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L Wiklund

Publications and source records attributed to L Wiklund.

At least 73 records · Page 4Linked to original sources
PubMed1997

Propofol induces a lowering of free cytosolic calcium in myocardial cells.

BACKGROUND: The intravenous anaesthetic drug propofol has been shown to depress myocardial contractility. Ketamine, on the other hand, is a well-documented cardiovascular stimulant. These differences could possibly be due to different effects of the drugs on the calcium homeostasis of the myocardium. METHODS: The fluorescent intracellular probe fura-2 acetoxymethyl ester (fura-2/AM) was used in this in vitro investigation to study the influence of intravenous anaesthetic drugs on free cytosolic calcium concentration in suspensions of isolated rat myocardial cells. RESULTS: Addition of 0.5-2.0 micrograms/mL propofol resulted in a significant and dose-dependent decrease of free cytosolic calcium concentration in the myocardial cells, while addition of 0.25-2.5 micrograms/mL ketamine did not affect this concentration significantly. CONCLUSION: The results imply that the previously demonstrated negative inotropic effect of propofol could possibly be related to its influence on calcium availability in the myocardium.

Anesthetics, Intravenous↗
PubMed1997

Cerebral normoxia in the rhesus monkey during isoflurane- or propofol-induced hypotension and hypocapnia, despite disparate blood-flow patterns. A positron emission tomography study.

BACKGROUND: Due to a few reports of cerebral dysfunction in connection with isoflurane-induced hypotension and concomitant hypocapnia, positron emission tomography (PET) was used to measure cerebral oxygenation and blood flow during similar conditions with isoflurane or propofol. METHODS: The short-lived radionuclide 15O was used for measurement of cerebral metabolic rate of oxygen (CMRO2), cerebral blood flow (CBF) and oxygen extraction ratio (OER) regionally in rhesus monkeys during normotensive/normocapnic and hypotensive/hypocapnic conditions, mean arterial pressure 100-110 and 50-65 mmHg and PaCO2 4.4-5.4 and 3.4-4.4 kPa, respectively. Isoflurane or propofol anaesthesia was given (n = 4 in both groups), supported with 70% nitrous oxide and preceded by ketamine anaesthesia (baseline). RESULTS: PET revealed wide variations in CBF between regions during isoflurane anaesthesia, particularly in comparison with propofol anaesthesia, while rCMRO2 decreased globally in a dose-dependent manner during both isoflurane and propofol anaesthesia. The metabolism-flow coupling was intact during propofol but not during isoflurane anaesthesia. Hypotension reduced rCBF, and rOER increased globally with both study drugs when changing from normo- to hypotension. However, this rOER increase was not significant when using PaCO2 as a covariate, and rOER was never above an arbitrary limit for hypoxia of 70%. Thus, hypocapnia, rather than hypotension, was responsible for the somewhat higher rOER measured. CONCLUSION: PET indicated adequate cerebral oxygenation during isoflurane and propofol anaesthesia, despite disparate blood-flow patterns. Hypotension and concomitant moderate hyperventilation reduced rCBF, but did not result in hypoxia.

Anesthesia↗
PubMed1997

Effects of mononuclear cells on pulmonary arteries from rejecting transplanted lungs.

Experiments were designed to determine responses of pulmonary arteries from an acutely rejecting, transplanted lung to rejection-activated mononuclear cells. Pulmonary arteries and macrophage-depleted mononuclear cells were obtained from unoperated dogs (control) and dogs with rejecting single lung allotransplants (transplanted, rejecting). In some arteries, the endothelium was removed deliberately. Pulmonary arteries were suspended for measurement of isometric force in organ chambers. Contractions to potassium chloride (60 M) were greater in rings of pulmonary arteries from rejecting compared with control dogs. Mononuclear cells from both control and transplanted dogs caused cell number-dependent contractions of autogenous pulmonary arteries. Contractions to cells were decreased when the endothelium was present only in arteries from control dogs; these contractions were increased by the L-arginine analog N(G)-monomethyl-L-arginine (10(-4) M) but not by indomethacin (10(-5) M). Contractions to mononuclear cells were reduced by superoxide dismutase (150 U/ml) and catalase (1,200 U/ml) in arteries without endothelium from control but not transplanted dogs. In arteries from transplanted dogs, contractions to mononuclear cells were reduced by desferoxamine (10(-3) M). Results suggest that interactions between mononuclear cells and pulmonary arteries are modified during rejection of lung allografts so that, during rejection, 1) endothelium-derived nitric oxide no longer antagonizes contractions to substances produced by the mononuclear cells and 2) contractions of smooth muscle from rejecting arteries to mononuclear cells may be mediated by radicals other than superoxide.

Acute Disease↗
PubMed1997

Increased levels of circulating nitrates and impaired endothelium-mediated vasodilation suggest multiple roles of nitric oxide during acute rejection of pulmonary allografts.

Experiments were designed to determine whether changes in pulmonary artery function could be reduced by treatment with a lipid peroxidation inhibitor (H 290/51) during acute rejection of pulmonary allografts. Single lung transplantation was performed in three groups of dogs: group 1 was maintained on immunosuppression for 8 days after operation (immunosuppressed, n = 5); in group 2, immunosuppression was discontinued on postoperative day 5, so that rejection occurred on postoperative day 8 (rejecting, n = 6); in group 3, immunosuppression was discontinued after 5 days, and the lipid peroxidation inhibitor H 290/51 (25 mg/kg) was given perorally for 3 days (rejecting + H 290/51, n = 6). Plasma nitric oxide (NO(x)) was measured by use of chemoluminescence. On postoperative day 8 rejection was observed in groups 2 and 3. Contractions to angiotensin I and endothelium-dependent relaxations to adenosine diphosphate were reduced in pulmonary arteries from rejecting lungs. Responses of rings from dogs treated with H 290/51 were similar to those from rejecting lungs. Rejection did not alter relaxations to exogenous nitric oxide. However, plasma levels of NO(x) increased significantly during rejection independently of treatment with H 290/51. Results of this study confirm that endothelium-dependent relaxation of pulmonary arteries is reduced during acute rejection of lung allografts. The result extends these observations to suggest that treatment with a lipid peroxidation inhibitor neither protects the pulmonary artery function nor affects levels of circulating NO(x). Therefore mechanisms other than lipid peroxidation participate in vascular changes associated with allograft rejection.

Acute Disease↗
PubMed1997

Decreased measures of experimental anxiety in rats bred for high alcohol preference.

A prevalent notion holds that acute anti-anxiety actions of ethanol are important for the reinforcing properties of this drug, and might predispose individuals with pre-existing anxiety disorders for developing ethanol dependence. This notion remains controversial, and human studies have yielded conflicting results. Ethanol dependence is likely a heterogenous disorder, and the discrepancies might be explained by a different relationship between anxiety and alcohol reinforcement in different subtypes of alcoholism. Recent results in experimental animals suggest that antianxiety actions of ethanol are important reinforcers of voluntary ethanol consumption in heterogeneous rats. Here, we examined whether the relationship is different in the AA line of rats bred for high voluntary ethanol intake. Behavior was studied in two established animal models of anxiety, a punished drinking conflict test, and the elevated plus maze. In the conflict test, the AA line displayed a markedly disinhibited behavior over a range of shock intensities, compared both with their counterpart, the ANA line, and with regular Wistar rats. On the plus maze, both AA and Wistar rats showed lower measures of experimental anxiety than ANA subjects. The phenotype of the animals was confirmed using a two-bottle free choice alcohol drinking procedure. The disinhibited behavior and spontaneous ethanol preference of the AA line differs from what has been found in heterogeneous rats, and displays similarities to genetically transmitted type II alcoholism according to the nomenclature of Cloninger.

Alcohol Drinking↗
PubMed1996

Influence of alkaline buffers on cytoplasmic pH in myocardial cells exposed to metabolic acidosis.

The influence of different clinically used alkaline buffers on cytoplasmic pH in normal as well as acidotic rat myocardial cells was investigated in this study by means of the fluorescent intracellular probe 2',7'-bis-(carboxyethyl)-5,6-carboxyfluorescein acetoxymethyl ester (BCECF-AM). It was shown that both sodium bicarbonate and Tris buffer mixture (Tribonat) caused a significant and dose-dependent acidification of the cytoplasm of suspended myocardial cells with normal initial intracellular pH. This decrease was followed by a slow increase during the observation period. The initial cytoplasmic pH value was more easily reached when Tris buffer mixture was used. Ringer's acetate also caused a decrease of intracellular pH, but this change persisted and was further amplified during the experiment. Carbicarb in larger dosages as well as pure trometamol (Tris) caused a pronounced dose-dependent and lasting intracellular alkalinization. Intracellular acidosis was achieved by preincubating the cells in sodium acetate. Addition of sodium bicarbonate caused an initial and dose-dependent acidification of the cytoplasm followed by a slow increase to values slightly above the induced acidosis. In contrast, Tris buffer mixture showed a tendency towards an initial acidification only when larger dosages were used, and correction of the induced acidosis was possible by use of moderate to large volumes. Ringer's acetate produced a lasting and dose-dependent decrease of cytoplasmic pH, while Carbicarb and pure trometamol caused an immediate, pronounced and persistent alkalinization. Myocardial cells with low initial cytoplasmic pH due to preincubation in an acid buffer also showed an early decrease of intracellular pH after addition of sodium bicarbonate and Tris buffer mixture. In the case of sodium bicarbonate correction of the acid-base disturbance was not achieved during the observation period, while this was accomplished by use of larger volumes of Tris buffer mixture. Carbicarb in larger volumes caused an increase in intracellular pH. The most significant and persistent increases of cytoplasmic pH was achieved by use of pure trometamol. In conclusion, the present in vitro study implies that Tris buffer mixture (Tribonat) is well-suited for correction of intracellular acidosis since it acts without causing a pronounced initial intracellular acidosis or a later potentially hazardous huge cytoplasmic alkalinization.

Animals↗
PubMed1996

Future directions for resuscitation research. IV. Innovative advanced life support pharmacology.

The topics discussed in this session include a partial review of laboratory and clinical studies examining the effects of adrenergic agonists on restoration of spontaneous circulation after cardiac arrest, the effects of varying doses of epinephrine, and the effects of novel vasopressors, buffer agents (NaHCO3, THAM, 'Carbicarb') and anti-arrhythmics (lidocaine, bretylium, amiodarone) in refractory ventricular fibrillation. Novel therapeutic approaches include titrating electric countershocks against electrocardiographic power spectra and of preceding the first countershocks with single or multiple drug treatments. These approaches need to be investigated further in controlled animal and patient studies. Epidemiologic data from randomized clinical outcome studies can give clues, but cannot document pharmacologic mechanisms in the dynamically changing events during attempts to achieve restoration of spontaneous circulation from prolonged cardiac arrest. Also, rapid drug administration by the intraosseous route was compared with intratracheal and intravenous (i.v.) drug administration. Many studies on the above treatments have yielded conflicting results because of differences between healthy hearts of animals and sick hearts of patients, differences in arrest (no-flow) times and cardiopulmonary resuscitation (CPR) (low-flow) times, different pharmacokinetics, different dose/response requirements, and different timing of drug administration during low-flow CPR versus during spontaneous circulation. The need to stabilize normotension and prevent rearrest by titrated novel drug administration, once spontaneous circulation has been restored, requires research. Most of the above topics require some re-evaluation in clinically realistic animal models and in cardiac arrest patients, especially by titration of old and new drug treatments against variables that can be monitored continuously during resuscitation.

Adrenergic Agonists↗
PubMed1996

Effect of tris buffer on free cytosolic calcium in myocardial cells.

OBJECTIVE: To study the effect of tris buffer on free cytosolic calcium in vitro. DESIGN: Open, randomized, control trial of dispersed rat myocardial cells. SETTING: Experimental laboratory in a large university hospital. SUBJECTS: Dispersed myocardial cells from Sprague-Dawley rats. INTERVENTIONS: The influences of pure trometamol (tris) and a tris butter mixture, as well as conventional sodium bicarbonate on free cytosolic calcium in suspended rat myocardial cells were studied with the fluorescent intracellular probe fura-2. MEASUREMENTS AND MAIN RESULTS: Addition of pure trometamol (tris) resulted in a significant increase of free cytosolic calcium in myocardial cells suspended in a buffer containing 1.25 mM of ionized calcium. The actions of trometamol display a dose-dependency in relation to the concentration of external ionized calcium since the ionized calcium response was reduced in a buffer with 0.5 mM of extracellular ionized calcium. Furthermore, removal of external ionized calcium totally prevented trometamol induced increases of ionized calcium, indicating that this increase is dependent on transmembrane ionized calcium fluxes. When tris buffer mixture was investigated in 1.25 mM of calcium, as well as 0.5 mM of external ionized calcium, a decrease of ionized calcium was noted initially, followed by an increase during the observation period. Addition of sodium bicarbonate to the two experimental settings resulted in a more prominent initial decrease of ionized calcium, followed by a slower increase which did not reach the initial values during the 20-min observation period. Extracellular pH was also included as a variable. When the cells were suspended in a buffer containing 1.25 mM of ionized calcium with a pH of 6.80 instead of 7.40 (as above), addition of pure trometamol also resulted in an increase of ionized calcium; however, after 20 mins this increase was smaller as compared with the results above. When tris buffer mixture as well as sodium bicarbonate was added, initial decreases of ionized calcium were recorded, followed by smaller increases during the observation period, compared with the increase in buffers with a pH of 7.40. CONCLUSIONS: Pure trometamol (tris) induces an increase in free cytosolic calcium in suspended myocardial cells.

Animals↗
PubMed1996

Effects of prolonged exposure to oxygen-derived free radicals in canine pulmonary arteries.

Experiments were designed to evaluate endothelium-dependent responses of pulmonary arteries following prolonged exposure to oxygen-derived free radicals. Rings of canine pulmonary arteries with and without endothelium were suspended for measurement of isometric force in organ chambers and incubated with xanthine (10(-4)M) plus xanthine oxidase (0.015 U/ml) for 1 h in the absence and presence of either superoxide dismutase (SOD, 150 U/ml), catalase (1,200 U/ml), deferoxamine (10(-3)M), or a combination of all three scavengers. Xanthine plus xanthine oxidase caused significantly greater contractions of rings without compared with those with endothelium. In rings with endothelium, contractions were reduced by SOD or catalase but not by deferoxamine. Following 1 h of exposure to xanthine plus xanthine oxidase, endothelium-dependent relaxations to ADP were reduced but not those to bradykinin or the calcium ionophore A-23187 (calcimycin). Relaxations to ADP were not corrected by incubation with the antioxidants used singly or in combination during the exposure to xanthine plus xanthine oxidase. These results suggest that oxygen-derived free radicals generated from exogenously applied xanthine plus xanthine oxidase cause contractions of canine pulmonary arteries. In addition, even when contractions of rings with endothelium were prevented by SOD and catalase, subsequent expression of some but not all endothelium-dependent relaxations were reduced. Therefore, scavenging of oxygen-derived free radicals may prevent some but not all of the vascular injury caused by oxygen-derived free radicals.

Adenosine Diphosphate↗
PubMed1996

Carbon dioxide formation and elimination in man. Recent theories and possible consequences.

Systemic metabolism results in a production of not only carbon dioxide, water and urea but also bicarbonate ions. Most of these bicarbonate ions are generated during the catabolism of glutamine. In order to be eliminated as carbon dioxide in the lungs bicarbonate ions must be protonised. This protonisation of the bicarbonate ion seems to take place in a number of tissue compartments in which acid-base balance is maintained. One of the most important processes for protonisation of the bicarbonate ion is the hepatic ureagenesis from ammonia/ammonium ions. A substantial part of the ammonia/ammonium ions are generated during the catabolism of amino acids. Terminal oxidation of glutamine in the gut seems to be of great significance for this process. In certain conditions the enteric generation of ammonium ions seems so important that an ATP-driven enterohepatic recirculation of ammonium ions/urea constituting an amplifying mechanism for the protonisation of the bicarbonate ion is motivated.

Acid-Base Equilibrium↗
PubMed1996

Faecal microflora and urease activity during the first six months of infancy.

Gastrointestinal degradation of urea might, according to a new hypothesis, have consequences for the regulation of acid-base balance as well as control of breathing during infancy. Thirteen infants were investigated from their first few days of life to the age of 6 months by collecting faecal samples at the age of 3 days, 2, 3, and 6 months, respectively. The faecal microflora was determined after aerobic and anaerobic cultivation and the faecal urease activity was assessed after 36 h aerobic and anaerobic preincubation. The infants were mostly breast fed and had a faecal microflora containing anaerobic bacteria such as Bifidobacteria, Bacterioides and Lactobacilli but also aerobics such as Escherichia coli, Enterococci and sometimes Klebsiella. The faecal pH increased from approximately 5.30 to 5.90, the pH after anaerobic preincubation being on an average 0.2 pH units lower than after aerobic preincubation. Simultaneously the nitric oxide production of the faecal specimens increased approximately 10-fold and the urease activity decreased by a factor of 3 to 5. We also found an inhibitory action of nitrate, nitrite (in mumolar concentration) and nitric oxide (in parts per million concentration) on the faecal urease activity. Hence, the present results warrant further research in order to determine more precisely the action of different concentrations of various nitrous oxides on individual bacterial species, and furthermore, to assay the faecal urease activity in victims of sudden infant death syndrome as well as in infants dead due to other causes.

Bacteria, Aerobic↗
PubMed1996

Resuscitation from severe hemorrhage.

The potential to be successfully resuscitation from severe traumatic hemorrhagic shock is not only limited by the "golden 1 hr", but also by the "brass (or platinum) 10 mins" for combat casualties and civilian trauma victims with traumatic exsanguination. One research challenge is to determine how best to prevent cardiac arrest during severe hemorrhage, before control of bleeding is possible. Another research challenge is to determine the critical limits of, and optimal treatments for, protracted hemorrhagic hypotension, in order to prevent "delayed" multiple organ failure after hemostasis and all-out resuscitation. Animal research is shifting from the use of unrealistic, pressure-controlled, hemorrhagic shock models and partially realistic, volume-controlled hemorrhagic shock models to more realistic, uncontrolled hemorrhagic shock outcome models. Animal outcome models of combined trauma and shock are needed; a challenge is to find a humane and clinically realistic long-term method for analgesia that does not interfere with cardiovascular responses. Clinical potentials in need of research are shifting from normotensive to hypotensive (limited) fluid resuscitation with plasma substitutes. Topics include optimal temperature, fluid composition, analgesia, and pharmacotherapy. Hypotensive fluid resuscitation in uncontrolled hemorrhagic shock with the addition of moderate resuscitative (28 degrees to 32 degrees C) hypothermia looks promising in the laboratory. Regarding the composition of the resuscitation fluid, despite encouraging results with new preparations of stroma-free hemoglobin and hypertonic salt solutions with colloid, searches for the optimal combination of oxygen-carrying blood substitute, colloid, and electrolyte solution for limited fluid resuscitation with the smallest volume should continue. For titrating treatment of shock, blood lactate concentrations are of questionable value although metabolic acidemia seems helpful for prognostication. Development of devices for early noninvasive monitoring of multiple parameters in the field is indicated. Molecular research applies more to protracted hypovolemic shock followed by the systemic inflammatory response syndrome or septic shock, which were not the major topics of this discussion.

Animals↗
PubMed1995

Protective effects of an indenoindole antioxidant on coronary endothelial function after long-term storage.

Experiments were designed to evaluate function of the endothelium and smooth muscle of coronary arteries following storage of hearts in cardioplegia containing an inhibitor of lipid peroxidation (H 290/51, cis-7-methyl-9-methoxy-5,5a, 6,10b tetrahydroindeno [2,1-b] indole). Canine hearts were perfused with crystalloid cardioplegia (Plegisol, 15 ml/kg, 4 degrees C) and left circumflex arteries were isolated and studied either immediately (group I, n = 6), or after storage of the hearts at 4 degrees C for 10 (group II, n = 6) or 24 hr with (group III, n = 6) or without (group IV, n = 6) addition of H 290/51. The final concentration of H 290/51 was 1 mumol/L. Arteries were removed, cut into rings, and suspended in organ chambers for measurements of isometric force. In selected rings, the endothelium was removed in order to study the function of the smooth muscle. In order to discriminate effects of ischemia/reperfusion and protective properties on coronary endothelium or smooth muscle, drugs with different mechanisms were used. The function of the endothelium were studied with the alpha 2-adrenergic agonist UK 14,304, bradykinin and A 23187. The smooth muscle function were studied with isoproterenol and nitric oxide. Endothelium-dependent relaxations to the alpha 2-adrenergic agonist UK 14,304 and bradykinin, but not to A 23187, were reduced significantly in arteries from hearts stored for 24 hr in cardioplegic solution alone. Relaxations of arteries from hearts stored for 24 hr with H 290/51 were comparable to those arteries from hearts that were not stored. Endothelium-independent relaxations to isoproterenol and nitric oxide among the different groups were comparable. These results suggest that storage of canine hearts with crystalloid cardioplegia selectively inhibits endothelium-dependent relaxations mediated by receptor activation. Inhibition of lipid peroxidation with H 290/51 preserves these relaxations and may therefore represent a therapeutic alternative to preserve hearts used for transplantation.

Adrenergic alpha-Agonists↗
PubMed1995

[von Hippel-Lindau hereditary tumor syndrome. Mutational analysis may improve prognosis].

The von Hippel-Lindau disease is a familial tumour syndrome characterised by greatly increased risks of developing central nervous haemangioma, renal cell carcinoma, retinal angioma and pheochromocytoma. Carriers have inherited a mutated tumour suppressor gene located at chromosome 3p25-26. The VHL gene has recently been cloned, three exons identified and the DNA sequence determined. A Swedish kindred comprising four generations and 41 individuals was investigated. Three living individuals with clinically verified VHL disease demonstrated a single base deletion of a cytosine residue at position 761 of the VHL gene, corresponding to amino acid 254. Among the remaining family members, two asymptomatic carriers of this VHL mutation were identified and offered a clinical follow-up programme for early detection and treatment of future VHL manifestations.

Adult↗
PubMed1995

Plasmapheresis as a rescue therapy to resolve cardiac rejection with vasculitis and severe heart failure. A report of five cases.

The predominant causes of late graft loss and death after cardiac transplantation are graft rejection and infection. The histopathological classification of acute rejection is based on cellular phenomena such as lymphocytic infiltration and myocyte damage. The adverse prognostic importance of vascular or humoral rejection has been reported, but there is no well-documented treatment available. In our experience, comprising 151 orthotopic transplants, five patients presented with graft rejection characterized by a lymphocytic vasculitis that did not respond to conventional therapy. Because of a deteriorating condition, in spite of vigorous antirejection treatment that included inotropic drugs and circulatory support. plasmapheresis was tried as a last, desperate means to stop the process from developing further. The clinical symptoms rapidly subsided in all five patients after the first couple of plasma exchanges. All of the patients are alive and well after 2-3.5 years of follow-up. Although the mechanism of action is unclear, plasmapheresis was beneficial in these critically ill patients.

Adolescent↗
PubMed1995

Blood flow and perfusion pressure during open-chest versus closed-chest cardiopulmonary resuscitation in pigs.

OBJECTIVE: To evaluate the blood flow and perfusion pressure differences observed during open- vs. closed-chest cardiopulmonary resuscitation (CPR), including the effects of epinephrine and sodium bicarbonate administration. DESIGN: Prospective, randomized, controlled trial. SETTING: Experimental animal laboratory in a university hospital. SUBJECTS: A total of 35 anesthetized piglets. INTERVENTIONS: After tracheostomy and insertion of arterial, right atrial, and pulmonary arterial catheters, thoracotomy was performed with placement of a pulmonary arterial flow probe and left atrial catheter. Ventricular fibrillation was induced and followed by 15 mins of either open-chest (n = 14) or closed-chest (n = 21) CPR. A 4-min infusion of 50 mmol of sodium bicarbonate or saline was added at the start of CPR. After 8 mins of CPR, 0.5 mg of epinephrine was given intravenously, and after 15 mins, direct current (DC) shocks were used to revert the heart to sinus rhythm. MEASUREMENTS AND MAIN RESULTS: Blood flow was studied using transit-time ultrasound flowmetry. In an extended group, intrathoracic pressure was measured for calculation of transmural pressure. Before epinephrine administration, mean pulmonary arterial flow (cardiac output) was reduced: a) during closed-chest CPR relatively more than pulmonary perfusion pressure but in proportion to systemic perfusion pressure; b) during open-chest CPR relatively less than pulmonary perfusion pressure but still in proportion to systemic perfusion pressure. Epinephrine administration temporarily increased systemic perfusion pressure during both closed- and open-chest CPR but temporarily decreased pulmonary perfusion pressure only during closed-chest CPR. After epinephrine administration, cardiac output temporarily decreased during both closed-and open-chest CPR. CONCLUSIONS: Open-chest CPR resulted in better cardiac output and systemic perfusion pressure than closed-chest CPR. However, cardiac output values obtained with both methods were much lower than previously reported. After epinephrine administration, cardiac output became extremely low with both methods.

Animals↗