pituitrin and Epilepsy--Tonic-Clonic

In a porcine model, we compared the efficacy of epinephrine, vasopressin, or the combination of epinephrine and vasopressin with that of saline placebo on the survival rate after bupivacaine-induced cardiac arrest. After the administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 3 +/- 1 min (mean +/- SD) until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of cardiac arrest. After 2 min of CPR, 28 animals received, every 5 min, epinephrine; vasopressin; epinephrine combined with vasopressin; or placebo i.v.. Three minutes after each drug administration, up to 3 countershocks (3, 4, and 6 J/kg) were administered; all subsequent shocks were 6 J/kg. Blood was drawn throughout the experiment for the determination of plasma bupivacaine concentration. In the vasopressin/epinephrine combination group, all pigs survived (P < 0.01 versus placebo); in the vasopressin group 5 of 7, in the epinephrine group 4 of 7, and in the placebo group none of 7 swine survived. The plasma concentration of total bupivacaine showed no significant difference among groups. In this model of bupivacaine-induced cardiac arrest, CPR with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group.. Although cardiovascular collapse occurs mostly immediately after rapid injection of a local anesthetic in the presence of anesthesiologists, resuscitation may be difficult, and the outcome is usually poor. In this model of bupivacaine-induced cardiac arrest, cardiopulmonary resuscitation with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group.

Topics: Anesthetics, Local; Animals; Bupivacaine; Cardiac Output; Drug Combinations; Epilepsy, Tonic-Clonic; Epinephrine; Female; Heart Arrest; Hemodynamics; Injections, Intravenous; Male; Survival; Swine; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

The time course and extent of changes in plasma prolactin, noradrenaline, vasopressin and oxytocin levels is reported following serial observations of a prolonged epileptic seizure arising in the temporal lobe, recorded by video-EEG-telemetry, in which the epileptic activity evolved from a simple partial to complex partial to secondarily generalised attack. The prolactin levels were markedly elevated during the phase of the simple partial seizure, at a time when consciousness was preserved, when motor activity was minimal and when EEG activity was highly localised. The hormonal levels continued to rise during the subsequent seizure evolution, suggesting that the duration (or intensity) of the seizure is an important, perhaps the most important, factor determining the degree of prolactin release during limbic seizures. Indeed, the prolactin elevation in this case (26 times the baseline level) is higher than any previously recorded, reflecting the unusual duration and intensity of this seizure. We did not observe the phenomenon of "exhaustion" of prolactin release and levels peaked after 49 min, and were high for over 2 h after the onset of the seizure, and after the convulsion had ceased. The concentrations of vasopressin, oxytocin and noradrenaline remained low during the aura, but rapidly increased during the phase of generalisation. The oxytocin and noradrenaline levels peaked during the phase of generalised convulsion, but the vasopressin levels peaked well into the post ictal phase, and remained high for several hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Electroencephalography; Epilepsies, Partial; Epilepsy, Temporal Lobe; Epilepsy, Tonic-Clonic; Evoked Potentials; Female; Humans; Hypothalamus; Limbic System; Monitoring, Physiologic; Neural Inhibition; Norepinephrine; Oxytocin; Prolactin; Temporal Lobe; Vasopressins

Topics: Animals; Enkephalin, Methionine; Epilepsy, Tonic-Clonic; Immunohistochemistry; Male; Neuropeptides; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Vasopressins

A patient with acute lymphocytic leukemia is described who developed meningeal leukemia 14 months after the initial diagnosis was made. As part of his antileukemic therapy, at that time, he received prednisone and vincristine, given prophylactically to maintain a bone marrow remission. He inadvertently received 15 mg of vincristine instead of 1.5 mg. Following this overdosage he developed pancytopaenia, mild neurotoxicity and subsequently a grand mal seizure associated with the delayed onset of hyponatremia. This was presumed to be due to the inappropriate secretion of antidiuretic hormone (ADH) secondary to vincristine toxicity. This responded to fluid restriction and anti-epileptiform therapy.

Topics: Adolescent; Anemia, Aplastic; Epilepsy, Tonic-Clonic; Humans; Hyponatremia; Male; Medication Errors; Peripheral Nervous System Diseases; Vasopressins; Vincristine

Topics: Adult; Body Water; Body Weight; Diuresis; Epilepsy, Tonic-Clonic; Female; Furosemide; Humans; Hypertonic Solutions; Hyponatremia; Injections, Intravenous; Male; Osmolar Concentration; Potassium; Potassium Chloride; Sodium; Sodium Chloride; Syndrome; Urine; Vasopressins

Topics: Adult; Craniocerebral Trauma; Epilepsy, Tonic-Clonic; Hematoma, Subdural; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Vasopressins

Topics: Child; Coma; Epilepsy, Tonic-Clonic; Humans; Hyponatremia; Hypotension; Leukemia, Lymphoid; Male; Reflex, Abnormal; Vasopressins; Vincristine

Topics: Adult; Body Weight; Diabetic Retinopathy; Epilepsy, Tonic-Clonic; Female; Humans; Hyponatremia; Male; Middle Aged; Palliative Care; Pituitary Gland; Postoperative Complications; Tremor; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adrenal Glands; Adrenocorticotropic Hormone; Epilepsy, Tonic-Clonic; Female; Humans; Hypothalamo-Hypophyseal System; Male; Metyrapone; Phenytoin; Pituitary Gland; Vasopressins