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J D O'Benar

Publications and source records attributed to J D O'Benar.

12 recordsLinked to original sources
PubMed1998

Hemodynamic and metabolic responses to repeated hemorrhage and resuscitation with hypertonic saline dextran in conscious swine.

Previous work in our laboratory has demonstrated that HSD is an effective small-volume resuscitation fluid for the treatment of hemorrhagic hypotension, but limitations to its usefulness in severe hemorrhage have not been explored. In the present study, animals (N = 12) were bled from an arterial line at a rate of 1 mL/kg/min until continuously monitored aortic blood flow was reduced to one-half its baseline value, and then they were immediately resuscitated with 7.5% NaCl/6% dextran 70 (hypertonic saline dextran, 4 mL/kg) administered intravenously over 3 min. After recording the maximum improvement in blood pressure, blood samples were obtained and the hemorrhage-resuscitation sequence was repeated until no further measurable increase in cardiac index or blood pressure could be elicited by resuscitation. In the majority of the animals, cardiac index and right and left ventricular stroke work could be improved at least through two bleedings and resuscitation. These improvements sufficed to increase oxygen delivery and consumption, despite the decreases in hematocrit induced by bleeding, transcapillary refill, and asanguinous fluid administration. Under these severe hemorrhage conditions, the acid-base imbalance was not improved by hypertonic saline dextran, and the rate of increase in acidosis was not affected by its administration. We observed a progressive decrease in base excess from +1.35+/-3.19 (mean +/- standard error) to -12.9+/-2.1 mEq/L even when resuscitation improved oxygen consumption significantly by 95+/-20%. In animals that survived as many as three bleedings and resuscitation, the depletion of buffering capacity of the blood was most predominant, and bicarbonate reached a nadir of 7.62 mEq/L with a base excess of -22.4 mEq/L. It is evident that restoration of perfusion in shock treats only a portion of the physiologic dysfunction, leaving major metabolic derangements uncorrected.

Acid-Base Equilibrium↗
PubMed1987

Beta-endorphin, ACTH, and cortisol response to hemorrhage in conscious pigs.

Some of the interrelations of neuroendocrine changes associated with hypovolemia were investigated in a model simulating an arterial hemorrhage. beta-Endorphin, adrenocorticotropin hormone (ACTH), and cortisol levels were measured by radioimmunoassay before, during, and after controlled bleeding of conscious splenectomized pigs. All animals showed significant (P less than 0.05) increases in the three neuroendocrine substances during hemorrhage. beta-Endorphin values initially were 55 +/- 7 pg/ml (+/- SE) and rose to a peak of 386 +/- 44 pg/ml at the nadir of blood pressure (mean arterial pressure = 47.5 mmHg). ACTH showed a similar pattern, increasing from 49 +/- 10 to a peak of 518 +/- 56 pg/ml. Cortisol values reached their peak of 18.2 +/- 2.5 micrograms % during the recovery phase. beta-Endorphin values displayed a close inverse correlation to blood pressure during hemorrhage, but returned to basal levels more rapidly than blood pressure during the recovery period. Plasma ACTH levels rose significantly more slowly than beta-endorphin as the hemorrhage progressed. An equimolar ratio of ACTH and beta-endorphin returned only as levels declined following the hemorrhagic insult. In awake pigs therefore an arterial hemorrhage is accompanied by endorphin release proportional to the decrement in blood pressure, a somewhat retarded buildup of ACTH, and a still later cortisol peak during recovery.

Adrenocorticotropic Hormone↗
PubMed1987

A computer model of hemorrhagic shock in domestic swine.

We used a modified version of the computer model of the circulation developed by C.V. Greenway (Pharmacol Rev 33:213-251, 1982) to study the volume-pressure relationship of the systemic venous circulation during and immediately after massive blood loss. Our theoretical predictions were based on experimental measurements performed in conscious, chronically instrumented swine subjected to massive and rapid loss of a predetermined amount of blood. These animals were subjected to an exponential removal of either 50% of their calculated blood volume in 1 hour or a linear removal of 60% in 15 minutes. Our computer model indicates a hysteresis effect between the volume-pressure curves during and immediately following hemorrhage. The results emphasize the importance of venous capacitance changes as a compensatory response to blood loss.

Animals↗
PubMed1985

Naloxone: ineffective in improving cardiac performance after hypoperfusion in swine.

A study was done to measure beta-endorphin immunoreactivity (beta-EI) in swine subjected to cardiopulmonary bypass at normal aortic perfusion pressures and during low-flow states such as can occur with shock. Fifteen pigs, divided into three groups of five each, were placed on total and right heart bypass and perfused as follows: group I, normal blood pressure (80 mmHg); group II, low blood pressure (45 mmHg); and group III, low flows (25 ml/kg/hr). beta-endorphin immunoreactivity was assayed six times during the procedure. Ventricular performance was evaluated by measuring stroke volume (SV) while controlling preload, afterload, and heart rate. Determinations of SV were made at the beginning of bypass, after a 1-hr pump run, and after administration of naloxone (1.1 mg/kg). There were no significant changes in beta-EI in any of the groups during the study. The initial SV in group III (23 +/- 6 ml) decreased significantly (p less than 0.05) after 1 hr of decreased cardiac perfusion (8.0 +/- 7 ml) and was not improved by naloxone (5.0 +/- 7 ml). Ventricular performance was not improved in any group following naloxone administration. In our study, naloxone administered to swine following inadequate myocardial perfusion did not effect a significant cardiac hemodynamic response.

Animals↗
PubMed1985

Naloxone does not prevent death after rapid hemorrhage in swine.

Despite the array of hemorrhage models, animal species and experimental designs, it seems clear that naloxone with or without volume replacement has no place in the treatment of rapidly exsanguinating traumatized patients. In this situation, the adrenergic hemodynamic effects, indirectly due to naloxone, further decrease tissue perfusion leading to a deleterious outcome. We suggest that the membrane stabilizing effects rather than the hemodynamic effects of naloxone should be pursued in the treatment of low perfusion states with longer survival times than rapid hemorrhage, such as septic and cardiogenic shock.

Animals↗
PubMed1984

Cessation of arterial and venous flow at a finite driving pressure in porcine coronary circulation.

We investigated the hypothesis that coronary capacitance is responsible for epicardial coronary artery flow stopping at arterial pressures greater than the coronary venous pressure. Using an in situ blood-perfused swine heart preparation, we compared the arterial pressures at which coronary artery inflow and coronary sinus outflow ceased. A pressure change was used that had the time course of aortic pressure during diastole. Data were obtained in hypocalcemic-arrested, adenosine-vasodilated preparations before and after pharmacologic interventions simulating the coronary circulation of the intact beating heart. The effect of extravascular compression was studied with barium contracture, while acetylcholine was infused to increase coronary vasomotor tone. The arterial pressure when arterial flow ceased was 13 +/- 5 mmHg in the arrested-vasodilated preparations, 37 +/- 10 mmHg after acetylcholine, and from 18 to 150 mmHg during barium contracture. Coronary sinus outflow ceased when arterial pressure was slightly less than the arterial pressure at which arterial flow had stopped. The differences between the arterial and venous zero flow arterial pressures were as follows: arrested-vasodilated 4 +/- 3 mmHg, acetylcholine 9 +/- 4, and barium contracture 0 +/- 3. The arteriovenous pressure gradients across the coronary bed at the instant venous flow ceased were as follows: arrested-vasodilated 5 +/- 6 mmHg, acetylcholine 23 +/- 6, and from 12 to 128 during barium contracture. These data do not support the suggestion that cessation of epicardial artery flow is solely a capacitance phenomenon.

Acetylcholine↗
PubMedDate not supplied

Electrophysiology of neural units in goldfish optic tectum.

Axons of retinal ganglion cells showed responses not previously emphasized: (a) many tonic units discharged oscillations, 2--12 spikes per burst, interburst intervals 20--300 msec; (b) phasic units showed concentric or flanking ON and OFF fields, response frequency depended on balance of retinal excitation and inhibition; (c) directional sensitivity was maximal for retinal stimuli moving in naso-temporal direction; (d) in anterior tectum deep afferent layer (DAL) provides for deep electrical sink, fibers of DAL have small fields, mostly in front of fish; (e) color-opponent units are prevalent in the superficial terminal layers, color is spatially and temporally represented. Tectal cell responses were distinguished by large visual fields, spontaneity, multiple spikes and long latencies to optic nerve stimulation, failure to follow above 60 per sec, plasticity of response. Tectal neurons of three classes included (a) cells of one type in upper layers were inhibited in ongoing activity by visual input, receptive fields exceeded 100 degrees, were often oblong, responses did not habituate; (b) cells of second type were excited by visual stimuli, became unresponsive (habituated) or responsive only to stimuli in different position or direction (newness cells); lability precluded field mapping and dishabituation was produced by change in background, extraneous stimulation, and spontaneous firing; (c) pyriform cells in periventricular layer were abundant, difficult to isolate electrically, discharged spontaneously in bursts at intervals of several seconds and responded to visual input by interruption of firing. Some tectal cells responded to non-visual stimuli as well.

Afferent Pathways↗