dinoprost and Cardiac-Output--Low

Diabetic patients manifest an increased incidence of heart failure (HF) after myocardial infarction (MI), which presages an increase in morbidity and mortality. Although oxidative stress has been implicated in diabetic complications, oxidative stress status associated with comorbid conditions that frequently accompany diabetes remains unknown. Therefore, we examined antioxidants and oxidative stress in the surviving myocardium in relation to ventricular function during diabetic HF following MI. MI was produced in diabetic and nondiabetic rats by ligation of the left coronary artery. At 4 weeks post-MI, LV systolic pressure (LVSP), rate of pressure rise (+dP/dt), and rate of pressure decay (-dP/dt) were depressed to a significantly greater extent in diabetic compared to nondiabetic MI animals. Higher levels of myocardial 8-isoprostane (8-iso PGF(2alpha)), oxidized glutathione (GSSG), as well as greater upregulation of superoxide dismutase (SOD) and catalase (CAT) protein expression paralleled by increases in enzymatic activity was observed in the diabetic MI animals, indicating higher oxidative stress. These data demonstrate a greater derangement of oxidative stress in the surviving tissues of diabetic post-MI rat hearts concomitant with an increased functional severity of HF, and suggest that chronic antioxidant therapy may be useful for the prophylaxis of subsequent HF after MI associated with diabetes.

Topics: Animals; Antioxidants; Cardiac Output, Low; Catalase; Diabetes Mellitus, Experimental; Diabetic Angiopathies; Dinoprost; Glutathione Disulfide; Male; Myocardial Infarction; Myocardium; Oxidative Stress; Proteins; Rats; Rats, Sprague-Dawley; Superoxide Dismutase

Topics: Aged; Biomarkers; Cardiac Output, Low; Cardiac Surgical Procedures; Coronary Artery Bypass; Dinoprost; F2-Isoprostanes; Female; Heart Valve Prosthesis Implantation; Humans; Male; Postoperative Complications

A case of severe reaction to extraamniotically administered prostaglandin F2 alpha, with cardiorespiratory collapse and pulmonary oedema necessitating transfer to an intensive care unit, is presented. Attention is drawn to the profound haemodynamic effects of systemically administered prostaglandin, and the need for caution and ready availability of facilities for resuscitation when this potent substance is administered. Treatment for the effects of intravascular absorption of prostaglandin F2 alpha is discussed.. A case of severe vasoconstriction treated as cardiorespiratory collapse in a woman given extraamniotic PGF2alpha for midtrimester abortion is described, with comments on management of this rare reaction. The patient was having elective termination because of confirmed spina bifida with hydrocephalus by ultrasound and elevated AFP at 18 weeks gestation. She was given a 4 mg test dose of PGF2alpha (Dinoprost, Upjohn Pty, Ltd) in viscous gel (Tylose MH300, Hoechst Australia Ltd) via extraamniotic Foley catheter. She immediately developed dyspnea, abdominal and breast pain, hypotension of 50 mm Hg systolic, peripheral vasoconstriction, cyanosis and confusion. She was treated with iv Hartmann's solution 600 ml, oxygen 8 1/min, and sc adrenaline 1/1000 0.5 ml. She seemed to improve after receiving 500 ml 3.5% polygeline colloid (Haemaccel, Behringwerke AG), and 5 ml 1/10,000 adrenaline iv, as her systolic blood pressure rose to 70 mm Hg measured indirectly. 500 ml more iv colloid was given, and blood pressure rose to 90 mm Hg. Then she suddenly deteriorated with florid pulmonary edema. Oxygen saturation fell and positive pressure ventilation was begun. She was given furosemide 160 mg iv and hydrocortisone 500 mg iv. Anaphylactic reaction was ruled out on the basis of blood count; amniotic fluid embolism was ruled out because of minor changes in clotting parameters. The events seen here most likely occurred as a result of inadvertent injection of PGF2alpha into the arterial circulation, causing increased pulmonary arterial pressure and vascular resistance, systemic vasoconstriction interpreted as hypotension, all exacerbated by adrenaline and exogenous fluid load. Severe hypertension after extraamniotic PGF2alpha has been reported before in a similar case of apparent hypotension treated with agents to increase blood pressure. PGF2a should not be used without facilities to treat such adverse reactions.

Topics: Abortion, Therapeutic; Adult; Cardiac Output, Low; Dinoprost; Female; Humans; Pregnancy; Pregnancy Complications, Cardiovascular; Pregnancy Trimester, Second; Pulmonary Edema; Respiratory Insufficiency

A case report is presented of a parturient who suffered severe hypotension and pulmonary oedema following an overdose of intramyometrial prostaglandin F2 alpha. Oxytocin induction of labour in this patient led to a rapid delivery, followed by a hypotonic uterus and postpartum haemorrhage. After resuscitation with blood and crystalloid fluids, the uterus was explored under general anaesthesia. The uterus was free of retained products but the lower uterine segment failed to contract despite bimanual uterine compression and intravenous oxytocin. Prostaglandin F2 alpha was injected into the lower uterine segment via a transvaginal approach. This was rapidly followed by cardiovascular collapse and later by pulmonary oedema. The differential diagnosis and subsequent management are discussed.

Topics: Adult; Cardiac Output, Low; Dinoprost; Female; Humans; Hypotension; Injections; Myometrium; Postpartum Hemorrhage; Pregnancy; Pulmonary Edema