Effects of catecholamines on oxygen consumption and oxygen delivery in critically ill patients (original) (raw)
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Effects of catecholamines on regional perfusion and oxygenation in critically ill patients
Acta Anaesthesiologica Scandinavica, 1995
Multiple organ failure is the major cause of death in patients with sepsis. Bacterial translocation from the gut is considered to induce and maintain sepsis. Therefore, the splanchnic region plays an important role in the pathogenesis and treatment of sepsis. There is evidence for a very high risk of imbalance between oxygen delivery and oxygen consumption especially in the splanchnic region. Consequently, there is a crucial interest whether it is possible to influence the splanchnic perfusion by specific catecholamines. Unfortunately, only a few, conflicting studies have looked at the effects of the various catecholamines on regional blood flow. Therefore, a clear recommendation for a specific catecholamine regimen in septic shock is impossible. Furthermore, it is unknown whether the choice of a specific catecholamine in the treatment of septic shock affects the patient's outcome. In most patients, the use of vasopressors is indispensable because adequate haemodynamic perfusion pressure is not achieved with fluid therapy alone. The negative effects of vasopressors on splanchnic perfusion are known from studies carried out under non septic conditions. Norepinephrine and dopamine in doses of 10 micrograms/kg/min in septic animals are without negative effects on splanchnic perfusion. Preliminary results show Preliminary results show a decrease in splanchnic oxygenation in patients with septic shock treated with epinephrine. Catecholamines with beta mimetic effects are often used to increase DO2. The question as to whether dobutamine or dopamine should be used first in treatment of septic shock cannot be answered yet. Whether treatment with low dose dopamine or dopexamine actually improves renal function and splanchnic oxygenation is the purpose of ongoing studies.
Journal of pharmacological methods, 1991
Restrained conscious rats have been widely used for physiological and pharmacological hemodynamic studies. In this condition, the variability of the circulation is unclear. Repeated measurements in restrained normal rats showed stable systemic hemodynamics (cardiac output ranging from 130 +/- 14 to 174 +/- 10 mL/min, mean arterial pressure ranging from 109 +/- 9 to 117 +/- 5 mmHg) and splanchnic hemodynamics (splanchnic blood flow ranging from 8.51 +/- 1.89 to 13.01 +/- 1.45 mL min-1 100 g-1 body wt) over a period of 1 hr. Slight but not significant hemodynamic variations, however, occurred in pulmonary blood flow. Similarly, plasma noradrenaline concentrations did not vary over this period (plasma noradrenaline level ranging from 186 +/- 36 to 358 +/- 64 pg/mL). These plasma noradrenaline concentrations were similar to those measured in a group of conscious unrestrained rats 3 hr after recovery from surgery (292 +/- 60 pg/mL). A significant correlation was observed between plasma n...
Catecholamines and Vasopressin During Critical Illness
Critical Care Clinics, 2006
Life-threatening disease is a severe stress that induces a set of neuroendocrine responses, including the activation of the sympathetic nervous system and secretion of epinephrine from the adrenal medulla [1]. This response has an impact on blood pressure, vital organ perfusion, and supply of metabolic substrates, all of which affect survival . Although most plasma norepinephrine is derived from synaptic nerve clefts, circulating epinephrine is produced largely in the adrenal gland. Unlike norepinephrine, which is a neurotransmitter of the sympathetic nervous system, epinephrine functions as a circulating hormone . Interestingly, the enteric nervous system, which contains more than 100 million neurons, is capable of releasing a previously unrecognized proportion of total sympathetic outflow . Mesenteric organs were shown to produce considerable amounts of norepinephrine [4] and dopamine , which accounts for 37% and N 50%, respectively, of the total amount of these catecholamines formed in the body. Given this capability of the gut, the interaction of enteric bacteria and toxins 0749-0704/06/$ -see front matter D
Australian Journal of Experimental Biology and Medical Science, 1972
Infusions of the catecholaniines noradrenaline, adrenaline and isoprenaline in anaesthetized rats under artificial ventilation caused a fall in arterial blood pH and a slight ri.se in P^.Q. The order of potency of the catecholaniines in producing metabolic acidosis was isoprenaline > adrenaline > noradrenaline. Thi.s effect of isoprenaline was abolished by propranolol but was not changed by phenoxybcnzaniine. The effect of noradrenaline was abolished by phenoxybenzaniine and was potentiated Iiy propranolol. The decrease in cardiovascular respon.ses to catecholaniines that follows an infusion may be partly due to the resultant acidosis. since acidosis produced by infusions of hydrochloric acid resulted in decreases of the responses of the heart and blood pressure to noradrenaline and isoprenaline. The decreased cardiovascular respoases caused by catecholamine infusions were partly restored when the blood pH was returned to normal levels by administration of Tris buffer.
Effects of injected sympathomimetic amines on plasma catecholamines and circulatory variables in man
Life Sciences - LIFE SCI, 1983
We measured blood pressure, heart rate (HR), and plasma catecholamine responses to a 5-minute infusion of 0.3 mg/kg d-amphetamine (d-A) and to graded bolus injections of tyramine (Tyr) to a similar increment in systolic pressure (BPs), in 9 and 7 healthy people, respectively. Both sympathomimetic agents dramatically increased BPs (mean increases peaking at 39 and 36 mm Hg for d-A and Tyr), associated with increased plasma norepinephrine (NE) (224 and 149 pg/ml) but unassociated with changes in plasma epinephrine or HR. The time course of BPs and NE responses to Tyr was much shorter than to d-A, but the pattern was similar. The results are consistent with the hypotheses that both agents increase BPs via increased synaptic cleft NE, and that circulating plasma NE reflects "spillover" from the cleft into the general circulation. D-amphetamine and tyramine increase blood pressure in man apparently due to an indirect sympathomimetic effect; that is, they do not directly stimulate post-synaptic noradrenergic receptors so much as induce norepinephrine release by displacing NE from storage vesicles (i). In animals, dependence of the pressor responses to d-A and Tyr on NE release has been demonstrated by abolition of the response after pre-treatment with reserpine and by closely parallel pressure and plasma catecholamine responses to d-A and Tyr which are attenuated similarly by guanethidine (2). In man, the strongest evidence for such an indirect mode of action would be the lack of a pressor response to d-A or Tyr in patients with peripheral sympathetic neuronal failure, and this has been reported in a few cases (3-5). Most patients with idiopathic orthostatic hypotension, however, show intact pressor responses to Tyr, possibly because denervation hypersensitivity occurs concomitantly with decreased NE release (6). Depletion of catecholamines by reserpine attenuates the pressor response to Tyr in man (7).
Metabolism, 1997
This study was undertaken to determine the impact of portal adrenergic blockade on the gluconeogenic effects of epinephrine (EPI) and norepinephrine (NE). Experiments were performed on 18-hour fasted conscious dogs and consisted of a 100-minute equilibration, a 40-minute basal, and two 90-minute test periods. A pancreatic clamp was used to fix insulin and glucagon levels at basal values. Propranolol (1 Ixg/kg • min) and phentolamine (2 I~g/kg • min) were infused intraportally during both test periods. Portal infusion of ~-and ~-adrenergic blockers alone (first test period) slightly increased hepatic glucose production from 2.4-+ 0.4 to 2,8-+ 0.5 mg/kg • min (nonsignificant [NS]) NE (500 ng/kg • min) and EPI (180 ng/kg • min) were infused peripherally during the second test period. Arterial NE and EPI increased from 186-+ 63 to 6,725-+ 913 pg/mL and 76 _+ 25 to 2,674 +-344 pg/mL, respectively. Portal NE and EPI increased from 135 _+ 32 to 4,082-+ 747 pg/mL and 28-+ 8 to 1,114 _+ 174 pg/mL, respectively, Hepatic glucose production, the maximal gluconeogenic rate, and gluconeogenic efficiency increased from 2.8-+ 0.5 to 3.8-+ 0.4 mg/kg • min (P < .05), 0.7-+ 0.3 to 2.1-+ 0.6 mg/kg • min (P < .05}, and 21% _+ 8% to 60% _+ 13% (P < .05), respectively, in response to catecholamine infusion. Net hepatic lactate balance changed from output (1.5-. 3.3 Fmol/kg • min) to uptake (-11.0-4-3.8 i~mol/kg • min, P < .05}. Net hepatic glycerol uptake increased from-1.5-+ 0.7 to-5.5-+ 2.0 i~mol/kg • min (P < .05). Net hepatic uptake of gluconeogenic amino acids did not change significantly. Similarly, hepatic glycogenolysis did not increase during catecholamine infusion. In conclusion, portal delivery of adrenergic blockers selectively inhibits the glycogenolytic effects of EPI and NE on the liver, but allows a marked gluconeogenic response to the catecholamines.