dinoprost and Heart-Arrest

Lipid peroxidation induced by free-radical species plays a prominent role in myocardial injury following ischemia and reperfusion. However, there is a lack of data in different oxygen concentrations on myocardial lipid peroxidation during the early phase of reperfusion. In this study, we investigated whether ventilation with medium or normal concentration of oxygen would decrease the severity of myocardial lipid peroxidation and postresuscitation myocardial dysfunction.. Prospective, randomized, controlled experimental study.. University-affiliated animal research institution.. Sixty-three healthy male Sprague-Dawley rats.. Animals were randomized into three groups: 1) 100% group, 2) 50% group, and 3) 21% group. Ventricular fibrillation was induced and untreated for 8 minutes, and defibrillation was attempted after 8 minutes of cardiopulmonary resuscitation. Ventilation with 100%, 50%, or 21% oxygen was initiated in all groups during cardiopulmonary resuscitation and 1 hour following the return of spontaneous circulation. Normoxic ventilation was maintained thereafter.. Myocardial function, including ejection fraction and myocardial performance index, were measured at baseline, 4, or 72 hours after resuscitation. Blood samples were drawn at baseline, 15 minutes, 1, 4, or 72 hours after resuscitation for the measurements of blood gas or biomarkers. Significantly better myocardial function and longer duration of survival were observed in the 50% group. Compared with the 21% and 100% groups, a mild hyperoxia and greater oxygen extraction with lower 8-iso-prostaglandin F2α were observed in the 50% group. Pearson correlation analysis confirmed that 8-iso-prostaglandin F2α was positively correlated with myocardial performance index at 4 hours postresuscitation.. In a rat model of cardiac arrest and resuscitation, ventilation with 50% inspired oxygen during early postischemic reperfusion phase contributed to a decreased lipid peroxidation and a better myocardial function and duration of survival.

Topics: Animals; Biomarkers; Blood Gas Analysis; Cardiopulmonary Resuscitation; Dinoprost; Dose-Response Relationship, Drug; Heart Arrest; Heart Function Tests; Lipid Peroxidation; Myocardial Reperfusion Injury; Myocardium; Oxidative Stress; Oxygen; Prospective Studies; Rats; Rats, Sprague-Dawley; Respiration, Artificial; Time Factors; Troponin I

Sudden cardiac arrest is a leading cause of death worldwide. Three-fourths of cardiac arrest patients die before hospital discharge or experience significant neurological damage. Hydrogen-rich saline, a portable, easily administered, and safe means of delivering hydrogen gas, can exert organ-protective effects through regulating oxidative stress, inflammation, and apoptosis. We designed this study to investigate whether hydrogen-rich saline treatment could improve survival and neurological outcome after cardiac arrest and cardiopulmonary resuscitation, and the mechanism responsible for this effect.. Sprague-Dawley rats were subjected to 8 minutes of cardiac arrest by asphyxia. Different doses of hydrogen-rich saline or normal saline were administered IV at 1 minute before cardiopulmonary resuscitation, followed by injections at 6 and 12 hours after restoration of spontaneous circulation, respectively. We assessed survival, neurological outcome, oxidative stress, inflammation biomarkers, and apoptosis.. Hydrogen-rich saline treatment dose dependently improved survival and neurological function after cardiac arrest/resuscitation. Moreover, hydrogen-rich saline treatment dose dependently ameliorated brain injury after cardiac arrest/resuscitation, which was characterized by the increase of survival neurons in hippocampus CA1, reduction of brain edema in cortex and hippocampus, preservation of blood-brain barrier integrity, as well as the decrease of serum S100β and neuron-specific enolase. Furthermore, we found that the beneficial effects of hydrogen-rich saline treatment were associated with decreased levels of oxidative products (8-iso-prostaglandin F2α and malondialdehyde) and inflammatory cytokines (tumor necrosis factor-α, interleukin-1β, and high-mobility group box protein 1), as well as the increased activity of antioxidant enzymes (superoxide dismutase and catalase) in serum and brain tissues. In addition, hydrogen-rich saline treatment reduced caspase-3 activity in cortex and hippocampus after cardiac arrest/resuscitation.. Hydrogen-rich saline treatment improved survival and neurological outcome after cardiac arrest/resuscitation in rats, which was partially mediated by reducing oxidative stress, inflammation, and apoptosis.

Topics: Administration, Intravenous; Animals; Antioxidants; Apoptosis; Biomarkers; Blood-Brain Barrier; Brain; Brain Injuries; Cardiopulmonary Resuscitation; Caspase 3; Cytokines; Dinoprost; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Administration Schedule; Fluid Therapy; Heart Arrest; Hydrogen; Inflammation Mediators; Male; Malondialdehyde; Neurons; Neuroprotective Agents; Oxidative Stress; Phosphopyruvate Hydratase; Rats; Rats, Sprague-Dawley; S100 Calcium Binding Protein beta Subunit; Sodium Chloride; Time Factors

Glucagon-like peptide-1 (GLP-1) has protective effects in the heart. We hypothesized that GLP-1 would mitigate coronary microvascular and left ventricular (LV) dysfunction if administered after cardiac arrest and resuscitation (CAR). Eighteen swine were subjected to ventricular fibrillation followed by resuscitation. Swine surviving to return of spontaneous circulation (ROSC) were randomized to receive an intravenous infusion of either human rGLP-1 (10 pmol·kg(-1)·min(-1); n = 8) or 0.9% saline (n = 8) for 4 h, beginning 1 min after ROSC. CAR caused a decline in coronary flow reserve (CFR) in control animals (pre-arrest, 1.86 ± 0.20; 1 h post-ROSC, 1.3 ± 0.05; 4 h post-ROSC, 1.25 ± 0.06; P < 0.05). GLP-1 preserved CFR for up to 4 h after ROSC (pre-arrest, 1.31 ± 0.17; 1 h post-ROSC, 1.5 ± 0.01; 4 h post-ROSC, 1.55 ± 0.22). Although there was a trend toward improvement in LV relaxation in the GLP-1-treated animals, overall LV function was not consistently different between groups. 8-iso-PGF(2α), a measure of reactive oxygen species load, was decreased in post-ROSC GLP-1-treated animals [placebo, control (NS): 38.1 ± 1.54 pg/ml; GLP-1: 26.59 ± 1.56 pg/ml; P < 0.05]. Infusion of GLP-1 after CAR preserved coronary microvascular and LV diastolic function. These effects may be mediated through a reduction in oxidative stress.

Topics: Animals; Antioxidants; Cardiopulmonary Resuscitation; Coronary Circulation; Dinoprost; Endothelium, Vascular; Female; Glucagon-Like Peptide 1; Heart Arrest; Heart Ventricles; Humans; Male; Microvessels; Reactive Oxygen Species; Swine; Ventricular Dysfunction, Left; Ventricular Fibrillation

Cerebral oxidative stress and metabolic dysfunction impede neurological recovery from cardiac arrest-resuscitation. Pyruvate, a potent antioxidant and energy-yielding fuel, has been shown to protect against oxidant- and ischemia-induced neuronal damage. This study tested whether acute pyruvate treatment during cardiopulmonary resuscitation can prevent neurological dysfunction and cerebral injury following cardiac arrest.. Anesthetized, open-chest mongrel dogs underwent 5 min cardiac arrest, 5 min open-chest cardiac compression (OCCC), defibrillation and 3-day recovery. Pyruvate (n=9) or NaCl volume control (n=8) were given (0.125 mmol kg(-1) min(-1) i.v.) throughout OCCC and the first 55 min recovery. Sham dogs (n=6) underwent surgery and recovery without cardiac arrest-resuscitation.. Neurological deficit score (NDS), evaluated at 2-day recovery, was sharply increased in NaCl-treated dogs (10.3+/-3.5) versus shams (1.2+/-0.4), but pyruvate treatment mitigated neurological deficit (NDS=3.3+/-1.2; P<0.05 versus NaCl). Brain samples were taken for histological examination and evaluation of inflammation and cell death at 3-day recovery. Loss of pyramidal neurons in the hippocampal CA1 subregion was greater in the NaCl controls than in pyruvate-treated dogs (11.7+/-2.3% versus 4.3+/-1.2%; P<0.05). Cardiac arrest increased caspase-3 activity, matrix metalloproteinase activity, and DNA fragmentation in the CA1 subregion; pyruvate prevented caspase-3 activation and DNA fragmentation, and suppressed matrix metalloproteinase activity.. Intravenous pyruvate therapy during cardiopulmonary resuscitation prevents initial oxidative stress and neuronal injury and enhances neurological recovery from cardiac arrest.

Topics: Analysis of Variance; Animals; Antioxidants; Brain; Cardiopulmonary Resuscitation; Caspase 3; Cerebrovascular Circulation; Dinoprost; Dogs; Energy Metabolism; Heart Arrest; In Situ Nick-End Labeling; Matrix Metalloproteinases; Oxidative Stress; Peroxidase; Pyruvic Acid; Regional Blood Flow

To determine whether antithrombin (AT) administration during cardiopulmonary resuscitation (CPR) increased cerebral circulation and reduced reperfusion injury.. Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. The animals were randomised into two groups. The treatment group received AT (250 U/kg) and the control group received placebo, after 7 min of CPR. Defibrillation was attempted after 9 min of CPR. If restoration of spontaneous circulation (ROSC) was achieved, the animals were observed for 4 h. Cortical cerebral blood flow was measured using laser-Doppler flowmetry. Cerebral oxygen extraction was calculated to reflect the relation between global cerebral circulation and oxygen demand. Measurements of eicosanoids (8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha)), AT, thrombin-antithrombin complex (TAT) and soluble fibrin in jugular bulb plasma were performed to detect any signs of cerebral oxidative injury, inflammation and coagulation.. There was no difference between the groups in cortical cerebral blood flow, cerebral oxygen extraction, or levels of eicosanoids, TAT or soluble fibrin in jugular bulb plasma after ROSC. In the control group reduction of AT began 15 min after ROSC and continued throughout the entire observation period (P < 0.05). Eicosanoids and TAT were increased compared to baseline in all animals (P < 0.01).. In this experimental model of CPR, AT administration did not increase cerebral circulation or reduce reperfusion injury after ROSC.

Topics: Animals; Antithrombin III; Antithrombins; Brain; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Dinoprost; Fibrin; Heart Arrest; Laser-Doppler Flowmetry; Oxygen Consumption; Peptide Hydrolases; Reperfusion Injury; Swine; Time Factors; Ventricular Fibrillation

Recovery of neurological function in patients following cardiac arrest and cardiopulmonary resuscitation (CPR) is a complex event. Free radical induced oxidative stress is supposed to be involved in this process. We studied levels of 8-iso-PGF2alpha (indicating oxidative injury) and 15-keto-dihydro-PGF2alpha (indicating inflammatory response) in venous plasma obtained from the jugular bulb in a porcine model of experimental cardiopulmonary resuscitation (CPR) where 2, 5, 8, 10 or 12 min of ventricular fibrillation (VF) was followed by 5 or 8 min of closed-chest CPR. A significant increase of 8-iso-PGF2alpha was observed immediately following restoration of spontaneous circulation in all experiments of various duration of VF and CPR. No such increase was seen in a control group. When compared between the groups there was a duration-dependent maximum increase of 8-iso-PGF2alpha which was greatest in animals subjected to the longest period (VF12 min + CPR8 min) of no or low blood flow. In contrast, the greatest increase of 15-keto-dihydro-PGF2alpha was observed in the 13 min group (VF8 min + CPR5 min). Thus, a time-dependent cerebral oxidative injury occurs in conjunction which cardiac arrest and CPR.

Topics: Animals; Brain; Brain Injuries; Cardiopulmonary Resuscitation; Dinoprost; Eicosanoids; F2-Isoprostanes; Female; Free Radicals; Heart Arrest; Inflammation; Male; Oxidative Stress; Radioimmunoassay; Swine; Time Factors; Ventricular Fibrillation

An investigation of the free radical scavenger sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) and the weak vasodilatator Tris buffer mixture (TBM) on cerebral cortical blood flow (CCBF) and the jugular bulb concentration of two eicosanoids, indicators of oxidative stress and inflammation, was undertaken in 30 anaesthetized piglets during cardiopulmonary resuscitation (CPR) and after restoration of spontaneous circulation (ROSC).. Thirty animals were subjected to 8 min of untreated circulatory arrest followed by 8 min of closed-chest CPR. During CPR, the animals were randomized to receive 60 mg/kg S-PBN, 1 mmol/kg TBM or 2 ml/kg normal saline (n = 10 in each group). Systemic haemodynamic variables, CCBF and jugular bulb plasma concentrations of 8-iso-PGF2alpha and 15-keto-dihydro-PGF2alpha were measured.. The CCBF during reperfusion after ROSC was greater in the TBM group than in the S-PBN group, the regression coefficient between CCBF and mean arterial blood pressure being lower in the S-PBN group than in the TBM group. The jugular bulb plasma concentration of 8-iso-PGF2alpha during the first 30 min after ROSC was greater in the TBM group than in the S-PBN group. Administration of TBM after vasopressin did not attenuate the pressor effect of vasopressin.. Administration of S-PBN during CPR results in less cerebral oxidative stress, possibly by promoting normal distribution of cerebral blood flow.

Topics: Animals; Blood Pressure; Brain; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Dinoprost; F2-Isoprostanes; Female; Heart Arrest; Hydrogen-Ion Concentration; Male; Oxidative Stress; Reperfusion Injury; Swine

We report the case of a 31-year-old woman who delivered twins by Caesarean section in whom atonic uterine haemorrhage developed 6 h postoperatively. During conservative treatment with the high-dose prostaglandin analogs sulprostone (PGE(2)) and dinoprost (PGF(2alpha)), acute pulmonary oedema and cardiac decompensation developed and, subsequently, the patient suffered cardiopulmonary arrest. After a 2h-period of cardiopulmonary resuscitation (CPR), it was possible to restore and stabilize circulation under the highest dose of catecholamines. Despite 2h of CPR, the patient was discharged from hospital 3 months later without any major physical or neurocognitive deficit.

Topics: Adult; Cardiopulmonary Resuscitation; Cesarean Section; Dinoprost; Dinoprostone; Female; Heart Arrest; Heart Failure; Heart Massage; Humans; Oxytocics; Postoperative Hemorrhage; Pregnancy; Pulmonary Edema; Uterine Contraction; Uterine Hemorrhage

In experimental cardiopulmonary resuscitation (CPR) aortic balloon occlusion, vasopressin, and hypertonic saline dextran administration improve cerebral blood flow. Free radical scavenger alpha-phenyl-N-tert-butyl-nitrone (PBN) and cyclosporine-A (CsA) alleviate neuronal damage after global ischemia. Combining these treatments, we investigated neurological outcome after experimental cardiac arrest.. : Thirty anesthetized piglets, randomly allocated into three groups, were subjected to 8 min of ventricular fibrillation followed by 5 min of closed-chest CPR. The combined treatment (CT) group received all the above-mentioned modalities; group B was treated with balloon occlusion and epinephrine; and group C had sham balloon occlusion with epinephrine. Indicators of oxidative stress (8-iso-PGF(2 alpha)), inflammation (15-keto-dihydro-PGF(2 alpha)), energy crisis (hypoxanthine and xanthine), and anoxia/hypoxia (lactate) were monitored in jugular bulb venous blood. Neurological outcome was evaluated 24 h after CPR.. : Restoration of spontaneous circulation (ROSC) was more rapidly achieved and neurological outcome was significantly better in the CT group, although there was no difference in coronary perfusion pressure between groups. The jugular venous PCO2 and cerebral oxygen extraction ratio were lower in the CT group at 5-15 min after ROSC. Jugular venous 8-iso-PGF(2 alpha) and hypoxanthine after ROSC were correlated to 24 h neurological outcome. : A combination of cerebral blood flow promoting measures and administration of alpha-phenyl-N-tert-butyl-nitrone and cyclosporine-A improved 24 h neurological outcome after 8 min of experimental normothermic cardiac arrest, indicating an ongoing neuronal injury in the reperfusion phase.

Topics: Angioplasty, Balloon, Coronary; Animals; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Cyclosporine; Dinoprost; Epinephrine; Free Radical Scavengers; Heart Arrest; Hypoxanthine; Lactic Acid; Nervous System Diseases; Saline Solution, Hypertonic; Swine; Treatment Outcome; Vasoconstrictor Agents; Vasopressins; Xanthine

In a porcine model of cardiopulmonary resuscitation (CPR), we investigated changes in the plasma levels of 8-iso-PGF(2alpha), a marker for oxidative injury, and 15-keto-dihydro-PGF(2alpha), an inflammatory response indicator during the post-resuscitation period after cardiac arrest. Twelve piglets were subjected to either 2 or 5 min (VF2 and VF5 group) of ventricular fibrillation (VF) followed by 5 min of closed-chest CPR. Six piglets without cardiac arrest were used as controls. In VF5 group, 8-iso-PGF(2alpha) in the jugular bulb plasma (draining the brain) increased four-fold. Jugular bulb 8-iso-PGF(2alpha) in the control group remained unchanged. The 15-keto-dihydro-PGF(2alpha) also increased four-fold in the VF5 group. Thus, 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) measurements in jugular bulb plasma may be used as biomarkers for quantification of free radical catalyzed oxidative brain injury and inflammatory response in reperfusion injury.

Topics: Animals; Biomarkers; Cardiopulmonary Resuscitation; Dinoprost; Disease Models, Animal; F2-Isoprostanes; Female; Free Radicals; Heart Arrest; Jugular Veins; Male; Molecular Structure; Myocardial Reperfusion Injury; Swine; Ventricular Fibrillation

Hypoxia and ischemia cause endothelial cell damage with consequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was tested.. Prospective, observational cohort study.. Emergency Department and general Intensive Care Unit in a city hospital.. Basic and advanced life support.. Forty-seven out-of-hospital cardiac arrest patients. The patients were classified into two groups, those who were resuscitated (n = 18) and those who died (n = 29).. Serial levels of platelet aggregation, thromboxane B2 (TXB2), 11-dehydro-TXB2 and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured. The results of measurements and demographic data were compared between the groups. Platelet counts decreased at the end of cardiopulmonary resuscitation (CPR), the decrease of the platelet counts showed statistical significance especially in the patients who died (p < 0.001). Platelet aggregation induced by adenosine diphosphate, epinephrine and collagen decreased to the lower limits of normal during and after CPR. Although high values of TXB2 and 11-dehydro-TXB2 continued throughout the study period in the resuscitated patients, 6-keto-PGF1 alpha decreased to the normal range (22.7 +/- 3.6 pg.ml-1. p < 0.05 at -24 h after arrival at the Emergency Department.. Platelet activation with the massive formation of thromboxane A2 (TXA2) occurs in patients with out-of-hospital cardiac arrest. Successful resuscitation is not associated with the balanced production of PGI2 against the TXA2 formation.

Topics: Aged; Analysis of Variance; Cardiopulmonary Resuscitation; Chi-Square Distribution; Cohort Studies; Dinoprost; Female; Heart Arrest; Humans; Male; Middle Aged; Platelet Activation; Prospective Studies; Prostaglandins F; Reperfusion Injury; Thromboxane A2

To assess differences in plasma prolactin and prostaglandin concentrations in resuscitated and nonresuscitated patients during cardiopulmonary resuscitation (CPR), and to compare changes of prostaglandin and prolactin concentrations with hemodynamic variables in the immediate postresuscitation phase.. Prospective, descriptive study.. Emergency medical service at a university hospital.. Twenty-nine patients ranging in age from 39 to 87 yrs with out-of-hospital cardiac arrest.. Venous blood samples were taken during CPR and at 5, 15, 30, and 60 mins after restoration of spontaneous circulation in order to measure plasma concentrations of prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 by immunoassay. Heart rate and blood pressure were measured at 5, 15, 30, and 60 mins after restoration of spontaneous circulation.. In 15 patients, restoration of spontaneous circulation was achieved; in the remaining 14 patients, successful resuscitation was not possible. During CPR, the mean plasma prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 concentrations were 95.9 +/- 13.6 micrograms/L, 357 +/- 61 ng/L, 228 +/- 28 ng/L, 277 +/- 66 ng/L, and 375 +/- 78 ng/L, respectively, in resuscitated patients, and 23.9 +/- 5.6 micrograms/L (p = .0001), 192 +/- 22 ng/L (p = .005), 202 +/- 31 ng/L (p = .528), 221 +/- 40 ng/L (p = .713), and 344 +/- 77 ng/L (p = .780), respectively, in nonresuscitated patients. At 60 mins after restoration of spontaneous circulation, the mean plasma prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 concentrations were 50.1 +/- 9.5 micrograms/L, 306 +/- 42 ng/L, 503 +/- 87 ng/L, 278 +/- 55 ng/L, and 355 +/- 30 ng/L, respectively. Mean values of systolic arterial blood pressure were 114 +/- 12 mm Hg at 30 mins and 123 +/- 18 mm Hg at 60 mins. No significant correlations were found between hemodynamic values and plasma concentrations of prolactin or prostaglandins.. Prolactin and prostaglandin concentrations were increased during cardiac arrest and CPR. Successful initial resuscitation was associated with increased prolactin and prostaglandin F2 alpha concentrations during CPR. Decreased concentrations in non-resuscitated patients may have been a result of exhaustion of the neuroendocrine and eicosanoid systems, or may be due to differences in bioavailability at the site of blood sampling based upon differences in hemodynamics.

Topics: Adult; Aged; Aged, 80 and over; Cardiopulmonary Resuscitation; Dinoprost; Female; Heart Arrest; Hemodynamics; Humans; Male; Middle Aged; Prolactin; Prospective Studies; Thromboxane B2; Time Factors; Treatment Failure

Topics: Abortion, Induced; Brain Injuries; Dinoprost; Drug Industry; Expert Testimony; Female; Heart Arrest; Humans; Illinois; Malpractice; Nursing Staff, Hospital; Pregnancy; Pregnancy Trimester, Second; Resuscitation

Topics: Animals; Brain; Dinoprost; Heart Arrest; Male; Prostaglandins D; Radioimmunoassay; Rats; Rats, Inbred Strains; Resuscitation; Thromboxane B2

Prostaglandins are mainly used in clinical medicine for midterm abortion and to terminate pregnancy. Systemic adverse reactions include nausea and vomiting, which occur in approximately half of the patients and, to a lesser extent, diarrhea. Although bronchospasm occurs infrequently, PGF2 should be avoided in asthmatics. Cardiorespiratory failure culminating in prolonged coma and death has been reported. Moreover, convulsions and EEG changes have been observed in a comparatively small number of cases.

Topics: Abortifacient Agents; Abortion, Induced; Bronchial Spasm; Diarrhea; Dinoprost; Dinoprostone; Female; Heart Arrest; Humans; Pregnancy; Prostaglandins; Prostaglandins E; Prostaglandins E, Synthetic; Prostaglandins F; Seizures; Vomiting