pituitrin and Hypothermia

To determine the rate of return of spontaneous circulation (ROSC) in animal models performing resuscitation from induced ventricular fibrillation (VF) in severe hypothermia (<30 degrees C).. A medical literature database search from 1966 to present was performed identifying placebo controlled trials using anti-arrhythmic or vasopressor medications to treat ventricular fibrillation in the setting of severe hypothermia.. 7 controlled studies were identified (n=117) testing 6 combinations of resuscitative medications. ROSC rates for treatment versus control groups were as follows: amiodarone (6% vs. 18%, p=0.6, n=34), bretylium (35% vs. 35%, p=1.0, n=40), intermediate- and high-dose epinephrine (adrenaline) (36% vs. 27%, p=1.0, n=22), vasopressin (60% vs. 0%, p<0.0001, n=39), vasopressin and amiodarone (0% vs. 0%, p=NS, n=11), low-dose epinephrine and amiodarone (91% vs. 30%, p=0.0075, n=21). Cumulatively, among all studies administering vasopressors, the rate of ROSC was 62% in treatment groups contrasted to 17% in control groups (p<0.0001, n=77).. In controlled animal models of severe hypothermia, ROSC rates for induced ventricular fibrillation are higher with utilization of vasopressor medications. Current guidelines which recommend withholding these medications in the setting of hypothermic cardiac arrest should be re-evaluated.

Topics: Animals; Anti-Arrhythmia Agents; Disease Models, Animal; Hypothermia; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation

Hypothermia preserves gastric mucosal microvascular oxygenation (μHbO2) during hemorrhagic shock. Additionally, hypothermia activates the sympathetic nervous system that leads to the release of vasopressin. The aim of this study was to evaluate whether the effect of hypothermia is mediated via the sympathetic nervous system and/or via vasopressin.. In prospective and randomized experiments on five anesthetized dogs (foxhounds, cross-over design, 6 groups with n=5 per group) we analyzed the effects of hemorrhage on μHbO2 during mild hypothermia (HT, 34 °C), during additional thoracic epidural anesthesia (HT/TEA) and during additional vasopressin V1 receptor blockade (HT/VB). As control groups, effects of hemorrhage were studied under normothermia alone (NT), during additional thoracic epidural anesthesia (NT/TEA) and during additional vasopressin V1 receptor blockade (NT/VB).. Hemorrhage decreased μHbO2 from 81 ± 3 to 49 ± 8%. In contrast, in the presence of hypothermia, μHbO2 was significantly higher during hemorrhagic shock (from 79 ± 3 to 66 ± 9%) despite a similar decrease in DO2. The effect of hypothermia on μHbO2 was reduced in the presence of thoracic epidural anesthesia or vasopressin receptor blockade.. Hypothermia preserves μHbO2 during hemorrhagic shock. This effect is partially abolished during thoracic epidural anesthesia or during vasopressin receptor blockade. The sympathetic nervous system and the vasopressin V1 receptor are partially involved in mediating the effect of hypothermia on gastric oxygenation during hemorrhage.

Topics: Anesthesia, Epidural; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Dogs; Female; Gastric Mucosa; Hemorrhage; Hypothermia; Lidocaine; Oxygen; Sympathetic Nervous System; Vasopressins

Topics: Accidents, Traffic; Adult; Brain Edema; Brain Injuries; Catecholamines; Fatal Outcome; Glasgow Coma Scale; Hematoma, Subdural; Humans; Hyperglycemia; Hyperkalemia; Hypokalemia; Hypothermia; Insulin; Intracranial Hypertension; Male; Mannitol; Norepinephrine; Potassium; Vasopressins

To report a cardiopulmonary resuscitation attempt in a 20-month-old child employing a combination of vasopressin and epinephrine.. Case report.. Out-of-hospital cardiopulmonary resuscitation.. A 20-month-old child found in cardiac arrest after submersion.. Dispatcher-assisted basic life support was initiated immediately after pulling the child out of the water. The emergency medical service crew arrived approximately 6 mins later and found a hypothermic, cyanotic child in cardiocirculatory arrest. The first electrocardiogram showed sinus bradycardia. After intubation and administration of epinephrine and atropine with no effect, an intravenous bolus of 0.2 mg of epinephrine and 10 IU of vasopressin resulted in restoration of spontaneous circulation. The boy was flown to a hospital and was discharged 23 days later to a rehabilitation facility. He returned home 6 months after the accident, where further rehabilitation efforts are pending.. Bystander cardiopulmonary resuscitation, early and aggressive advanced life support, rewarming, and the combination of intravenous epinephrine and vasopressin were associated with sustained return of spontaneous circulation following hypothermic submersion-associated cardiac arrest.

Topics: Cardiopulmonary Resuscitation; Drug Therapy, Combination; Epinephrine; Heart Arrest; Humans; Hypothermia; Infant; Male; Near Drowning; Vasoconstrictor Agents; Vasopressins

Recent animal data have challenged the common clinical practice to avoid vasopressor drugs during hypothermic cardiopulmonary resuscitation (CPR) when core temperature is below 30 degrees C. In this report, we describe the case of a 19-year-old-female patient with prolonged, hypothermic, out-of-hospital cardiopulmonary arrest after near drowning (core temperature, 27 degrees C) in whom cardiocirculatory arrest persisted despite 2 mg of intravenous epinephrine; but, immediate return of spontaneous circulation occurred after a single dose (40 IU) of intravenous vasopressin. The patient was subsequently admitted to a hospital with stable haemodynamics, and was successfully rewarmed with convective rewarming, but died of multiorgan failure 15 h later. To the best of our knowledge, this is the first report about the use of vasopressin during hypothermic CPR in humans. This case report adds to the growing evidence that vasopressors may be useful to restore spontaneous circulation in hypothermic cardiac arrest patients prior to rewarming, thus avoiding prolonged mechanical CPR efforts, or usage of extracorporeal circulation. It may also support previous experience that the combination of both epinephrine and vasopressin may be necessary to achieve the vasopressor response needed for restoration of spontaneous circulation, especially after asphyxial cardiac arrest or during prolonged CPR efforts.

Topics: Adult; Blood Circulation; Cardiopulmonary Resuscitation; Epinephrine; Fatal Outcome; Female; Heart Arrest; Hemodynamics; Humans; Hypothermia; Multiple Organ Failure; Near Drowning; Rewarming; Vasoconstrictor Agents; Vasopressins

Aim of this experimental animal study was to investigate the influence of vasopressin and amiodarone on cardiopulmonary resuscitation (CPR) outcome in a pig model of hypothermic cardiac arrest.. After surface cooling to a core temperature of 26 degrees C, ventricular fibrillation was induced in 14 12-16-week-old domestic pigs. After 15 min of untreated cardiac arrest, a manual closed chest CPR was started and pigs were randomly assigned to two treatment groups: Group 1 pigs (n = 7) received vasopressin 0.4 U kg-1 as initial drug therapy, followed by a combination vasopressin (0.4 U kg-1) and amiodarone (4 mg kg-1) as subsequent drug therapy. Subsequent drug therapy was administered in animals without permanent restoration of spontaneous circulation after a first series of electrical countershocks 10 min after drug administration. Group 2 pigs (n = 7) received saline placebo as initial drug therapy and saline placebo and amiodarone (4 mg kg-1) as subsequent drug therapy.. Vasopressin significantly increased coronary perfusion pressure and defibrillation success (successful defibrillation in five of seven Group 1 vs. none of seven Group 2 pigs, P = 0.02). Due to refibrillation within 30-150 s, the 60-min survival rate was not improved by vasopressin. Subsequent drug therapy with amiodarone had no further effect on defibrillation success or the refibrillation rate.. Data from this experimental animal model suggest that vasopressin and amiodarone may not be beneficial for treatment of ventricular fibrillation associated with severe hypothermia when concomitant measures at core rewarming are not applied.

Topics: Amiodarone; Animals; Blood Pressure; Cardiopulmonary Resuscitation; Coronary Vessels; Disease Models, Animal; Heart Arrest; Hypothermia; Survival Rate; Swine; Vasopressins

The aim of the present study was to examine whether minimizing plasma volume loss due to cold-induced diuresis can increase the survival time of rats maintained in long-term stable hypothermia (~24 h at a body temperature of 19 degrees C). Infusion of desmopressin (0.5-2.0 microg), a potent antidiuretic agent, during the cooling period enhanced survival over saline controls in a dose-related manner. The enhanced survival was accompanied by a significant delay in the expected increase of hematocrit and decrease of plasma volume as compared with those seen in saline controls. In contrast, treating the rats with the same dose range of another vasopressin analog, [beta-mercapto-beta,beta-cyclopentamethyl enepropionyl]-vasopressin, which has no antidiuretic action, failed to enhance survival over saline control. Further, treating the rats with the optimal dose of desmopressin (1 microg) at the later stage of hypothermia failed to elicit any beneficial effect. Our results indicate that by using desmopressin early during the cooling phase of the hypothermia, plasma volume and rheological parameters important for sustaining microcirculation can be better maintained than those seen in saline controls. These improvements may have contributed to the observed longer survival time in hypothermia.

Topics: Animals; Deamino Arginine Vasopressin; Diuresis; Hematocrit; Hypothermia; Infusions, Intravenous; Male; Microcirculation; Plasma Volume; Rats; Rats, Sprague-Dawley; Renal Agents; Rheology; Survival Rate; Time Factors; Vasopressins

During hypothermic cardiopulmonary resuscitation with a body core temperature <30 degrees C administration of a vasopressor to support coronary perfusion pressure is controversial. The purpose of the current study was to assess the effects of a single 0.4-unit/kg dose of vasopressin on coronary perfusion pressure, defibrillation success, and 1-hr survival in a pig model of hypothermic closed-chest cardiopulmonary resuscitation combined with rewarming.. Prospective, randomized study in an established pig model.. University hospital research laboratory.. Fifteen 12- to 16-wk-old domestic pigs.. Pigs were surface cooled to a body core temperature of 26 degrees C and ventricular fibrillation was induced. After 15 mins of untreated cardiac arrest, manual closed-chest cardiopulmonary resuscitation and thoracic lavage with 40 degrees C warmed tap water were started. After 3 mins of external chest compression, animals were assigned randomly to receive vasopressin (0.4 units/kg, n = 8; or saline placebo, n = 7). Defibrillation was attempted 10 mins after drug administration.. Compared with saline placebo treated-animals, coronary perfusion pressure in vasopressin-treated pigs was significantly higher 90 secs (36 +/- 5 mm Hg vs. 7 +/- 4 mm Hg, p =.000) to 10 mins (24 +/- 4 mm Hg vs. 8 +/- 4 mm Hg, p =.000) after drug administration. Restoration of spontaneous circulation and 1 hr survival were significantly higher in vasopressin animals compared with saline placebo (8 of 8 vasopressin pigs vs. 0 of 7 placebo pigs, p <.001).. A single 0.4-unit/kg dose of vasopressin administered at a body core temperature <30 degrees C significantly improved defibrillation success and 1-hr survival in a pig model of hypothermic cardiopulmonary resuscitation.

Topics: Animals; Cardiopulmonary Resuscitation; Hypothermia; Lactates; Rewarming; Swine; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo.. Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.

Topics: Animals; Blood Pressure; Body Temperature; Cardiopulmonary Resuscitation; Coronary Circulation; Epinephrine; Female; Heart Arrest; Hypothermia; Male; Swine; Vasoconstrictor Agents; Vasopressins

The aim of this study was to investigate whether the increased diuresis in consequence of hypothermia is due to a depression of the hypothalamic release of antidiuretic hormone (ADH). The plasma concentration of antidiuretic hormone and the effect of intravenous (i.v.) administration of 65 ng kg-1 desmopressin (selective V2-receptor agonist) were determined in the anaesthetized rat. In spite of a 50% (P < 0.001) decrease in glomerular filtration rate, urine flow increased sixfold (P < 0.01) and urine sodium excretion increased sevenfold (P < 0.05), whereas urine osmolality decreased (P < 0.001). At the same time plasma antidiuretic hormone decreased from 7.5 +/- 1.1 to 3.8 +/- 0.4 pg mL-1 (P = 0.01). After injection of desmopressin urine flow was completely restored, whereas urine osmolality and sodium excretion were only partially normalized. Since tubular conservation of water and fractional water reabsorption decreased during hypothermia, the diuresis must have resulted from an augmented loss of water. This is further supported by the fact that osmolal excretion was not influenced either by hypothermia or by desmopressin. It is concluded that the diuresis in consequence to hypothermia is due both to a decrease in the release of ADH and to a reduction of renal medullary hypertonicity.

Topics: Anesthesia; Animals; Blood Pressure; Cold Temperature; Deamino Arginine Vasopressin; Diuresis; Glomerular Filtration Rate; Hypothermia; Injections, Intraperitoneal; Kidney; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Vasopressins

Previously, we have reported that intravenous administration of bacterial endotoxin (lipopolysaccharide, LPS) in rats kept at a subthermoneutral ambient temperature of 24 degrees C results in a fall in colonic temperature that involved the release of antipyretic products by peripheral macrophages. Here, we demonstrate that treatment of rats with a biologically active antiserum to tumor necrosis factor (TNF) markedly attenuates the hypothermia in response to administration of LPS (0.5 mg/kg). Moreover, this hypothermia was prevented by central injection of a selective antagonist of V1 vasopressin receptors, dPTyr(Me) arginine vasopressin (AVP; 2 micrograms icv). AVP is thought to act as an antipyretic in the ventral septal area (VSA) of the brain. Because the AVP content of this area has been shown to be eliminated after long-term castration, we have tested the hypothesis that castration would attenuate the hypothermia in response to administration of LPS. Castrated rats displayed a markedly less hypothermic response than age-matched controls in response to administration of LPS. We conclude that hypothermia in response to intravenous injection of LPS involves the release of TNF from peripheral macrophages. Moreover, our results are consistent with the possibility that androgen-dependent vasopressinergic neurons in the VSA are mediating the hypothermia in response to intravenous administration of LPS.

Topics: Animals; Arginine Vasopressin; Endotoxins; Escherichia coli; Hypothermia; Injections, Intraventricular; Lipopolysaccharides; Male; Orchiectomy; Rabbits; Rats; Rats, Wistar; Tumor Necrosis Factor-alpha; Vasopressins

We describe a 71 year old man with a neurodegenerative condition who developed chronic inappropriate antidiuretic hormone secretion and hypothermia resulting in recurrent episodes of impaired consciousness. This combination of abnormalities is attributable to hypothalamic disease and has not to our knowledge been previously reported with clearly documented antidiuretic hormone excess.

Topics: Aged; Chronic Disease; Demyelinating Diseases; Humans; Hyponatremia; Hypothermia; Male; Vasopressins; Water Intoxication

Topics: Animals; Body Weight; Dehydration; Drinking Behavior; Environment, Controlled; Environmental Exposure; Feeding Behavior; Hypothermia; Hypoxia; Kidney; Kidney Concentrating Ability; Male; Organ Size; Osmolar Concentration; Oxygen Consumption; Rats; Regression Analysis; Time Factors; Urination; Vasopressins; Water

Topics: Agenesis of Corpus Callosum; Cerebral Ventriculography; Child; Child, Preschool; Diabetes Insipidus; Drinking Behavior; Dwarfism, Pituitary; Electroencephalography; Epilepsy; Humans; Hypothermia; Male; Puberty, Precocious; Recurrence; Vasopressins

Topics: Aminohippuric Acids; Animals; Dogs; Hypothermia; Inulin; Kidney; Kidney Concentrating Ability; Osmolar Concentration; Potassium; Sodium; Urea; Urine; Vasopressins; Water; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Body Temperature; Hypophysectomy; Hypothermia; Hypothermia, Induced; Pharmacology; Rats; Research; Vasopressins

Topics: Angiotensins; Blood Pressure; Endocrinology; Hypophysectomy; Hypothermia; Hypothermia, Induced; Pharmacology; Rats; Renin; Research; Vasopressins

Topics: Blood Pressure; Heart; Histamine; Hypophysectomy; Hypothermia; Hypothermia, Induced; Kidney; Perfusion; Pharmacology; Rats; Research; Serotonin; Vasopressins

Topics: Arginine Vasopressin; Biomedical Research; Humans; Hypothermia; Hypothermia, Induced; Mental Disorders; Surgical Procedures, Operative; Vasopressins