Opioids and opiates: analgesia with cardiovascular, haemodynamic and immune implications in critical illness

Abstract

Abstract. Molina PE (Louisiana State University Health Sciences Center, New Orleans, LA, USA). Opioids and opiates: analgesia with cardiovascular, haemodynamic and immune implications in critical illness (Review). J Intern Med 2006; 259: 138-154.Traumatic injury, surgical interventions and sepsis are amongst some of the clinical conditions that result in marked activation of neuroendocrine and opiate responses aimed at restoring haemodynamic and metabolic homeostasis. The central activation of the neuroendocrine and opiate systems, known collectively as the stress response, is elicited by diverse physical stressor conditions, including ischaemia, glucopenia and inflammation. The role of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system in counterregulation of haemodynamic and metabolic alterations has been studied extensively. However, that of the endogenous opiates/opioid system is still unclear. In addition to activation of the opiate receptor through the endogenous release of opioids, pharmacotherapy with opiate receptor agonists is frequently used for sedation and analgesia of injured, septic and critically ill patients. How this affects the haemodynamic, cardiovascular, metabolic and immune responses is poorly understood. The variety of opiate receptor types, their specificity and ubiquitous location both in the central nervous system and in the periphery adds additional complicating factors to the clear understanding of their contribution to the stress response to the various physical perturbations. This review aims at discussing scientific evidence gathered from preclinical studies on the role of endogenous opioids as well as those administered as pharmacological agents on the host cardiovascular, neuroendocrine, metabolic and immune response mechanisms critical for survival from injury in perspective with clinical observations that provide parallel assessment of relevant outcome measures. When possible, the clinical relevance and corresponding scenarios where this evidence can be integrated into our understanding of the clinical implications of opiate effects will be examined. Overall, the scientific basis to enhance clinical judgment and expectations when using opioid sedation and analgesia in the management of the injured, septic or postsurgical patient will be discussed.

Skin Conductance Reflects Drug-Induced Changes in Blood Levels of Cortisol, Adrenaline and Noradrenaline in Dogs

“…In healthy male humans, increasing doses of fentanyl induced a significant dose-dependent increase in plasma catecholamine levels [9]. This process is not yet clearly understood, but it is suggested that opioid-induced catecholamine release is mediated by a particular type of opioid receptor in the CNS [15]. In the present study, both SC and catecholamine levels increased in the fentanyl treatment group.…”

Hematologic changes in propofol-anesthetized dogs with or without tramadol administration

“…Opioids may suppress immune system cells, such as leukocytes and lymphocytes, via an indirect mechanism operating through the central nervous system (CNS) (Chang, 1984;Molina, 2006). This CNS influence occurs by regulating the systemic concentration of humoral substances such as cortisol and epinephrine (Straub et al, 1998).…”

Urinary Cortisol and Catecholamine Excretion after Burn Injury in Children

“…However, the impact of opioids and opiate use in the presence of persistent stressful stimuli has yet to be fully elucidated. Opiatemediated effects have been hypothesized to result from either direct interaction with opioid receptors on cells of the immune system (37,38) or indirectly through the activation of opioid receptors within the central nervous system and the resulting modulation of HPA axis and the sympathetic nervous system (39,40).…”