Alteration of the cardiac effects of isoproterenol and propranolol by hypothermia in isolated rat atrium

Melnikov, A. L.; Løkebø, Jan Eirik; Lathrop, David A.; Helgesen, Knut G.

doi:10.1016/0306-3623(95)02078-0

Cited by 8 publications

(4 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Early diastolic filling is improved even in spontaneous HR, even if the diastolic duration here is shortened due to the elevated HR. An inotropic stimulation of atrial contraction may have contributed to a better diastolic filling of the LV (Melnikov et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Function During Epinephrine Stimulation and Hypothermia: Effects at Spontaneous and Paced Heart Rates in a Porcine Model

Espinoza

Kerans

Bugge

et al. 2021

Therapeutic Hypothermia and Temperature Management

View full text Add to dashboard Cite

Postcardiac arrest patients treated with hypothermia, frequently require vasopressors and inotropic medication. The aim of this experimental study was to investigate the effect of epinephrine on left ventricular (LV) function during hypothermia. In an open-chest porcine model, seven animals were equipped with LV micromanometer and epicardial ultrasound transducers to provide LV pressure, Tau, and wall thickness and thickening velocities in systole (S¢) and early diastole (e¢). Arterial, central venous, and pulmonal artery pressures were recorded. Cardiac output (CO) was measured by transit-time flow probe on the ascending aorta. Hypothermia was induced using a cooling catheter through the femoral vein. Pacemaker leads were attached to the right atrium for pacing. LV volumes were obtained by two-dimensional echocardiography. Measurements were made at normothermia (38°C) and hypothermia (33°C), without and with epinephrine infusion (0.03 lg/kg/min), at spontaneous and paced heart rates (HRs) 120 and 140 beats/min. Hypothermia reduced LV stroke volume (SV). Epinephrine during hypothermia increased the SV with reduced end-systolic volumes. LV dP/dt max and wall-thickening velocity increased. During normothermia, epinephrine increased CO mainly due to accelerated HR, but during hypothermia, the increased CO resulted from augmented SV and, to a lesser degree, elevated HR. The incomplete relaxation and shortened diastolic filling time and the following reduction in SV seen in hypothermic animals, was repealed by epinephrine. The CO remained elevated also due to a shortened systolic duration, which gave time for complete relaxation during higher HRs. Epinephrine infusion improved systolic and diastolic function during hypothermia, and thereby reversed the effects induced by hypothermia considerably. Epinephrine augmented CO at hypothermia through increases in both SV and HR, in contrast to a mainly HRdependent effect during normothermia. Systolic duration was shortened, which gave sufficient diastolic duration for complete relaxation. This allowed diastolic filling and maintained CO at elevated HRs.

show abstract

Section: Discussionmentioning

confidence: 99%

Left Ventricular Function During Epinephrine Stimulation and Hypothermia: Effects at Spontaneous and Paced Heart Rates in a Porcine Model

Espinoza

Kerans

Bugge

et al. 2021

Therapeutic Hypothermia and Temperature Management

View full text Add to dashboard Cite

show abstract

“…No effect on CO [50, 51]. Negative or depressed inotropic effect (in vitro) [52, 53]. Positive inotropic effects (in vitro) [22, 24, 54].…”

Section: Methodsmentioning

confidence: 99%

“…This alteration in response to β-receptor stimulation also remained after rewarming as only the highest dose of isoprenaline managed to elevate SV above baseline [51]. In vitro studies have shown depressed β 1 -mediated inotropic effect of isoprenaline in rat left atrial preparations at 28 and 20 °C, compared to at 35 °C [52]. This finding finds support in another study reporting reduced inotropic response to both isoprenaline and adrenaline in hypothermic rabbit atria at 23 °C [53].…”

Section: Methodsmentioning

confidence: 99%

Altered pharmacological effects of adrenergic agonists during hypothermia

Dietrichs

Sager

Tveita

2016

Scand J Trauma Resusc Emerg Med

View full text Add to dashboard Cite

Rewarming from accidental hypothermia is often complicated by hypothermia-induced cardiac dysfunction, calling for immediate pharmacologic intervention. Studies show that although cardiac pharmacologic support is applied when rewarming these patients, a lack of updated treatment recommendations exist. Mainly due to lack of clinical and experimental data, neither of the international guidelines includes information about pharmacologic cardiac support at temperatures below 30 °C. However, core temperature of accidental hypothermia patients is often reduced below 30 °C. Few human studies exploring effects of adrenergic drugs during hypothermia have been published, and therefore prevailing information is collected from pre-clinical studies. The most prominent finding in these studies is an apparent depressive effect of adrenaline on cardiac function when used in doses which elevate cardiac output during normothermia. Also noradrenaline and isoprenaline largely lacked positive cardiac effects during hypothermia, while dopamine is a more promising drug for supporting cardiac function during rewarming. Data and information from these studies are in support of the prevailing notion; not to use adrenergic drugs at core temperatures below 30 °C.

show abstract

“…Y.). The 34°C temperature is considered normothermic for the heart, and temperature-related functional changes to adrenergic agents are seen with temperatures at 28°C [16]. The cells had either 2 ml L15 or L15 with drug solution added to the culture dishes.…”

Section: Methodsmentioning

confidence: 99%

Acute effects of adrenergic agents on post-defibrillation arrest time in a cultured heart model

Krauthamer

Smith

2004

CMLS, Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Possible drug interactions with electrical defibrillation were examined. We tested the hypothesis that adrenergic agents (epinephrine, norepinephrine, isoproterenol) and a calcium channel blocker (verapamil), when applied acutely, alter the duration of arrest following a defibrillator shock. A secondary hypothesis (based on observations) was that the drugs alter the occurrence of changes to normal rhythms following the shock. Dissociated heart cells from 10-day chicken embryos were cultured to form spherical aggregates and plated in petri dishes. In the experiments, the spheres were paced at 0.75 V/cm above contraction threshold, and a biphasic defibrillator shock was applied for 1 ms at 46 V/cm. The arrest time and occurrence of rhythm changes were recorded. The adrenergic agents shortened the duration of arrest following a defibrillator shock, while the calcium channel blocker lengthened the arrest time. Comparisons with the control proportion of double beats showed no significant change with the adrenergic agents and a decrease with verapamil.

show abstract

Alteration of the cardiac effects of isoproterenol and propranolol by hypothermia in isolated rat atrium

Cited by 8 publications

References 10 publications

Left Ventricular Function During Epinephrine Stimulation and Hypothermia: Effects at Spontaneous and Paced Heart Rates in a Porcine Model

Left Ventricular Function During Epinephrine Stimulation and Hypothermia: Effects at Spontaneous and Paced Heart Rates in a Porcine Model

Altered pharmacological effects of adrenergic agonists during hypothermia

Acute effects of adrenergic agents on post-defibrillation arrest time in a cultured heart model

Contact Info

Product

Resources

About