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Biomedical subjects

B C White

Publications and source records attributed to B C White.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1983

Calcium blockers in cerebral resuscitation.

Recent studies on cerebral resuscitation following an ischemic anoxic insult suggest that both inadequate reperfusion and direct neuronal death are partially initiated by calcium entry into vascular smooth muscle and neurons. To investigate the effects of calcium blocking agents on cerebral resuscitation, a controlled perfusion arrest model with cardiopulmonary bypass was used. Post-resuscitation regional cerebral cortical blood flow (rCCBF) and intracranial pressures (ICP) were monitored in five control dogs and in 12 study dogs resuscitated after a prolonged (20-minute) cardiac arrest. The resuscitation included dexamethasone and three agents thought to be calcium entry antagonists and to offer potential cerebral protection after complete prolonged cerebral ischemic anoxia. Prearrest rCCBF measured by a thermal dilution method with a thermistor placed on the cerebral cortex was 2.0 +/- 0.6 (S.D.) ml/gm/min on bypass at 100 mm Hg mean arterial pressure. Twenty minutes after resuscitation was begun, the rCCBF in ml/min/gm were: controls 1.1 +/- 0.3; dexamethasone (2 mg/kg) 1.2 +/- 0.4; MgSO4 (100 mg/kg) 1.8 +/- 0.5; verapamil (0.15 mg/kg) 1.9 +/- 0.4; and lidoflazine (1 mg/kg) 1.5 +/- 0.3. Ninety minutes following the beginning of resuscitation the rCCBF were: controls 0.1 +/- 0.1; dexamethasone 0.1 +/- 0.1; MgSO4, 1.7 +/- 0.3; verapamil, 1.9 +/- 0.4; and lidoflazine, 1.5 +/- 0.3 ml/gm/min. Thus the Ca2+ entry antagonists maintained cerebral blood flow at 20 and 90 minutes following a prolonged ischemic anoxic insult. Dexamethasone was no better than control. These data suggest that calcium entry blockers can maintain rCCBF and may have a significant role in cerebral resuscitation following cardiac arrest.

Animals↗
PubMed1983

Physiology of resuscitation.

Ischemia ultimately leads to loss of thermodynamic order in all cells. During ischemia and reperfusion, the influx of Ca2+ ions appears to initiate a number of cell processes, the reversal of which depends on the re-establishment and maintenance of adequate organ perfusion and high energy metabolism. Promising therapeutic approaches for accomplishing these goals include substrate augmentation, inhibition of calcium-activated injury, membrane stabilization, manipulation of the cycloxygenase and lipoxygenase reactions, and the use of free radical scavengers.

Adenosine Triphosphate↗
PubMed1982

Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest.

Twelve dogs were anesthetized and instrumental for determination of CVP, arterial pressure, intracranial pressure, left atrial pressure, and frontal cerebral cortical blood flow (CCBF) by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls. Pre-arrest determinations of hemoglobin, glucose, CCBF, and cerebral A-V oxygen differences were taken. Full circulatory arrest was carried out for 20 minutes by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected quickly, and pre-arrest perfusion pressure was achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. All pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. Five dogs were treated with 6 microgram/kg flunarizine administered IV drip over 10 minutes immediately post reperfusion. Five dogs were not treated post arrest. Treated animals had a prompt return of CCBF rates equal to or greater than pre-arrest flow, which persisted throughout the period of post-arrest observation. Untreated animals had markedly reduced CCBF and increased resistance. CCBF uniformly proceeded to near zero flow by 90 minutes. The ICP was not significantly altered by treatment.

Animals↗
PubMed1982

Canine cerebral cortical blood flow and vascular resistance post cardiac arrest.

seven dogs were anesthetized and instrumented for determination of central venous pressure (CVP), arterial pressure, intracranial pressure (ICP), left atrial pressure (LAP), and frontal cerebral cortical blood flow by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery, and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left-side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls for stability of the measured parameters on prolonged bypass. Pre-arrest determinations of hemoglobin, cerebral cortical blood flow, and cerebral A-V oxygen saturation differences were taken. Full circulatory arrest was carried out for 20 minutes in 5 dogs by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected and pre-arrest perfusion pressures were achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. Pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. A 50% reduction in cerebral cortical blood flow 20 minutes post resuscitation progressed to near zero flow 90 minutes post resuscitation. The changes in net cerebral perfusion pressure produced by the slowly rising intracranial pressure do not account for this flow reduction. Calculation of cerebral vascular resistance reveals a ten-fold increase in resistance post-arrest and -resuscitation.

Animals↗
PubMed1981

Peripheral vs central circulation times during CPR: a pilot study.

The circulation time during closed chest cardiac compression was studied using Cardio-Green injected in either the right antecubital vein or right subclavian vein during CPR. Arterial blood was obtained from a right femoral arterial catheter at 30-second intervals for five minutes following injection. Six patients, in two groups, comprised the study population. The arterial sample for Cardio-Green after central venous injection revealed a high concentration of the dye at 30 seconds and an emerging second peak at five minutes. After peripheral injection, no peak concentration of the dye was achieved during the five-minute sampling method. Our preliminary study indicates reduced concentrations and significant delay in arrival of injected agents that are introduced at a peripheral intravenous site during closed chest compression.

Blood Circulation Time↗
PubMed1981

Transthoracic pacing during CPR.

Twenty-seven patients had transthoracic pacemakers inserted by the subxiphoid approach during advanced cardiopulmonary resuscitation (CPR) in the emergency department of Detroit General Hospital between May 1977 and March 1979. Twenty-one charts were available for detailed review. Pacemaker indications in these 21 cases included electromechanical dissociation in four cases, asystole in 10 cases, pulseless idioventricular rhythm in five cases, and 3 degree heart block in two cases. All patients had failed to respond to conventional chronotropic and inotropic agents prior to pacemaker insertion. Good pacemaker capture was obtained in eight of the 21 patients. Two of the patients with good capture had pulses for about 15 min after capture. One of these two patients rearrested, with signs of pericardial tamponade which was confirmed during emergency thoractomy. Neither of the two patients who had pulses after pacemaker insertion and capture could be stabilized, and both died within 30 min post-insertion. Transthoracic pacemaker insertion during advanced CPR in the emergency department probably does not improve outcome in bradyasystolic arrests if there has been poor response to standard advanced cardiac life support management.

Adult↗
PubMed1980

Anxiety and muscle tension as consequences of caffeine withdrawal.

Regular consumers of caffeine had higher muscle tension after three or more hours of abstinence than low caffeine consumers. This difference was absent after double-blind administration of caffeine citrate or placebo. In a discriminative reaction time test, caffeine treatment improved performance. Among subjects receiving placebo, anxiety was highly correlated with prior caffeine use, suggesting that even a brief abstinence may produce anxiety in the regular user.

Adult↗
PubMed1980

Mitochondrial O2 use and ATP synthesis: kinetic effects of Ca++ and HPO4(-2) modulated by glucocorticoids.

We have studied the effect of increased Ca++ on rat liver mitochondrial O2 consumption and modulation of the effects of the Ca++ by varying levels of HPO4(-2). Moreover, we have studied the acute in vitro effects of glucocorticoids on this system. Our data indicate that: 1) 200 microM Ca++ produces uncoupled respiration by mitochondria and blocks ATP synthesis: 2) HPO4(-2) increases the velocity and duration of uncoupled O2 consumption induced by Ca++. The HPO4(-2) effect fits Michaelis-Menton kinetics, indicating a specific site for the action of HPO4(-2) with a Km (1/2 saturation constant) of 5 mM; 3) dexamethasone acts acutely (without prefeeding) as an allosteric inhibitor of the HPO4(-2) system; and 5) uptake kinetics done with tritium-labeled dexamethasone into fresh intact human leukocytes demonstrate equilibration into the cell within 60 sec with a very large Vmax of transport at the plasma membrane. Critically ill patients with reduced tissue perfusion have lowered ionized calcium blood levels. This reflects movement of this ion into the cytosol as the plasma membrane Ca++ pump begins to fail. Clinical implications of our study are that: 1) administration of therapeutic Ca++ in hypoperfused patients with low serum Ca++ levels may be contraindicated because this will only increase the Ca++ load on the mitochondria and further depress ATP synthesis; 2) glucocorticoids administered to these patients offer partial protection of the mitochondria from uncoupling and improve ATP synthesis; and 3) effective doses of glucocorticoids are probably near optimum at four to five times the K.

Adenosine Triphosphate↗
PubMed1979

Incidence, etiology, and outcome of pulseless idioventricular rhythm treated with dexamethasone during advanced CPR.

The cardiac resuscitation records of 458 patients who received advanced cardiac life support at Detroit General Hospital during the last two years were reviewed to identify patients who had pulseless idioventricular rhythm (PIVR) recognized and treated with dexamethasone. Twenty-five cases were identified. The initial successful resuscitation rate of 52% in these patients contrasts sharply with other published data indicating 100% failure with the use of conventional chronotropic drugs. The most common etiology of cardiac arrest in our patients who display PIVR during resuscitation is hypoperfusion shock. Dexamethasone may counteract the lethal arrhythmia by causing the release of aditional adenosine triphosphate into the cytoplasm from the mitochondria.

Adenosine Triphosphate↗
PubMed1979

His electrocardiographic characterization of terminal arrhythmias of hemorrhagic shock in dogs.

Pulseless idioventricular rhythm is the agonal arrhythmia identified in three models of hemorrhagic shock used in this study. This arrhythmia is preceded by atrial and then junctional arrest demonstrated by His electrocardiography in all nine dogs studied. Two additional dogs were used as controls. Acid-base and electrolyte changes were not sufficient to cause the progressive failure of conduction system function seen so consistently. Patients receiving cardiopulmonary resuscitation who have profound bradycardia without pulses may have been in shock prior to cardiopulmonary arrest.

Animals↗
PubMed1977

Unilateral catecholamine depletion of the corpus striatum and amphetamine-induced turning: an ontogenetic study.

Unilateral intrastriatal microinjections of alpha-methyl-p-tyrosine followed by systemic amphetamine treatment produced turning ipsilateral to the side of the injection in rats from 12 days of age to maturity, but not in rats younger than 12 days. These results are consistent with other findings that indicate rapid development of the striatal dopaminergic system and dopaminergic component of the amphetamine stereotypy in the second postnatal week.

Aging↗
PubMed1977

Effects of sodium bicarbonate administration during cardiopulmonary resuscitation.

To study whether sodium bicarbonate given in cardiopulmonary resuscitation may produce life-threatening hyperosmolality or hypernatremia, arterial blood was analysed for blood gas, alcohol, blood urea nitrogen, electrolyte and osmolality. The blood was drawn after resuscitation in successful cases, and while effective massage and ventilation were being applied in unsuccessful resuscitations. Seven of the 17 resuscitations were successful. Serum sodium concentrations ranged from 135 to 154 with one exception and did not correlate with the amount of sodium bicarbonate administered. Arterial pH ranged from 6.38 to 7.71; only one patient had metabolic alkalosis. Serum osmolality ranged from 301 to 407. The data suggests a net increase in osmolality of 6 mOsm/50 mEq of sodium bicarbonate.

Alkalosis↗