Biomedical subjects

O Henderson

Publications and source records attributed to O Henderson.

3 recordsLinked to original sources

PubMed1994

International Lp(a) standardization.

Two international surveys for Lp(a) measurements were organized from 1989 to 1991. The results of the first survey led to the conclusion that the lack of a common primary standard was the main cause of the large inter-laboratory variation observed. No major effects of techniques or antisera were observed. The same findings were confirmed during the second survey, which was extended to include more samples and a larger number of participants. During the second survey, no consistent effect due to freezing or lyophilization could be demonstrated, although there was a trend towards lower Lp(a) values in lyophilized samples. The inter- and intra-laboratory coefficients of variation did not vary significantly for the different Lp(a) phenotypes, and variability was comparable for lyophilized, liquid and frozen materials. Large intra-assay coefficients of variation were observed during both surveys. Results obtained in different laboratories using the same commercial reagents and standards also showed a large variation. These initial results demonstrate that the lack of a primary standard and poor assay precision are the main factors responsible for the high inter-laboratory variation observed during these surveys.

Analysis of Variance↗

PubMed1983

Prolonged hypoperfusion in the cerebral cortex following cardiac arrest and resuscitation in dogs.

Increasing cerebral vascular resistance and brain perfusion failure occur within 90 minutes following cardiac arrest and resuscitation. This study followed cortical perfusion for 18 hours after a 15-minute cardiac arrest. Six dogs were anesthetized with ketamine and gallamine and then mechanically ventilated. They were instrumented for arterial pressure, central venous pressure, and regional cerebral cortical blood flow (rCCBF) determined by thermodilution. A left thoracotomy and pericardiotomy were done. Two dogs served as non-arrest controls. Cardiac arrest was produced in four dogs with an intravenous bolus of KCl at 1 mEq/kg. After 15 minutes of cardiac arrest, the animals were resuscitated with internal massage, NaHCO3, epinephrine, and internal defibrillation. Cortical blood flow was followed for 18 hours. Arterial core temperature was never less than 35 C. Pre-arrest cortical blood flows were 0.86 cc/min/g (+/- 0.11). The two control animals had stable rCCBF (0.74 +/- 0.17) for all determinations during the 18-hour follow-up period. Determinations of rCCBF from 6 to 18 hours in post-arrest animals were 7% to 14% of pre-arrest values. We conclude that the post-resuscitation perfusion failure in the cortex is prolonged. Any potential for neuronal recovery, unless perfusion is protected, would not be realized given this phenomenon.

Animals↗

PubMed1983

Early amelioration of neurologic deficit by lidoflazine after fifteen minutes of cardiopulmonary arrest in dogs.

A prospective, controlled, blind study was done to test the effect of a calcium entry blocker on the neurologic integrity of dogs after cardiopulmonary arrest. Ten male mongrel dogs were anesthetized, prepared with sterile technique, and instrumented for pulmonary arterial (PA) and systematic arterial pressure monitoring. A left thoracotomy and pericardotomy were performed. Cardiac arrest was produced by injecting KCl (1 mEq/kg) through the PA line, and the respirator was stopped. Full arrest was maintained for 15 minutes. Thereafter, the dogs were resuscitated with ventilation, internal massage, fluids, bicarbonate, epinephrine, and internal defibrillation. All dogs were resuscitated within 6 to 10 minutes. Five control dogs received saline placebo, and five dogs were treated with lidoflazine (1 mg/kg) IV drip immediately post resuscitation. All dogs were scored neurologically every two hours by a deficit grading scale. All treated dogs had spontaneous ventilation, reactive pupils and corneals, voluntary movements, and responses to tactile stimulation at 12 hours post resuscitation. Four of five control dogs had maximum deficit scores without improvement. The difference in neurologic scores between the treated and control groups became increasingly divergent with time, and was statistically significant (P less than .05) by four hours post resuscitation. Thus the calcium antagonist lidoflazine produces improvement in neurologic recovery in the first 12 hours after cardiopulmonary arrest in dogs.

Animals↗