Cardiovascular Effects Of Epinephrine Research Articles

Cardiovascular Effects of Epinephrine During Experimental Hypothermia (32°C) With Spontaneous Circulation in an Intact Porcine Model

Aims: Rewarming from accidental hypothermia and therapeutic temperature management could be complicated by cardiac dysfunction. Although pharmacologic support is often applied when rewarming these patients, updated treatment recommendations are lacking. There is an underlying deficiency of clinical and experimental data to support such interventions and this prevents the development of clinical guidelines. Accordingly, we explored the clinical effects of epinephrine during hypothermic conditions.Materials and methods: Anesthetized pigs were immersion cooled to 32°C. Predetermined variables were compared at temperature/time-point baseline, after receiving 30 ng/kg/min and 90 ng/kg/min epinephrine infusions: (1) before and during hypothermia at 32°C, and after rewarming to 38°C (n = 7) and (2) a time-matched (5 h) normothermic control group (n = 5).Results: At 32°C, both stroke volume and cardiac output were elevated after 30 ng/kg/min administration, while systemic vascular resistance was reduced after 90 ng/kg/min. Epinephrine infusion did not alter blood flow in observed organs, except small intestine flow, and global O2 extraction rate was significantly reduced in response to 90 ng/kg/min infusion. Electrocardiographic measurements were unaffected by epinephrine infusion.Conclusion: Administration of both 30 ng/kg/min and 90 ng/kg/min at 32°C had a positive inotropic effect and reduced afterload. We found no evidence of increased pro-arrhythmic activity after epinephrine infusion in hypothermic pigs. Our experiment therefore suggests that β₁-receptor stimulation with epinephrine could be a favorable strategy for providing cardiovascular support in hypothermic patients, at core temperatures >32°C.

Comparison between cardiovascular effects of adrenaline and phenylephrine associated with lidocaine and the effects of felypressin with prilocaine during intrabucal anesthesia in ASA I patients

OBJECTIVE: Evaluate the cardiovascular effects by infiltration of 1:100.000 epinephrine and 1:2.500 phenylephrine associated with 2% lidocaine compared with the effects by infiltration of 0.03 IU/ml felypressin with 3% prilocaine, during surgery of third molars in ASA I patients.METHODS: Eighteen patients were divided into two groups. In group I (GI), the effects of epinephrine vs felypressin were evaluated and in group II (GII), the effects of phenylephrine vs felypressin. Cardiovascular parameters: systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) and oxygen saturation (SatO2) were measured in pre, trans and post-operative periods.RESULTS: Statistical analysis (T-TEST) on the cardiovascular parameters demonstrated with significance that, GI: felypressin presented HR average reduction in the postoperative period and SatO2 average reduction in trans and postoperative periods. For GII: felypressin presented SatO2 average reduction in the postoperative period; SBP averages for patients submitted to phenylephrine increased in trans and postoperative periods; and DBP averages for patients submitted to phenylephrine increased in pre and trans-operative periods.COCLUSION: We can conclude that phenylephrine may lead to increased SBP and DBP and felypressin generated a reduction in HR and SatO2. All these changes were well tolerated by ASA I patients.

Anaphylaxis and cardiovascular disease: therapeutic dilemmas.

Cardiovascular disease (CVD) increases the risk of severe or fatal anaphylaxis, and some medications for CVD treatment can exacerbate anaphylaxis. The aim of this article is to review the effect of anaphylaxis on the heart, the potential impact of medications for CVD on anaphylaxis and anaphylaxis treatment, and the cardiovascular effects of epinephrine. The therapeutic dilemmas arising from these issues are also discussed and management strategies proposed. PubMed searches were performed for the years 1990-2014 inclusive, using terms such as angiotensin-converting enzyme (ACE) inhibitors, adrenaline, allergic myocardial infarction, anaphylaxis, angiotensin-receptor blockers (ARBs), beta-adrenergic blockers, epinephrine, and Kounis syndrome. Literature analysis indicated that: cardiac mast cells are key constituents of atherosclerotic plaques; mast cell mediators play an important role in acute coronary syndrome (ACS); patients with CVD are at increased risk of developing severe or fatal anaphylaxis; and medications for CVD treatment, including beta-adrenergic blockers and ACE inhibitors, potentially exacerbate anaphylaxis or make it more difficult to treat. Epinephrine increases myocardial contractility, decreases the duration of systole relative to diastole, and enhances coronary blood flow. Its transient adverse effects include pallor, tremor, anxiety, and palpitations. Serious adverse effects (including ventricular arrhythmias and hypertension) are rare, and are significantly more likely after intravenous injection than after intramuscular injection. Epinephrine is life-saving in anaphylaxis; second-line medications (including antihistamines and glucocorticoids) are not. In CVD patients (especially those with ACS), the decision to administer epinephrine for anaphylaxis can be difficult, and its benefits and potential harms need to be carefully considered. Concerns about potential adverse effects need to be weighed against concerns about possible death from untreated anaphylaxis, but there is no absolute contraindication to epinephrine injection in anaphylaxis.

85: Cardiovascular Effects of Epinephrine During Neonatal Cardiopulmonary Resuscitation in a Piglet Model

85: Cardiovascular Effects of Epinephrine During Neonatal Cardiopulmonary Resuscitation in a Piglet Model

Effects of Nimesulide, a Selective COX-2 Inhibitor, on Cardiovascular Function in 2 Rat Models of Diabetes

Cyclooxygenase-2 (COX-2) has been found to be activated in diabetes. We investigated whether nimesulide (selective COX-2 inhibitor) alters cardiovascular responses to adrenaline in 2 rat models of diabetes. Wistar rats (5-week old) were continuously fed a normal or high-fructose diet (60% of caloric intake). At week 2, half of the rats in each diet regimen were given streptozotocin (STZ) (60 mg/kg, intravenously). At week 6, cardiovascular effects of adrenaline (6 and 16 × 10 mol·kg·min, intravenously) were measured in 4 groups of thiobutabarbital-anesthetized rats (control, fructose, STZ, and fructose-streptozotocin [F-STZ]) before and after the injection of nimesulide (3 mg/kg, intravenously). Both the STZ and F-STZ groups exhibited hyperglycemia and significantly (P < 0.05) reduced left ventricular contractility, mean arterial pressure, arterial and venous resistance, and mean circulatory filling pressure (index of venous tone) responses to adrenaline, relative to the control and fructose groups. Nimesulide did not affect responses in the control and fructose groups but increased the venous and, to a less extent, arterial constriction to adrenaline in both the groups of diabetic rats. The cardiac contractile responses, however, were not altered after nimesulide treatment. The results show that nimesulide partially restored arterial and venous constriction to adrenaline in rats with STZ- and F-STZ-induced diabetes.

Effects of Mepivacaine 2% With Epinephrine in the Cardiovascular Activity of Patients Undergoing Third Molar Surgery

Cardiovascular effects of epinephrine, especially on blood pressure (BP) and heart rate (HR), have been well documented. When present in dental local anesthetic solutions, epinephrine concentration ranges from 5 to 20 µg/mL. Doses less than 200 µg are recommended to be clinically safe. This study investigated the effects of the anesthetic solution of mepivacaine (2%) with epinephrine (10 µg/mL) in cardiovascular activity (HR and BP). Twenty-six patients underwent outpatient surgery for the removal of 2 unilateral (group I, n = 15) or 4 (group II, n = 11) third molars in a single session, being injected 5.4 and 10.8 mL of anesthetic solution, equivalent to 54 and 108 µg of epinephrine, respectively. The cardiovascular activity was monitored by cardioscope during the experimental period of 2 hours. Heart rate and BP were measured at the intervals of 0, 5, 10, 15, 20, 30, 40, 60, 90, and 120 minutes after anesthetic injection. After application of 2-way analysis of variance test, comparison between groups was not statistically significant for HR (P = 0.1388), systolic BP (P = 0.0228), and diastolic BP (P = 0.9846). However, patients from group II presented significantly greater sway in HR (P < 0.0001), systolic BP (P = 0.0169), and diastolic BP (P < 0.0001) in the course of 2 hours. Blood pressure did not present significant alterations after a local injection of 54 or 108 µg of epinephrine during surgery to remove 2 or 4 third molars. Although without significance, HR was more elevated in the 108-µg dose of epinephrine during the removal of 4 third molars.

There Is Minimal Risk for Adverse Events in Hypertensives Associated with the Use of Epinephrine in Local Anesthetics

Article Title and Bibliographic Iynformation Bader JD, Bonito AJ, Shugars DA. Cardiovascular Effects of Epinephrine on Hypertensive Dental Patients. Evidence Report/Technology Assessment Number 48. AHRQ Publication No. 02-E006. Level of Evidence 1A Purpose To identify the additional risks of adverse cardiovascular outcomes to controlled and uncontrolled hypertensive individuals represented by the use of epinephrine-containing anesthetic solutions and epinephrine-impregnated retraction cords during dental treatment. Source of Funding (Prepared by Research Triangle Institute under Contract No. 290-97-0011.) Rockville, MD: Agency for Healthcare Research and Quality; July 2002. Type of Study/design Systematic review

The Cardiovascular Effects of Adrenaline, Dobutamine and Milrinone in Rabbits Using Pressure-Volume Loops and Guinea Pig Isolated Atrial Tissue

This study evaluated the effects of milrinone, adrenaline and dobutamine with pressure-volume loops and isolated atrial tissue. Agonist dose-response curves to incremental drug infusions were acquired in 11 anesthetised rabbits using pressure-volume loops and preload recruitable stroke work indicated contractility. Agonist concentration-response curves were completed in eight guinea pig isolated atria, for effects on atrial rate and force. Adrenaline and dobutamine increased contractility (P = 0.006 and 0.044), whereas milrinone did not (P = 0.895). Only adrenaline increased myocardial stiffness (P < 0.001). Milrinone decreased vascular resistance (P < 0.001) and elicited the greatest fall in mean arterial pressure (P < 0.001) and increased ejection fraction (P < 0.001). Adrenaline decreased heart rate (P < 0.001), whereas dobutamine and milrinone increased it (P = 0.006 and 0.011). Milrinone increased the force of left atrial contraction, but its inotropic effect was weak and significantly less than with dobutamine and adrenaline (P < 0.001). Adrenaline acted as an inoconstrictor, dobutamine an inodilator and milrinone predominantly a vasodilator

Cardiovascular effects of epinephrine during rewarming from hypothermia in an intact animal model

Rewarming from accidental hypothermia is often complicated by "rewarming shock," characterized by low cardiac output (CO) and a sudden fall in peripheral arterial pressure. In this study, we tested whether epinephrine (Epi) is able to prevent rewarming shock when given intravenously during rewarming from experimental hypothermia in doses tested to elevate CO and induce vasodilation, or lack of vasodilation, during normothermia. A rat model designed for circulatory studies during experimental hypothermia and rewarming was used. A total of six groups of animals were used: normothermic groups 1, 2, and 3 for dose-finding studies, and hypothermic groups 4, 5, and 6. At 20 and 24 degrees C during rewarming, group 4 (low-dose Epi) and group 5 (high-dose Epi) received bolus injections of 0.1 and 1.0 microg Epi, respectively. At 28 degrees C, Epi infusion was started in groups 4 and 5 with 0.125 and 1.25 microg/min, respectively. Group 6 served as saline control. After rewarming, both CO and stroke volume were restored in group 4, in contrast to groups 5 and 6, in which both CO and stroke volume remained significantly reduced (30%). Total peripheral resistance was significantly higher in group 5 during rewarming from 24 to 34 degrees C, compared with groups 4 and 6. This study shows that, in contrast to normothermic conditions, Epi infused during hypothermia induces vasoconstriction rather than vasodilation combined with lack of CO elevation. The apparent dissociation between myocardial and vascular responses to Epi at low temperatures may be related to hypothermia-induced myocardial failure and changes in temperature-dependent adrenoreceptor affinity.

The Cardiovascular Effects of Epinephrine Used for Hemostasis under Enflurane-N2O Anesthesia during Tonsillectomy

The Cardiovascular Effects of Epinephrine Used for Hemostasis under Enflurane-N2O Anesthesia during Tonsillectomy

The early chick embryo as a model to evaluate cardiovascular effects of adrenaline and nicotine

During the early stages of development, chick embryos offer a good model for vascular and circulatory studies. The present experiments were carried out with nicotine and adrenaline as validation substances, to test whether this system can be applied to evaluate functional cardiovascular effects. Nicotine was injected into the yolk before incubation and administered topically on different days of incubation. Adrenaline was injected intravascularly to evaluate functional effects (heart rate and heart arrhythmia). Mortality rates following nicotine and adrenaline application were determined. An injection of nicotine prior to incubation resulted in a dose-related increase in undeveloped chick embryos, and the topical application led to hyperaemia and haemorrhages. The body weight of the embryos was reduced due to the repeated nicotine application. After iv injection of adrenaline, heart rate increase and the occurrence of heart arrhythmia showed dose-response effects and the mortality rate was three-fold higher as compared with the controls. These results show that, following the application of adrenaline and nicotine, effects on the early chick embryo are similar to those seen in other test systems. In addition to its use in toxicology, this model is suitable for the evaluation of functional cardiovascular effects. The system does not require living animals, and uses stages of development during which the nervous system is still immature.

Intracisternal administration of cholecystokinin-8 counteracts the central cardiovascular effects of adrenaline and NPY. A study based on the coexistence of cholecystokinin, phenylethanolamine N-methyltransferase and neuropeptide Y immunoreactivity in neurons of the nucleus tractus solitarius

(1) In the present study the occlusion method was employed to evaluate the overall coexistence of neuropeptide Y and phenylethanolamine-N-methyl transferase, neuropeptide Y and tyrosine hydroxylase as well as cholecystokinin and phenylethanolamine-N-methyl transferase immunoreactivity in nerve cell bodies of the dorsal subnuclei of the nucleus tractus solitarius of the male rat. A high degree of coexistence was established for neuropeptide Y/phenylethanolamine-N-methyl transferase, cholecystokinin/phenylethanolamine-N-methyl transferase and for tyrosine hydroxylase/neuropeptide Y immunoreactivity. (2) Sulfated [(12)I]cholecystokinin-8 was used as radioligand to study the densities of cholecystokinin-8 binding sites in the dorsal medulla oblongata by means of quantitative receptor autoradiography. High densities of binding sites were observed in parts of the nucleus tractus solitarius and in the area postrema. Labeling was also observed in the dorsal motor nucleus of the vagus. (3) In the physiological studies adrenaline (0.15-1.0 nmol), neuropeptide Y (0.075-0.75 nmol) and sulfated cholecystokinin-8 (0.3-3.0 nmol) were administered alone or in combination with neuropeptide Y or adrenaline intracisternally into ?-chloralose anaesthetized male rats. Especially the hypotensive and bradycardic responses of adrenaline were counteracted in the adrenaline/cholecystokinin co-treated animals, whereas the cardiovascular effects of neuropeptide Y when co-administered with cholecystokinin-8 (0.3 nmol) appeared to be more resistant to the antagonistic effect of cholecystokinin 8. In addition, cholecystokinin-8 further enhanced the neuropeptide Y-induced bradynpnea and increase in the tidal volume. The present results indicate the existence of neuropeptide Y, adrenaline and cholecystokinin-8 immunoreactivity in the same neurons of the dorsal subnuclei of the nucleus tractus solitarius. Furthermore, binding sites for cholecystokinin-8 seem to at least partly co-distribute with ?-2 adrenergic and neuropeptide Y binding sites in the nucleus tractus solitarius. In the functional analysis, an antagonistic interaction between cholecystokinin-8 and adrenaline as well as between cholecystokinin and neuropeptide Y is demonstrated opening up the possibility that cholecystokinin peptides act as intrinsic modulators in the putative cholecystokinin/neuropeptide Y/adrenaline synapses in the nucleus tractus solitarius.

A Comparative Study of the Haemostatic Properties and Cardiovascular Effects of Adrenaline and Ornipressin in Children during Enflurane Anaesthesia

In a randomized, double-blind trial, haemostatic and cardiovascular effects of ornipressin and adrenaline were compared in 30 children requiring surgery for "bat-ear" deformity. Mean total blood loss was 14.3 ml with ornipressin and 11.7 ml with adrenaline, this difference being insignificant. There was a significant and progressive reduction in mean heart rate in children who received ornipressin, from 134 to 116 bpm (P less than 0.05), and a significant rise from 127 to 134 bpm (P less than 0.05) with adrenaline. Mean systolic pressure was unaltered by ornipressin but was significantly increased from 97 to 105 mmHg (P less than 0.05) in children receiving adrenaline. Ornipressin is as effective a haemostatic agent as adrenaline and the rises in heart rate and systolic pressure associated with adrenaline, which are factors known to predispose to the onset of ventricular dysrhythmias, do not occur with ornipressin.

Effects of cardioselective and non-cardioselective beta-blockade on adrenaline-induced metabolic and cardiovascular responses in man.

In 12 normal volunteers the interaction between the metabolic and cardiovascular effects of adrenaline and either a cardioselective (atenolol 150 mg p. o. for 1 week) or a non-selective beta-blocker with intrinsic sympathomimetic activity (pindolol 15 mg p. o. for 1 week) were studied. Equiactive doses of the beta-blockers were investigated with respect to their metabolic effects. There were profound differences in the metabolic profile of the two substances: the non-cardioselective beta-blocker caused significant inhibition of the lipolytic, glycogenolytic and the growth hormone-releasing effects of adrenaline when compared to the cardioselective agent. The results indicate that, during non-cardioselective beta-blockade, metabolic effects occur which should favourably influence myocardial oxygen consumption by making myocardial performance more economical.

Acute Asthma. Part II. The effects of therapy on heart rate and blood pressure

This study evaluated cardiovascular effects of epinephrine in the treatment of asthma. Heart rates, systolic and diastolic blood pressures were monitored in 64 patients treated for acute asthma. Treatment regimens included subcutaneous epinephrine in doses of 0.1 to 0.5 mg. Pretreatment heart rates ranged from 64 to 136 beats per minute and systolic and diastolic blood pressures from 80 to 190 and 50 to 108 mm Hg respectively. Epinephrine in all doses and repeated as often as three times did not raise blood pressure or heart rates, and in the highest dose or in patients with pressures in the hypertensive range exerted a hypotensive effect. Adverse cardiovascular effects of epinephrine observed in normal subjects are significantly modified in acute asthma and its use should be considered in light of these findings.

Metabolic and cardiovascular effects of adrenaline and alprenolol (Aptin�) in human subjects

Changes in blood pressure, heart rate, hematocrit, O2 consumption, blood glucose, lactate, pyruvate and FFA during intravenous adrenaline infusion alone and after pre-treatment with alprenolol (Aptin®), a beta-adrenergic receptor blocker, were studied in four healthy fasting male subjects according to double-blind technique with saline infusions as control. Adrenaline alone caused increases in heart rate, hematocrit and systolic blood pressure and a decrease in diastolic pressure. After alprenolol, adrenaline infusion gave a decrease in heart rate with an increase in both systolic and diastolic blood pressure, while the hematocrit was unchanged. The adrenaline infusion caused significant rises in all the metabolic variables studied. Pre-treatment with alprenolol abolished all these rises with the exception of blood glucose.