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Biomedical subjects

J H Milde

Publications and source records attributed to J H Milde.

82 records · Page 5Linked to original sources
PubMed1976

Porcine malignant hyperthermia induced by halothane and succinylcholine: failure of treatment with procaine or procainamide.

Metabolic, hemodynamic and neuroendocrine responses to the combined use of halothane and succinylcholine (SCh) were measured in five normal swine and five swine susceptible to malignant hyperthermia (MH). Constant-volume ventilation was used, and no therapy was instituted. The overall response in susceptible swine was fulminant, in that it involved the rapid onset of SCh-induced MH combined with the more severe metabolic, endocrine, and cardiovascular effects of halothane-induced MH. Maximal changes in VO2 were equivalent with either drug or both combined, while changes in lactate, potassium (K+), pH, and catecholamines were perhaps synergistic. Utilizing similar measurements, procaine or procainamide was used in 20 susceptible swine in attempts to prevent MH initiated by halothane, SCh, or both. Recommended therapeutic doses of either drug did not prevent characteristic MH changes in oxygen consumption, cardiac output, lactate, K+, pH, catecholamines, or temperature.

Animals↗
PubMed1976

Dantrolene in porcine malignant hyperthermia.

The effectiveness of intravenous administration of dantrolene in prevention and treatment of fulminant malignant hyperthermia (MH) initiated by halothene and succinylcholine (SCh) in genetically susceptible swine was assessed. In six animals, prior administration of dantrolene in doses of 5 mg/kg or more prevented MH, while 1 or 3 mg/kg attenuated MH, and 0.1 mg/kg had no effect. In ten additional swine, therapy was not started until MH was fulminant. Five of these were then given supportive therapy only (discontinuation of anesthesia, hyperventilation with oxygen, surface cooling, and NaHCO3). The remaining five received the same supportive therapy, plus dantrolene (7.5 mg/kg). With supportive therapy only, arterial blood pH, Po2 and Pco2 returned toward normal, but oxygen consumption (Vo2), blood lactate, potassium (K+), catecholamines, and temperature continued to increase and the course of MH was unaltered. When dantrolene was added to supportive therapy, Vo2, lactate, K+, catecholamines, and temperature decreased, and the course of MH was dramatically slowed and, apparently, reversed.

Animals↗
PubMedDate not supplied

Failure of flunarizine to improve cerebral blood flow or neurologic recovery in a canine model of complete cerebral ischemia.

Ten minutes of cerebral ischemia was produced in 12 dogs by temporary ligation of the venae cavae and aorta. After reperfusion the dogs received the calcium entry blocker, flunarizine, 6 micrograms/kg infused over a ten minute period. Cerebral blood flow (CBF) and metabolism (CMRO2) were measured pre-ischemia and for 2 h post-ischemia in 6 dogs. At the end of the study brain biopsies were analyzed for cerebral metabolites. Neurologic recovery was evaluated for up to 48 h post-ischemia in an additional 6 dogs. The results of each study were compared to those previously obtained in untreated animals. The cerebral blood flows (when expressed as a percent of the pre-ischemic control value) of the flunarizine-treated and untreated groups were similar throughout the post-ischemic period. Following an initial hyperemia, the CBF fell to significantly less than the pre-ischemic control values, and remained approximately 26% of control during the final 90 min in both groups. The CMRO2 was also the same for both groups. Cerebral metabolites were similar although abnormal in both groups. Flunarizine produced pulmonary edema in 5 of 6 dogs studied for neurologic recovery. Four of these dogs died within 12 h and another dog demonstrated severe neurologic damage. None of the untreated dogs developed pulmonary edema, but 6 of 7 dogs evidenced severe neurologic damage or were dead at 48 h. Thus, flunarizine failed to improve either cerebral blood flow or neurologic outcome when given after complete cerebral ischemia in the dog. A cardiodepressive effect of flunarizine might have contributed to the poor neurologic outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Failure of deferoxamine, an iron chelator, to improve neurologic outcome following complete cerebral ischemia in dogs.

Eleven minutes of complete cerebral ischemia was produced in 17 dogs by temporary ligation of the venae cavae and aorta. Immediately prior to the ischemic episode, 7 dogs received deferoxamine, an iron chelator, 50 mg/kg i.v., and 10 dogs received an equivalent volume of saline placebo i.v. Five dogs failed to meet preestablished protocol criteria and were excluded from data analysis. Neurologic recovery was evaluated by an observer blind to the treatment groups in the remaining 12 dogs at 48 hours postischemia. The neurologic effects of complete cerebral ischemia were compared between dogs treated with deferoxamine and those receiving placebo treatment. One of 6 deferoxamine-treated dogs was normal and 5 were moderately to severely damaged. Similarly, 1 of 6 placebo-treated dogs was normal and 5 were moderately to severely damaged. The authors conclude that deferoxamine does not provide cerebral protection in this model of complete cerebral ischemia.

Animals↗
PubMedDate not supplied

Influence of anesthetics on metabolic, functional and pathological responses to regional cerebral ischemia.

Regional cerebral ischemia was produced by common carotid artery occlusion in gerbils and by middle cerebral artery occlusion in dogs, cats, and squirrel monkeys. Anesthesia was induced with either pentobarbital or halothane and maintained for two to three hours after vessel occlusion. In acute studies, the effect of regional cerebral ischemia on cerebral concentrations of ATP, phosphocreatine, lactate, and pyruvate was determined at the end of this period in gerbils, cats, and squirrel monkeys. In chronic studies, the degree of neurological deficit and size of cerebral infarction were determined 48 hours after a two-hour to three-hour period of vessel occlusion in cats and squirrel monkeys and permanent occlusion in dogs. In gerbils, dogs, and cats, there were no differences in the metabolis, functional, or pathological effects of anesthesia with pentobarbital or halothane. However, in the squirrel monkey, in acute studies the metabolic alterations were significantly less with pentobarbital, and in chronic studies the frequency and magnitude of functional deficits and cerebral infarction were significantly less. We conclude that pentobarbital does provide a degree of protection during regional cerebral ischemia but that such effects are only consistently demonstrable in primates. In nonprimates, we assume that variability in the collateral circulation renders demonstration of significant differences difficult or impossible.

Adenosine Triphosphate↗
PubMedDate not supplied

Failure of prolonged hypocapnia, hypothermia, or hypertension to favorably alter acute stroke in primates.

The effects of induced hypocapnia, hypothermia, and hypertension were surveyed in a primate model of acute stroke during and following a 48-hour period of intensive care. The results were compared to a group of nine control animals previously studied. Hypocapnia (PaCO2=25 torr) was examined in five animals and did not appear to alter the expected mortality, degree of neurological deficit, or frequency of infarction. There was, however, a suggestion that the size of infarction may be reduced. Hypothermia (29 degrees C) in five animals had a detrimental effect in that no animals survived following the intensive care period and all had infarction with massive edema. We speculate that hypothermia caused a sufficient increase in blood viscosity as to compromise collateral flow, thereby accounting for this detrimental effect. Induced hypertension (to 20% above control levels) was abandoned after three animals because of severe systemic effects (cardiac failure and pulmonary edema) resulting in death during the period of intensive care.

Acute Disease↗