When, during continuous infusion of DADLE 10 micrograms/kg/min, and after return of MAP to the pre-DADLE level, dynorphin 1 microgram/kg/min or DADLE 10 micrograms/kg/min was infused additionally, the effect of dynorphin was unchanged, whereas that of DADLE was almost abolished. We conclude that the opioid peptides as well as bremazocine decrease action potential-evoked release of noradrenaline and, secondarily, blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Neuronal and postjunctional components in the blood pressure effects of dopamine and bromocriptine in rabbits.

We have studied the contribution of neuronal and postjunctional dopamine (DA) receptors and of the DA1 and DA2 receptor subtypes to the blood pressure effects of DA and bromocriptine in the rabbit. The norepinephrine release rate, i.e., the rate of entry of endogenous norepinephrine into the plasma, was derived from the plasma level of endogenous norepinephrine and the plasma [3H]norepinephrine clearance. Bromocriptine (40 micrograms kg-1) lowered the norepinephrine release rate and the arterial blood pressure both in anesthetized rabbits and in pithed rabbits with electrically stimulated sympathetic outflow. These effects were antagonized by the selective DA2 antagonist domperidone but not by the selective DA1 antagonist SCH 23390. DA (10-160 micrograms kg-1 min-1) dose-dependently increased the norepinephrine release rate and caused only transient hypotension in anesthetized rabbits. However, after treatment with desipramine, DA did not change the norepinephrine release rate and produced a persistent fall in blood pressure. When DA and domperidone were given simultaneously to desipramine-treated rabbits, the hypotensive effect of DA was unchanged, but now DA increased the norepinephrine release rate. When DA and SCH 23390 were given simultaneously to desipramine-treated rabbits, DA failed to lower blood pressure and decreased the norepinephrine release rate. Propranolol did not change the effects of DA in desipramine-treated rabbits. These results suggest that bromocriptine decreases blood pressure by activating ganglionic and/or prejunctional, inhibitory DA2 receptors in the peripheral sympathetic nervous system. DA also activates these receptors, but in addition releases norepinephrine in the manner of an indirectly acting sympathomimetic amine and activates postjunctional vascular DA1 receptors, and the latter seems to be the main component in DA-induced hypotension.

Anesthesia↗

PubMed1984

Ethylketocyclazocine decreases noradrenaline release and blood pressure in the rabbit at a peripheral opioid receptor.

Rabbits were pithed and their sympathetic outflow was stimulated electrically via the pithing rod. Arterial blood pressure, heart rate, the endogenous plasma noradrenaline level, the plasma 3H-noradrenaline clearance and the noradrenaline release rate (the rate of entry of endogenous noradrenaline into the plasma) were determined. Ethylketocyclazocine 0.1 mg kg-1 + 0.02 mg kg-1 h-1 and 1 mg kg-1 + 0.2 mg kg-1 h-1 but not 0.01 mg kg-1 + 0.002 mg kg-1 h-1 decreased blood pressure, the endogenous plasma noradrenaline level and the noradrenaline release rate. The effects of ethylketocyclazocine 1 mg kg-1 + 0.2 mg kg-1 h-1 were antagonized by naloxone 1 mg kg-1 + 0.5 mg kg-1 h-1. Given alone, naloxone caused no change. It is concluded that ethylketocyclazocine inhibits action potential-evoked release of noradrenaline from postganglionic sympathetic neurones, and hence can lower blood pressure, by a peripheral effect, possibly mediated by opioid receptors at the terminal axons.

Animals↗

PubMed1980

[Percutaneous catheter dilatation of carotid stenoses --animal experiments (author's transl)].

Thirty-one carotid artery stenoses were produced in thirty dogs by three different techniques. Twenty-three of these could be cured by transfemoral percutaneous catheter dilatation. High grade tight stenoses may present resistance which cannot be overcome by the catheter. Histological examination of the dilated vessels showed circumscribed changes in the vessel wall, with destruction of elastic membranes. From our experience of catheter dilatation of pelvic and lower limb arteries and of renal arteries, we consider it feasible to use this technique in selected patients with carotid stenosis.

Angiography↗

PubMedDate not supplied

Bremazocine causes sympatho-inhibition and hypotension in rabbits by activating peripheral kappa-receptors.

We have studied the effects of bremazocine on the peripheral sympathetic nervous system and the arterial blood pressure of pithed rabbits with electrically (2 Hz) stimulated sympathetic outflow, and compared them with the effects of Leu-enkephalin and fentanyl. The 3H-noradrenaline plasma clearance and the plasma concentration of noradrenaline were used to calculate the rate of spillover of endogenous noradrenaline into the plasma; the spillover rate reflects the overall release of noradrenaline from postganglionic sympathetic neurones. Bremazocine (10 and 100 micrograms kg-1, followed by an infusion of 2 and 20 micrograms kg-1 h-1, respectively, i.v.) persistently decreased the noradrenaline spillover rate as well as blood pressure. Both effects were antagonized by naloxone. Leu-enkephalin (70 and 350 micrograms kg-1 min-1 i.v.) caused only transient hypotension. Fentanyl decreased blood pressure only at a very high dose (250 micrograms kg-1, followed by an infusion of 500 micrograms kg-1 h-1 i.v.). The effects of Leu-enkephalin and fentanyl were also antagonized by naloxone. When the blood pressure of pithed rabbits was raised by an intravenous infusion of noradrenaline, rather than by electrical stimulation, bremazocine, Leu-enkephalin, and fentanyl failed to produce hypotension. The results indicate that bremazocine inhibits the release of noradrenaline and, in consequence, lowers arterial pressure by activation of peripheral, probably prejunctional, opioid receptors. The receptors appear to be of the kappa-type.

Analgesics↗