Naloxone Group Research Articles

Effect of naloxone on the secretion of LH in infantile and prepubertal Holstein bull calves

Administration of naloxone (100 mg i.v.; approximately 1.21 mg/kg body weight0.75) to 10 intact calves (24 weeks of age) caused an acute release of LH that was similar in amplitude and duration to spontaneous discharges of LH that occur at the same age. The naloxone-induced release of LH was abolished in 9/10 calves (intact and castrated) treated with oestradiol-17 beta. To determine the ontogeny of opioid control of secretion of LH, 12 calves were randomly assigned to receive saline or naloxone (1.21 mg/kg body weight0.75, i.v.) at 3, 5, 7, 9, 11, 13, 17 and 21 weeks of age. At each age, blood was collected at 10-min intervals for 4 h and saline or naloxone was administered (i.v.) after collection of the 120-min sample. Before administration of naloxone, plasma LH values increased with age (P less than 0.01) but did not differ between the control and naloxone groups (age x treatment, P greater than 0.05). Administration of naloxone caused concentrations of plasma LH to increase at 3, 11, 13, 17 and 21 weeks of age (treatment x time, P less than 0.001). Concentrations of LH (saline vs naloxone, ng/ml) reached a maximum within 20 min after treatment at Weeks 3 (0.3 vs 1.2), 11 (0.6 vs 2.6), 13 (0.6 vs 3.7), 17 (1.1 vs 2.6), and within 40 min after treatment at Week 21 (1.0 vs 3.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Narcotic reversal in hypercapnic dogs: comparison of naloxone and nalbuphine

Reversal of opioid effects by naloxone (NX) can lead to significant cardiovascular problems. We have reported previously that hypercapnic dogs develop greater increases in blood pressure and plasma catecholamine (CA) levels than hypocapnic ones when reversed with naloxone. We have also demonstrated differences between NX and nalbuphine (NBPH) in producing excitatory adrenergic responses when administered during normocapnia. The present study was designed to investigate possible dissimilarities in cardiovascular and sympathetic events after administration of either NX or NBPH in dogs made hypercapnic following fentanyl administration. After induction of anaesthesia with thiopentone and intubation, two groups of dogs were maintained with controlled ventilation on enflurane in oxygen anaesthesia and given 50 micrograms.kg-1 fentanyl IV. This caused a significant decrease in heart rate (HR) (P less than 0.001), mean arterial blood pressure (MAP) (P less than 0.001), and plasma concentrations of norepinephrine (NE) (P less than 0.002). Then, ventilation was decreased to produce a PaCO2 of 60 mmHg; this was accompanied by a significant elevation in plasma level of both epinephrine (EPI) (P less than 0.02) and NE (P less than 0.001). Administration of 20 micrograms.kg-1 NX to six dogs resulted in immediate increases in HR (P less than 0.01) and MAP (P less than 0.01), and a further rise in CA levels to greater than pre-fentanyl baseline values. In six other dogs, NBPH (0.3 mg.kg-1) caused increases in HR (P less than 0.001) and MAP (P less than 0.001) only, and the MAP rise was significantly less than that seen in the NX group (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Untersuchungen zur Therapie des hypovolämischen Schocks bei Kühen mit rechtsseitiger Labmagenverlagerung*

In this trial, the effect of supplementary administration of the opioid antagonist Naloxone was tested, in comparison to infusion of Ringer's-solution only, in the treatment of hypovolemic shock in cows suffering from right-sided abomasal displacement. Twenty cows were selected by several criteria (pulse rate greater than 95/min; plasma chloride content less than 90 mmol/l; body temperature less than 39.5 degrees C) and alternatively assigned to the Naloxone group and the control group. All animals were treated surgically by the usual clinical method. After opening the abdominal cavity paralumbally from the right, intravenous administration of 13 l of Ringer's-solution was started and continued for about 5 hours. In addition, the cows of the experimental group received 0.75 g Naloxone as an intravenous bolus before, and 1 g Naloxone dissolved in 7 l fluid during the first hour of the permanent drip infusion. Further treatments (additional fluid therapy or administration of purgatives and ruminomotorics on the following days) were given according to the condition of the animal. The evaluation of efficacy was done in regard to the clinical (course of disease), and clinicochemical (e.g. hemogram, blood gas analysis, plasma chloride, plasma lactate) parameters as well as to blood pressure. No statistically significant differences were found between both groups. Only nine of the twenty cows were sent home cured, one patient of each group died one day after surgery, and the remaining 9 animals had to be sent to the slaughterhouse within 3 to 22 days after surgery after only transient improvement. These results suggest, that under the conditions described, conventional fluid therapy is equivalent to fluid therapy with addition of Naloxone. Hypoxic damage of the abomasum caused by its displacement and the subsequent hypovolemic shock are discussed as main causes for the poor postsurgical prognosis of right-sided abomasal displacement.

Naloxone alters the early response to an inspiratory flow-resistive load

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.

Endotracheal naloxone in rabbits: No adverse effects on blood gases and lung tissue

52 Endotracheal Naloxone in Rabbits: No Adverse Effects on Blood Gases and Lung Tissue SC Rector, RW Geiss, K Beamer, P Legg/Emergency Service, and Departments of Surgery and Pathology, West Virginia School of Medicine, Morgantown We compared endotracheal naloxone with normal saline solution to study the effects on arterial blood gases and lung tissue in 16 rabbits. The pulmonary effects of endotracheal naloxone have not been studied previously. Eight rabbits received naloxone through an endotracheal tube, and eight controls received normal saline. Blood gases were sampled for 30 minutes. Four subject rabbits and four controls were killed after two days; the remaining rabbits were killed after six weeks. Microscopic analysis of lung tissue was done by a pathologist blinded to the identity of the specimens. There was no significant difference in blood gas values between the naloxone and control groups. By microscopy, there was no observed pattern of variance in pulmonary pathology between the subject and control groups. This experiment revealed no adverse effects on rabbit blood gases and lung tissue after one dose of endotracheal naloxone as compared with saline. Further study is needed before endotracheal naloxone can be considered safe for human use.

Effects of naloxone on cardiac energy metabolism in hypovolemic shock in rats

It has been reported that naloxone may be useful in the treatment of hypovolemic shock. However, the effects of naloxone on cardiac energy metabolism in hemorrhagic shock have not been investigated. The effects of naloxone on myocardial metabolism were evaluated in the rats which were bled to a systolic pressure of 40 mmHg and maintained at that pressure for 30 min. Naloxone (10 mg/kg) was administered intravenously 5 min before the heart was removed. Then the intramyocardial high energy phosphates, pyruvate, lactate, and glycogen were measured. Naloxone increased systolic blood pressure and decreased heart rate significantly. However, there were no significant differences in high energy phosphates, energy charge, pyruvate, lactate and glycogen between the control and naloxone groups. These data suggest that naloxone may have no direct effect on the cardiac energy metabolism in a 30-min hypovolemic shock.

Endogenous opiates in the mediation of early meal-induced jejunal absorption of water and electrolytes

The purpose of this study was to investigate the role of endogenous opiates in mediating meal-stimulated jejunal absorption. Jejunal Thiry-Vella loops, 25 cm long, were studied in awake conditioned dogs, using luminal perfusion with carbon-14 polyethylene glycol. Fluxes of water, sodium, and chloride were calculated every 15 minutes over a 1-hour basal period, followed by a 3-hour experimental period. The animals were divided into four groups: control, naloxone, meal, and meal plus naloxone. In the control and naloxone groups, the fluxes did not change over the 4-hour observation period. Meal alone immediately stimulated the absorption of water and electrolytes in the Thiry-Vella loop (p < 0.05). The addition of naloxone infusion to the meal stimulus resulted in significantly reduced absorption during the first hour after the meal (p < 0.05). We concluded that endogenous opiates play a role in meal-stimulated jejunal absorption.

Volume-regulated arginine vasopressin release in conscious dogs. Evidence for dopaminergic or opioid modulation?

The possibility of a dopaminergic and/or opioid modulation of the volume-regulated release of AVP was investigated in conscious dogs. Either bromocriptine, 10 micrograms/kg body weight po, or naloxone, 0.1 mg/kg body weight iv, was administered prior to induction of nonhypotensive hypovolemia. Volume contraction of 15 ml/kg body weight was induced gradually, over a period of 30 min. Basal plasma AVP levels in the bromocriptine group were not significantly different from control group values. Bromocriptine administration significantly augmented AVP release following volume contraction. Mean arterial pressure in the bromocriptine group decreased to a slightly, but significantly, lower level than that in the control group. Mean arterial pressures, however, did not adequately explain the magnitude of the AVP response in the bromocriptine group. In the naloxone group, neither baseline levels, nor AVP values following volume contraction, differed significantly from respective control group values. In conclusion, the results suggest the possibility of a stimulatory role for endogenous dopamine in the volume-regulated, but not the basal, release of AVP in conscious dogs.

Buprenorphine antagonism of ventilatory depression following fentanyl anaesthesia

In order to compare the effect of buprenorphine and naloxone on respiratory depression after fentanyl anaesthesia (25 micrograms/kg), 32 women scheduled for elective abdominal hysterectomy participated in a double-blind randomized investigation. At termination of anaesthesia, after antagonizing residual neuromuscular blockade, 20 normocapnic patients with a respiratory rate of 4 breaths/min or less entered the study, receiving either buprenorphine (0.6 mg in 20 ml NaCl) or naloxone (0.4 mg in 20 ml NaCl) 2 ml/min until 20 ml was given or until the respiratory rate exceeded 8 breaths/min. Respiratory rate, PaCO2, sedation score, and pain intensity were evaluated during a 3-h study period. Fifteen min after beginning the treatment, all the patients in both groups had their ventilatory depression antagonized. There were no statistically significant differences in respiratory rates between groups except at 15 min. On no occasion did either PaCO2 or a sedation score differ statistically significantly between the groups. At 15 min all patients in the buprenorphine group had no or mild pain, compared to the patients in the naloxone group, of whom 50% had moderate to severe pain (P less than 0.05). It seems as if buprenorphine is as effective as naloxone in antagonizing respiratory rate depression following fentanyl anaesthesia.

Effects of dichloroacetate and naloxone on hemodynamic performance and substrate use following endotoxin administration

We compared the effects of the opiate antagonist, naloxone, and a stimulator of pyruvate dehydrogenase, sodium dichloroacetate, on the hemodynamic performance and substrate use in a model of sustained low-flow state following endotoxin administration in dogs. We administered Escherichia coli 055:B5 endotoxin to 16 female mongrel dogs to induce a sustained drop in cardiac index. At 90 minutes following administration of endotoxin, we injected naloxone 2 mg/kg as a bolus followed by 2 mg/kg/hr infusion in six animals (naloxone group), and dichloroacetate 300 mg/kg/hr in five animals (dichloroacetate group). Five animals received endotoxin but neither naloxone nor dichloroacetate and served as the control group. No differences were observed in cardiac index, mean blood pressure, or oxygen consumption between the naloxone-treated animals and the control animals. Pyruvate concentrations in the serum were significantly higher in naloxone-treated animals than in controls. In contrast, dichloroacetate-treated animals had higher cardiac indices, higher oxygen consumption, lower systemic vascular resistance, and much lower pyruvate and lactate concentrations. We conclude that naloxone does not improve hemodynamic performance or substrate use when given 90 minutes after endotoxin exposure. Dichloroacetate, however, appears beneficial in the treatment of the hemodynamic and metabolic derangements of established endotoxin shock.

Modulation by endogenous opioids of pulmonary vasoconstrictor response to acute lung injury.

The effects of endogenously generated opioids on distribution of pulmonary perfusion (as assessed by radiolabeled microspheres) and overall gas exchange in acute acid-induced lung injury were studied. In 14 anesthesized dogs, sufficient acid was given to one lung to double shunt fraction (Qs/Qt) from 14.2 +/- 0.8 to 32.4 +/- 2.6% (SE). This resulted in a significant decrease in Po2 from 495 +/- 9 to 136 +/- 21 Torr, cardiac output from 2.47 +/- 0.27 to 1.46 +/- 0.15 1/min, and blood pressure from 139 +/- 3 to 116 +/- 5 mmHg and a significant rise in pulmonary arterial pressure from 9.6 +/- 0.8 to 14.9 +/- 0.8 mmHg. After acid instillation, microsphere distribution to the injured lung segments decreased to 50% of the base-line value. At the same time, microsphere distribution in the normal segments increased to 160% of base line. In 7 of the 14 dogs the effects of naloxone (1 mg/kg) given after lung injury were compared with the other 7 animals that were given saline. Naloxone administration caused a significant redistribution of regional pulmonary perfusion such that microsphere distribution in the injured lung segments increased by a factor of 2 at 35 min compared with the animals given saline. Consistent with this finding, Qs/Qt in the naloxone group increased to 34.7 +/- 5.0% at 35 min, whereas that of the saline group decreased to 28.2 +/- 2.5%. The difference between the two groups was significant at 35 min. These changes occurred without further alterations in cardiac output, pulmonary arterial pressure, or systemic blood pressure in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Opioids and hibernation. I. Effects of naloxone on bear hit's depression of guinea pig ileum contractility and on induction of summer hibernation in the ground squirrel

Summer hibernation in ground squirrels ( Citellus tridecemlineatus) can be induced by intravenous injection of hibernation-induction trigger (HIT) from winter bear plasma or its albumin fraction. In this study, we show that bear HIT depresses electrically-induced contraction of the guinea pig ileum myenteric plexus-longitudinal muscle preparation, and that naloxone, at 100, 1,000 or even 4,000 n M , fails to reverse that effect. In a simultaneous study, four sets of ground squirrels were implanted with osmotic minipumps which delivered solutions at a controlled and continuous rate. Two of the groups had pumps delivering naloxone at 1 mg/kg body weight per hour. The other two groups had saline-filled pumps (controls). One set of squirrels from each of the saline- and naloxone-filled pump groups were then injected intravenously with winter bear plasma. The remaining two groups of squirrels were injected with winter bear albumin fraction. Hibernation frequency was determined by measurements of core temperature (from surgically-implanted radio capsules), respiratory rate, and bouts of activity. Squirrels with saline-filled pumps hibernated four times,more frequently than the naloxone groups. To confirm these findings, three squirrels from each naloxone group were reinjected with bear HIT after removal of the pumps. These six squirrels then hibernated over four times their previous frequency. Results sugest that bear HIT is not itself an opioid (since naloxone did not reverse bear HIT's depression of electrically-induced contraction of guinea pig ileum). The fact that bear HIT's effect of inducing summer hibernation in ground squirrels is effectively blocked in vivo by naloxone leads to the speculation that HIT may be either a precursor of endogenous opioids or a potent releaser of them, which, in turn, induce hibernation.

Naloxone does not improve hemodynamics following graded hemorrhage in a canine model

Two recent studies have demonstrated no improvement in hemodynamic parameters or survival following naloxone administration in hemorrhagic shock. This finding is in contrast to those of earlier studies, which consistently demonstrated a beneficial effect. The current study evaluated naloxone's ability to improve hemodynamics when administered following a fixed-volume hemorrhage, during a period of partial hemodynamic compensation. Thirteen conditioned beagles were anesthetized with pentobarbital (25 mg/kg intravenously), endotracheally intubated, and instrumented with a femoral arterial line and a pulmonary artery thermodilution catheter. Animals were then subjected to an estimated 50% graded hemorrhage (45 ml/kg) over one hour. Following hemorrhage, animals were observed for 90 minutes, then reinfused with shed blood over 30 minutes, and finally observed for an additional 60 minutes. Six animals received naloxone (2 mg/kg intravenously) 30 minutes after completion of hemorrhage and then 2 mg/kg/hr for the duration of the study. Seven control animals received an equivalent volume of saline. Heart rate, mean arterial pressure, central venous pressure, cardiac output, arterial and mixed venous blood gases, and serum lactate level were measured at regular intervals throughout the study. Cardiac index and systemic vascular resistance index were calculated at the same intervals. Overall, there were no statistically significant differences in the mean data values for mean arterial pressure, cardiac index, systemic vascular resistance index, or lactate, although lactate values were consistently higher in the naloxone group (two-tailed independent Student's t test). We conclude that naloxone does not significantly improve hemodynamics when administered after a fixed-volume hemorrhage.

Failure of Blood Transfusion or Naloxone to Improve Clinical Recovery After Experimental Spinal Cord Injury

Thirty adult Wistar rats underwent an extradural clip compression injury of 50 g of force for 1 minute at T-1. After injury, the animals were randomly separated into three groups: the control group received a saline infusion for the 2-hour treatment period; the second group was given a blood transfusion over 2 hours titrated to maintain mean systemic arterial pressure (MSAP) at preinjury levels; and the third group received an intravenous bolus dose of naloxone (10 mg/kg), followed by a 2-hour infusion of intravenous naloxone (2 mg/kg/minute). The rats were observed postoperatively for 15 weeks, during which their clinical recovery was measured weekly by the inclined plane technique. At 15 weeks, the spinal cords were removed and prepared for histological assessment. The blood pressure before, during, and immediately after injury did not differ statistically among the three groups. During the initial 2 hours after injury, blood transfusion produced a significant increase in MSAP (P less than 0.02) and hematocrit (P less than 0.001), but naloxone infusion did not result in a significant change in MSAP. Performance on the inclined plane at 15 weeks was 35.6 +/- 6 degrees, 32.7 +/- 4 degrees, and 36.1 +/- 6 degrees for the control, transfusion, and naloxone groups, respectively, and no significant differences were found (P greater than 0.05). Histological examination confirmed a consistent injury of moderate severity in all three groups with no major differences among groups. Thus, this study demonstrates no significant clinical benefit either from a blood transfusion to maintain MSAP or from naloxone given by bolus and infusion after an extradural clip compression injury of the rat spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of naloxone on breathing movements during hypercapnia in the fetal lamb.

To determine whether endogenous opioids influence the fetal breathing response to CO2 we have investigated the effect of the opiate antagonist, naloxone on the incidence, rate, and amplitude of breathing movements during hypercapnia in fetal lambs in utero. In 20 experiments in six pregnant sheep (130-145 days gestation) hypercapnia was induced by giving the ewe 4-6% CO2-18% O2 in N2 to breathe for 60 min. After 30 min of hypercapnia either naloxone (13 experiments) or saline (7 experiments) was infused intravenously for the remaining 30 min. During hypercapnia breath amplitude increased from 5.8 +/- 0.5 to 9.1 +/- 1.2 mmHg (P less than 0.001), and infusion of naloxone was associated with a further significant increase to 15.7 +/- 1.2 mmHg (P less than 0.001). Naloxone had no effect on the incidence or rate of breathing movements during hypercapnia. After hypercapnia there was a significant decrease in the incidence of fetal breathing movements in the naloxone group (14.7 +/- 3.2%). Infusion of saline during hypercapnia had no effect on incidence, rate, or amplitude of fetal breathing movements. These results suggest that endogenous opioids act to suppress or limit breath amplitude during hypercapnia but do not affect rate or incidence of breathing movements.

Effects of naloxone on cardiac energy metabolism in acute hemorrhage in rats.

It has been reported that naloxone may be useful in the treatment of hypovolemic shock. However, the effects of naloxone on cardiac energy metabolism in acute hemorrhage have not been investigated. The effects of naloxone on myocardial metabolism were evaluated in the rat during acute hemorrhage with crystalloid resuscitation. Intramyocardial high energy phosphates, pyruvate, lactate and glycogen were measured. There was no significant difference in high energy phosphates, energy charge, lactate and glycogen contents between control, 1 mg naloxone and 10 mg naloxone groups. However, pyruvate level in hearts in the 10 mg naloxone group was significantly higher than that in control group. Therefore, naloxone reduced the lactate/pyruvate (L/P) ratio. Although naloxone did not improve the mitochondrial function, it improved the oxidation-reduction state in cardiac energy metabolism.

Effect of the opiate antagonist naloxone on digitalis induced cardiac arrhythmias

To test the hypothesis that the endogenous opioid system is operative in digitalis arrhythmias, guinea pigs anesthetized with pentothal and breathing spontaneously were allocated to a control group or four naloxone groups: 0.1 mg/kg i.v., 1.0 mg/kg i.v., 2 mg/kg i.v. or 4 mg/kg i.v. after the induction of arrhythmias by digoxin 100 μg/kg i.v. every 15 min. Naloxone at higher doses resulted in a rapid development of fatal arrhythmias with high degree AV block being more frequent than ventricular tachycardiac or fibrillation. Survival was significantly and inversely related to naloxone dose. The role of theautomatic nervous system was studied using cervical cord transection at the C7 level or bilateral cervical vagotomy, or atropine 1.2 mg/kg pretreatment. Cord transection, but not vagotomy, was associated with a significantly higher digoxin dose to produce arrhythmias. Naloxone 4 mg/kg i.v. shortened survival in cord transected animals, but less than in intact animals. Naloxone did not alter survival in vagotomized animals or animals that were pretreated with atropine. Thus, naloxone accelerates the development of fatal cardiac arrhythmias suggesting that endogenous opioids are involved in digitalis toxic arrhythmias an effect interrelated to the autonomic, mainly parasympathetic, nervous system.

Lack of efficacy of naloxone in a fixed-volume hemorrhage model

Animal studies using a reservoir model of hemorrhagic shock have shown the narcotic antagonist naloxone to be of value in reversing the hemodynamic effects of severe hemorrhage. We conducted a study to evaluate the ability of naloxone to limit the deleterious effects of a fixed-volume hemorrhage. Fifteen mongrel dogs were bled 50% of their estimated blood volumes during one hour. This was followed by a one-hour stabilization period; reinfusion during a 30-minute period; and finally, an additional one-hour monitoring period. Eight dogs received 2 mg/kg IV naloxone 30 minutes prior to hemorrhage and 2 mg/kg/hr for the duration of the study. Seven control dogs received an equivalent volume of saline without naloxone. Pulmonary capillary wedge pressure, central venous pressure, cardiac output, heart rate, blood pressure, arterial and mixed venous blood gases, and serum lactate were measured at 19 intervals throughout the study period. Mean arterial pressure, cardiac index, and systemic vascular resistance were calculated for each sampling period. With the exception of serum lactates, which were higher in the naloxone group, there were no significant differences between the groups in the mean values calculated for each sampling interval (P less than .05, two-tailed independent t test). Furthermore, the changes in hemodynamic parameters observed during the hemorrhage, stabilization, reinfusion, and monitoring periods were not significantly different. We conclude that in this fixed-volume hemorrhage model, naloxone does not prevent or reverse hemodynamic deterioration.

Failure of Blood Transfusion or Naloxone to Improve Clinical Recovery after Experimental Spinal Cord Injury

Thirty adult Wistar rats underwent an extradural clip compression injury of 50 g of force for 1 minute at T-1. After injury, the animals were randomly separated into three groups: the control group received a saline infusion for the 2-hour treatment period; the second group was given a blood transfusion over 2 hours titrated to maintain mean systemic arterial pressure (MSAP) at preinjury levels; and the third group received an intravenous bolus dose of naloxone (10 mg/kg), followed by a 2-hour infusion of intravenous naloxone (2 mg/kg/minute). The rats were observed postoperatively for 15 weeks, during which their clinical recovery was measured weekly by the inclined plane technique. At 15 weeks, the spinal cords were removed and prepared for histological assessment. The blood pressure before, during, and immediately after injury did not differ statistically among the three groups. During the initial 2 hours after injury, blood transfusion produced a significant increase in MSAP (P less than 0.02) and hematocrit (P less than 0.001), but naloxone infusion did not result in a significant change in MSAP. Performance on the inclined plane at 15 weeks was 35.6 +/- 6 degrees, 32.7 +/- 4 degrees, and 36.1 +/- 6 degrees for the control, transfusion, and naloxone groups, respectively, and no significant differences were found (P greater than 0.05). Histological examination confirmed a consistent injury of moderate severity in all three groups with no major differences among groups. Thus, this study demonstrates no significant clinical benefit either from a blood transfusion to maintain MSAP or from naloxone given by bolus and infusion after an extradural clip compression injury of the rat spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of naloxone on the hemodynamics of the newborn piglet with septic shock.

Naloxone has been shown to reverse the hemodynamic sequelae of experimental septic shock in adult animal models. Its effectiveness in the newborn has not been studied. To further investigate the efficacy of naloxone, we instrumented 18 piglets for continuous measurement of mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, heart rate, left ventricular pressure, contractility, cardiac output, and O2. Oxygen consumption, systemic vascular resistance, and pulmonary vascular resistance were calculated. Following a stabilization period, group B beta-hemolytic Streptococci were infused over 30 min. Following the infusion, naloxone (1 mg/kg) was given followed by a continuous infusion of 1 mg/kg/h in nine treatment animals. Nine control animals were given an equal volume of saline. Both groups developed significant increases in mean pulmonary arterial pressure followed by a return to baseline. Oxygen consumption, cardiac output, contractility and mean arterial pressure decreased in both groups. Treatment with naloxone was associated with a cessation in the fall in the mean arterial pressure and the contractility. The difference in mean arterial pressure and contractility between groups was significant. The naloxone group had significantly improved 5-h survival. We speculate that naloxone may reverse some of the hemodynamic sequelae and improve survival in newborns with septic shock.