Biomedical subjects

Frederick J Goldstein

Publications and source records attributed to Frederick J Goldstein.

6 recordsLinked to original sources

PubMed2005

Preoperative intravenous morphine sulfate with postoperative osteopathic manipulative treatment reduces patient analgesic use after total abdominal hysterectomy.

CONTEXT: Administration of opioids for treatment of pain after total abdominal hysterectomy (TAH) is a common postoperative procedure, providing an excellent parameter for evaluating the efficacy of postsurgical osteopathic manipulative treatment (OMT). OBJECTIVE: To determine whether a combination of preemptive morphine sulfate and postoperative OMT could provide improved analgesic effects. DESIGN: Randomized double-blind controlled trial. SETTING AND PATIENTS: Thirty-nine hospitalized patients assigned to one of four treatment groups: (1) preoperative saline and postoperative sham manipulative treatment; (2) preoperative saline and postoperative OMT; (3) preoperative morphine and postoperative sham manipulative treatment; or (4), preoperative morphine and postoperative OMT. INTERVENTION: Saline (control) or morphine, 10 mg, delivered intravenously (IV) 10 minutes before surgical incision. All patients received a postoperative patient-controlled IV analgesia pump containing morphine. At specified intervals following preoperative IV injections, blood was drawn and analyzed for morphine concentrations. Subjects were also asked to rate their postoperative levels of pain, nausea, and vomiting. RESULTS: There were no differences in either pain, or nausea and vomiting scores among the four study groups. Patients in Group 4 used less morphine than those in the Group 3 for the first 24 hours (P=.02) and from 25-48 hours (P=.01) after elective TAH. Morphine blood concentrations were lower after 24 hours in Group 4 compared with Group 2 (P=.04). CONCLUSION: Administration of postoperative OMT enhanced pre- and postoperative morphine analgesia in the immediate 48-hour period following elective TAH, demonstrating that OMT can be a therapeutic adjunct in pain management following this procedure.

Analgesia, Patient-Controlled↗

PubMed2002

Adjuncts to opioid therapy.

Administration of opioids to alleviate moderate to severe acute pain and chronic cancer pain is an established management process. However, advancements in clinical pharmacologic research have shown that opioids are also effective in chronic noncancerous pain. Many patients properly treated for prolonged periods with opioids develop tolerance and subsequently, physical dependence. This process is not necessarily harmful to the patient and will not cause the patient to develop an addiction (properly defined as psychologic dependence). For many patients who have been on opioid therapy for months or years, analgesic effectiveness tragically becomes less. In addition, opioid-induced constipation can be severe and cause pain; patients do not develop tolerance to this adverse reaction. Therefore, such issues become a management problem and require additional intervention. Currently, many different classes of drugs can serve as effective adjuncts to opioids for treatment of pain. Adding adjunctive medication to opioid therapy improves pain management primarily by nonopioid mechanisms of action. Clinical outcomes of such combinations include greater analgesia and attenuation of opioid-induced adverse reactions such as nausea and vomiting, constipation, sedation, and respiratory depression. Adjuncts include acetaminophen, antiarrhythmics, anticonvulsants, antidepressants, antipsychotics, baclofen, benzodiazepines, capsaicin, calcium channel blockers, clonidine hydrochloride, central nervous system stimulants, corticosteroids, local anesthetics, N-methyl-D-aspartate receptor antagonists, nonsteroidal antiinflammatory drugs, pentoxifylline, and scopolamine. Some adjuncts (eg, acetaminophen) are routinely used today, whereas others (eg, nifedipine [calcium channel blocker]) are used on a limited basis but have great potential for more widespread application. All professionals (eg, nurses, pharmacists, physicians, physicians' assistants, social workers, members of the clergy) involved in treating patients with unresolved pain recognize this to be an extraordinary and delicate time. It is when patients are likely to request physicians to provide some method to accelerate their death. Thus, inadequate analgesia can become a suicidogen, ie, any factor that causes a patient to want to commit suicide. Incorporation of adjuncts to opioid therapy can serve to lessen pain and improve quality of life for a suffering patient.

Analgesics↗

PubMed1990

Effects of chronic clomipramine on central DADLE antinociception.

Equipotent antinociceptive doses, as determined by a tail-flick response, for centrally administered (periaqueductal gray) morphine (M) and D-Ala2, D-Leu5 enkephalin (DADLE) were established as 5 micrograms and 19 micrograms, respectively. Chronic (28 day) subcutaneous infusion of clomipramine (CMI) via an Alzet minipump attenuated both central M-and DADLE-induced analgesia by day 15; attenuation persisted for the duration of the infusion (day 29). Within 7 days following removal of the pump, antinociceptive responses to M and DADLE returned to near pre-CMI levels. Our results indicate a similarity between M and DADLE with regard to attenuation of their antinociceptive action by chronic CMI. This attenuation may be due to decreased mu opioid receptor sensitivity or density resulting from chronic tricyclic antidepressant administration.

Analgesia↗

PubMed1988

Opioid-monoamine interactions in spinal antinociception: evidence for serotonin but not norepinephrine reciprocity.

Anatomical and electrophysiological studies have demonstrated that enkephalinergic, noradrenergic, and serotonergic pathways projecting from the brain-stem to the dorsal horn inhibit nociceptive transmission at the spinal level. Previous attempts to delineate interactions between opioids, norepinephrine (NE), and serotonin (5-HT) in the production of spinal analgesia have produced conflicting results. The present study determined the effect of intrathecal (i.t.) pretreatment with opioid, NE, and 5-HT antagonists upon i.t. monoamine- and morphine-induced antinociception as assessed with the rat tail-flick model. Naloxone, at a dose which antagonized i.t. morphine analgesia, had no effect upon i.t. NE but inhibited i.t. 5-HT antinociception. Corynanthine or yohimbine (NE antagonists) reduced analgesia elicited by i.t. NE but not morphine, while pretreatment with methysergide or ketanserin (5-HT antagonists) attenuated both i.t. 5-HT- and morphine-induced antinociception. These results suggest that (1) an opioid link mediates spinal 5-HT but not NE antinociception, and (2) 5-HT but not NE participates in spinal morphine analgesia.

Analgesia↗

PubMed1984

Contrasting effects of acute vs. chronic tricyclic antidepressant treatment on central morphine analgesia.

Antinociception following central opioid microinjection in rats was assessed weekly via a tail-flick procedure during chronic tricyclic antidepressant (TCA) treatment. (1) Daily TCA: Subcutaneous injections of desipramine (DMI), 30 mg/kg, chlorimipramine (CMI), 10 mg/kg, or saline, 1 ml/kg, were given daily for 22 days. Morphine sulfate (M), 5 micrograms, was microinjected into the ventrolateral periaqueductal gray (VLPAG) at 7 day intervals. On day 1, DMI or CMI enhanced M analgesia whereas saline did not. Augmentation of M disappeared by days 8 and 15 for CMI and DMI, respectively, and was replaced by attenuation which was still observed on day 22 for both TCAs. L-Tryptophan (LT), 100 mg/kg, i.p., on days 15 and 22 temporarily restored TCA enhancement of M. Fourteen days after cessation of all daily TCA treatments, enhancement of M by CMI was similar to that observed on day 1, whereas recovery of DMI-induced facilitation was incomplete. (2) Weekly TCA: Weekly treatment with DMI, CMI, or saline in the same doses as above had similar effects. M analgesia was enhanced by the TCAs but not saline on day 1; this facilitation was absent by day 15. Attenuation of M by DMI or CMI was evident on day 22; 2 weeks after cessation of all weekly TCA treatments, complete recovery of TCA-induced augmentation was observed. Loss of M facilitation during chronic daily or weekly TCA administration may be related to reduction of central opioid and/or 5-HT2 receptors.

Analgesia↗

PubMed1982

Elevation in analgetic effect and plasma levels of morphine by desipramine in rats.

Pretreatment of rats with desipramine (30 mg/kg, s.c.) enhanced both peak intensity and duration of morphine sulfate (5 mg/kg, s.c.) analgesia as determined by measurement of tail flick latency. Morphine concentrations in plasma were also significantly elevated after desipramine. Increased narcotic analgetic responses following desipramine pretreatment appear related to higher circulating levels of unmetabolized morphine.

Animals↗