The Treatment of Shock With Beta Adrenergic Blockade

Berk, John L.; Hagen, Joan F.; G, Maly; Koo, R

doi:10.1001/archsurg.1972.04180010040011

Cited by 44 publications

(24 citation statements)

References 7 publications

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“…However, it was demonstrated that a nonselective as well as a ß 1 -selective ß-adrenergic blockade did not affect mean arterial blood pressure during systemic inflammation or following hemorrhagic shock in humans and animals [22][23][24][25]. Furthermore, coadministration of epinephrine that normally counteracts the cardiovascular suppression induced by propranolol augmented the effect of this drug on the survival and on cellular immune functions.…”

Section: Discussionmentioning

confidence: 99%

Adrenergic Modulation of Survival and Cellular Immune Functions during Polymicrobial Sepsis

Oberbeck

Schmitz

Wilsenack

et al. 2004

Neuroimmunomodulation

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Objective: An immunomodulatory effect of epinephrine has been reported that is supposed to be mediated via β-adrenergic receptors. The effect of epinephrine and/or β-adrenergic blockade on cellular immune functions during systemic inflammation has not yet been investigated. Methods: Male NMRI mice were treated with either an infusion of epinephrine (0.05 mg/kg/h i.p.), administration of the nonselective β-adrenoceptor antagonist propranolol (0.5 mg/kg s.c.), or a combination of epinephrine and propranolol after induction of a polymicrobial sepsis by cecal ligation and puncture. Forty-eight hours thereafter survival and cellular immune functions (splenocyte proliferation, splenocyte apoptosis and cytokine release, distribution of leukocyte subsets) were determined. Results: Infusion of epinephrine did not affect lethality of septic mice but induced alterations of splenocyte apoptosis, splenocyte proliferation and IL-2 release and was associated with profound changes of circulating immune cell subpopulations. Treatment with propranolol augmented the epinephrine-induced increase of splenocyte apoptosis, did not affect the decrease of splenocyte proliferation and IL-2 release, augmented the release of IL-6 and antagonized the mobilization of natural killer cells observed in epinephrine-treated animals. Furthermore, these immunologic alterations were accompanied by a significant increase of sepsis-induced mortality. Coadministration of propranolol and epinephrine augmented the propranolol-induced changes of splenocyte apoptosis and IL-6 release and was associated with the highest mortality of septic mice. Conclusion: Epinephrine infusion modulated cellular immune functions during systemic inflammation without an impact on survival. A pharmacologic β-adrenergic blockade partly augmented the epinephrine-induced immune alterations and was associated with a pronounced increase of mortality. This effect was further augmented by a combination of epinephrine infusion and β-adrenergic blockade. These data indicate that adrenergic mechanisms modulate cellular immune functions and survival during sepsis, with these effects being mediated via α- and β-adrenergic pathways.

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Section: Discussionmentioning

confidence: 99%

Adrenergic Modulation of Survival and Cellular Immune Functions during Polymicrobial Sepsis

Oberbeck

Schmitz

Wilsenack

et al. 2004

Neuroimmunomodulation

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“…A further study, which included patients with refractory septic shock, reported a 27.3% mortality rate in patients treated with propranolol; this was low compared to the 30–40% mortality rate reported in recent studies. It is important to note that the management of patients with septic shock in these early studies was significantly different to the modern medical care available today [61]. Despite the beneficial effects in patients with septic shock, β-adrenergic blockade therapy in septic shock is not widely established, as results are conflicting.…”

Section: Reviewmentioning

confidence: 99%

“…As the patient’s condition improves, the heart rate may return to baseline levels, before the onset of sepsis, without β-adrenergic blocker therapy. In the four clinical trials [61, 65–67] presented in Table 1, β-adrenergic blocker administration was adjusted to achieve a heart rate <95 bpm, and the heart rate was maintained between 80 and 95 bpm. Therefore, the optimum heart rate may be between 80 and 95 bpm.…”

Section: Reviewmentioning

confidence: 99%

Sepsis-induced cardiac dysfunction and β-adrenergic blockade therapy for sepsis

Suzuki

Okuda

et al. 2017

j intensive care

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Despite recent advances in medical care, mortality due to sepsis, defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, remains high. Fluid resuscitation and vasopressors are the first-line treatment for sepsis in order to optimize hemodynamic instability caused by vasodilation and increased vascular permeability. However, these therapies, aimed at maintaining blood pressure and blood flow to vital organs, could have deleterious cardiac effects, as cardiomyocyte damage occurs in the early stages of sepsis. Recent experimental and clinical studies have demonstrated that a number of factors contribute to sepsis-induced cardiac dysfunction and the degree of cardiac dysfunction is one of the major prognostic factors of sepsis. Therefore, strategies to prevent further cardiomyocyte damage could be of crucial importance in improving the outcome of sepsis.Among many factors causing sepsis-induced cardiac dysfunction, sympathetic nerve overstimulation, due to endogenous elevated catecholamine levels and exogenous catecholamine administration, is thought to play a major role. β-adrenergic blockade therapy is widely used for ischemic heart disease and chronic heart failure and in the prevention of cardiovascular events in high-risk perioperative patients undergoing major surgery. It has also been shown to restore cardiac function in experimental septic animal models. In a single-center randomized controlled trial, esmolol infusion in patients with septic shock with persistent tachycardia reduced the 28-day mortality. Furthermore, it is likely that β-adrenergic blockade therapy may result in further beneficial effects in patients with sepsis, such as the reduction of inflammatory cytokine production, suppression of hypermetabolic status, maintenance of glucose homeostasis, and improvement of coagulation disorders.Recent accumulating evidence suggests that β-adrenergic blockade could be an attractive therapy to improve the prognosis of sepsis. We await a large multicenter randomized clinical trial to confirm the beneficial effects of β-adrenergic blockade therapy in sepsis, of which mortality is still high.

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“…Three case series were found, two of them published in the early '70s by the group of Berk and colleagues who administered beta-blockers to patients with refractory septic shock of different etiologies 17,18 . In these two series the authors enrolled a total of 24 patients and the mortality rates were 15% and 27% respectively, considerably lower than the 50% mortality in their historic controls.…”

Section: Case Seriesmentioning

confidence: 99%