PubMed Health⌕ Search

Biomedical subjects

J W Holaday

Publications and source records attributed to J W Holaday.

At least 109 records · Page 6Linked to original sources
PubMed1982

Comparison of early and late naloxone treatment in experimental spinal injury.

The effects of early (1 hour posttrauma) and late (4 hours posttrauma) naloxone treatment on neurologic recovery were compared after experimental cervical spinal injury. Neurologic scores did not differ significantly between the early and late naloxone-treatment groups, and both naloxone groups showed significantly better neurologic recovery than saline-treated controls during a 6-week follow-up. These findings confirm the therapeutic benefit of opiate antagonists in experimental spinal injury and indicate that even delayed naloxone treatment is effective in improving neurologic outcome.

Animals↗
PubMed1981

Opiate-like electroencephalographic and behavioral effects of electroconvulsive shock in rats.

Rats were studied (a) after a single transauricular electroshock (acute ECS) and (b) following 10 consecutive once-daily shocks (chronic ECS). ECS produced a generalized convulsion marked by a polyspike EEG seizure. The seizure was followed by a period of postictal depression (PID) characterized by EEG high-voltage synchrony, EMG quietening, and an associated stuporous behavior in the rat. Acute ECS produced a maximal of 33 +/- 8 (S.E.) percent above control in the EEG voltage output during postictus, with the PID lasting 2680 +/- 658 sec. Chronic ECS resulted in a significant enhancement of these acute responses. Pretreating rats with naloxone (0.3-10 mg/kg s.c.) antagonized the postictal effects of acute ECS, but not of chronic ECS. These naloxone-sensitive postictal EEG and behavioral changes appear to reflect a release of endogenous opioid peptides during ictus, a finding consistent with the hypothesis that electroshock activates opioid systems.

Animals↗
PubMed1981

Thyrotropin-releasing hormone improves neurologic recovery after spinal trauma in cats.

Naloxone treatment improves neurologic outcome after experimentally induced spinal trauma, but this opiate-receptor antagonist may increase post-traumatic pain. In contrast, thyrotropin-releasing hormone appears to act in vivo as a partial physiologic opiate antagonist that spares analgesic systems; this activity prompted us to evaluate its effect in spinal injury. Cervical-spine trauma was produced in anesthetized cats by the Allen method. Six animals each received thyrotropin-releasing hormone, saline, or dexamethasone as an intravenous infusion over four hours, beginning one hour after injury. Neurologic recovery was significantly better after treatment with thyrotropin-releasing hormone than after saline or dexamethasone (P less than 0.01): at six weeks, the average animal given thyrotropin-releasing hormone was normal, whereas average control animals had marked spasticity. The beneficial effect of thyrotropin-releasing hormone in experimental spinal injury and its lack of effect on nociception indicate that it may have unique therapeutic potential in spinal trauma in human beings.

Animals↗
PubMed1981

Thyrotropin releasing hormone improves blood pressure and survival in endotoxic shock.

In conscious rats subjected to endotoxic shock, thyrotropin releasing hormone (TRH) is shown to produce a rapid increase in cardiovascular variables and respiratory rates at intravenous doses between 0.20 and 6.34 mg/kg. Moreover, these doses of TRH significantly improve survival following endotoxemia. The absence of an effect of TRH upon analgesic latencies, combined with its demonstrated efficacy in reversing shock, suggest that it may have therapeutic advantage over the opiate antagonist naloxone.

Animals↗
PubMed1981

Thyrotropin-releasing hormone improves cardiovascular function in experimental endotoxic and hemorrhagic shock.

Thyrotropin-releasing hormone significantly improved cardiovascular function when it was injected intravenously into conscious rats subjected to experimental endotoxic or hemorrhagic shock. Because thyrotropin-releasing hormone appears to be a "physiologic: opiate antagonist without effects on pain responsiveness, it may provide therapeutic benefits in the treatment of shock or acute hypotension.

Animals↗
PubMed1981

Dopamine partially mediates the cardiovascular effects of naloxone after spinal injury.

Following spinal injury, the opiate antagonist naloxone selectively elevates plasma dopamine levels, with the dopamine changes significantly correlated with improved cardiovascular function. Moreover, the cardiovascular effects of naloxone are significantly attenuated by pretreatment with the dopamine antagonist domperidone. From these data, it is concluded that the cardiovascular effects of naloxone after spinal injury are in part dopamine mediated.

Animals↗
PubMed1981

Opiate antagonist improves neurologic recovery after spinal injury.

The opiate antagonist naloxone has been used to treat cats subjected to cervical spinal trauma. In contrast to saline-treated controls, naloxone treatment significantly improved the hypotension observed after cervical spinal injury. More critically, naloxone therapy significantly improved neurologic recovery. These findings implicate endorphins in the pathophysiology of spinal cord injury and indicate that narcotic antagonists may have a therapeutic role in this condition.

Animals↗
PubMed1981

Endorphins in experimental spinal injury: therapeutic effect of naloxone.

An experimental model of cat spinal injury was used to investigate the hypotheses that endorphins are involved in the pathophysiology of spinal cord injury and that the opiate antagonist naloxone, by blocking the effects of endorphins, may improve physiological and neurological recovery. Experimental trauma to the cervical spine caused a reduction in blood pressure and spinal cord blood flow (SCBF) associated with increased plasma levels of beta-endorphin-like immunoreactivity; both blood pressure and SCBF were significantly improved by naloxone treatment. Naloxone-treated animals also showed less prominent spinal cord abnormalities and significantly improved neurological recovery compared with saline controls. Moreover, both the pathological and clinical findings correlated significantly with the blood pressure changes following treatment. The data support a pathophysiological role for endorphins in experimental spinal cord injury and suggest that opiate antagonists might improve the treatment of spinal trauma in humans.

Animals↗
PubMed1981

Hypophysectomy alters cardiorespiratory variables: central effects of pituitary endorphins in shock.

The possible involvement of pituitary endorphins in the pathophysiology of shock was evaluated by measuring cardiorespiratory variables after naloxone injection in conscious hypophysectomized and sham-hypophysectomized rats subjected to controlled hemorrhage. Additionally, the role of the central nervous system (CNS) in mediating the cardiodepressant effects of endorphins in shock was studied. After the induction of hypovolemic shock (20 min at below 40 mmHg), hypophysectomized and sham-hypophysectomized rats received intraventricular (ivt) injections of naloxone HCl (10 micrograms) or an equivalent volume of saline (20 microliters over 20 s). In sham-hypophysectomized rats, both injections significantly elevated mean arterial pressure and pulse pressure; however, the increase produced by naloxone was significantly greater than that produced by saline. By contrast, hypophysectomized rats showed no response to naloxone or saline. Intravenous (iv) administration of naloxone HCl (3 mg/kg) or saline to these same hypophysectomized rats 15 min after ivt administration had no additional cardiovascular effects; as before, only animals with intact pituitaries responded to naloxone. Heart rate and respiration rate were unaffected by ivt or iv naloxone. From these data we suggest that pituitary endorphins contribute to the pathophysiology of hypovolemic shock, at least in part through actions within the CNS.

Animals↗
PubMed1981

A role for endorphins in the pathophysiology of spinal cord injury.

These studies have demonstrated that the opiate-antagonist naloxone improves blood pressure and functional neurologic recovery after spinal injury. From these findings we suggest that endorphins are released in response to spinal injury and contribute to the hypotension and to the ultimate neurologic deficit. Naloxone's ability to reverse the presumed endorphin-mediated hypotension in this model supports the hypothesis that its therapeutic effects may be secondary to its improvement of spinal cord blood flow, thereby reducing the ischemic damage caused by spinal cord trauma.

Animals↗