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P J Manberg

Publications and source records attributed to P J Manberg.

At least 19 recordsLinked to original sources
PubMed1999

Computer simulation to determine how rapid anesthetic recovery protocols to decrease the time for emergence or increase the phase I postanesthesia care unit bypass rate affect staffing of an ambulatory surgery center.

UNLABELLED: Ambulatory surgery centers (ASC) are implementing new anesthetic techniques and rapid recovery protocols in the postanesthesia care unit (PACU) to achieve earlier discharge after general anesthesia. Using computer simulation, we addressed two questions. First, what is the decrease in an ASC's operating room (OR) staff if the time from which the surgery is finished to the time the patient leaves the OR is decreased? Second, what is the decrease in PACU nursing staffing if patients bypass phase I PACU (i.e., proceed from the OR directly to the phase II PACU)? The decrease in labor costs from rapid emergence or fast-tracking depends on how staff are compensated, how many ORs routinely run concurrently, and what percentage of patients undergo general anesthesia. The results show potential decreases in ASCs' labor costs ($7.39 per case) from technologies (e.g., new anesthetics or Bispectral Index [Aspect Medical Systems, Natick, MA] monitoring) to decrease emergence times or increase the phase I bypass rates. IMPLICATIONS: Decreases in operating room and postanesthesia care unit labor costs resulting from faster emergence and phase I postanesthesia care unit bypass vary depending on the amount of routine overtime, how the staff are compensated, and how many patients are routinely anesthetized each day.

Ambulatory Surgical Procedures↗
PubMed1989

Neurotensin-like immunoreactivity in cerebrospinal fluid of patients with schizophrenia, depression, anorexia nervosa-bulimia, and premenstrual syndrome.

Neurotensin (NT) concentrations in cerebrospinal fluid (CSF) were measured by a sensitive and specific radioimmunoassay in psychiatric patients and age- and sex-matched normal controls. No increase in CSF NT concentrations was observed after antipsychotic drug treatment. CSF NT concentrations were significantly lower in one group of schizophrenic subjects. NT concentrations were unaltered in patients with depression, anorexia/bulimia, or premenstrual syndrome, and no rostral-caudal gradient for NT in CSF was evident. NT concentrations were not related to age or sex, and probenecid treatment did not alter CSF NT concentrations. Finally CSF NT concentrations were unaltered in paranoid schizophrenic subjects. These findings confirm and extend previous studies of CSF NT that showed certain patients with schizophrenia, nonparanoid type, have reduced CSF concentrations of this tridecapeptide.

Adult↗
PubMed1986

Single-dose pharmacokinetics of clomiphene citrate in normal volunteers.

Twenty-four healthy adult female volunteers participated in a randomized, three-phase double-blind crossover trial comparing the single-dose (50 mg) pharmacokinetics of three formulations of clomiphene citrate (CC). Plasma levels of both the Z(cis) and E(trans) isomers of CC, as well as principal metabolites, were determined at periodic intervals; and no differences between formulations were observed. The active Z isomer attained peak blood levels later than the inactive E isomer and was eliminated much more slowly, significant plasma concentrations still being detected up to 1 month after treatment. The results of this study demonstrate that three commercially available formulations of CC are bioequivalent.

Adult↗
PubMed1985

Neuropeptides in CSF and post-mortem brain tissue of normal controls, schizophrenics and Huntington's choreics.

Studies describing the CNS distribution of neuropeptides can provide important new insights concerning their possible physiological functions. The rational for studying human post-mortem tissue, as well as some methodological constraints, are reviewed. The localization of NT in normal human brain is presented. Concentrations of NT, TRH, and SRIF were determined in brain tissue from normal controls and patients with schizophrenia or Huntington's chorea. Specific alterations in the levels of these neuropeptides were found in each disease. Appreciable quantities of NT immunoreactivity are present in human CSF. Sub-normal CSF-NT levels were found in a sub-group of unmedicated schizophrenics but were elevated back to normal concentrations following neuroleptic treatment. Although the pathophysiological significance of these findings is unclear, they nevertheless indicate that neuropeptides are important brain constituents which deserve further study.

Adult↗
PubMed1985

Problems in the development of neuropeptides as psychotherapeutic drugs.

Research describing the potent pharmacological effects of endogenous neuropeptides has stimulated considerable interest in possible psychotherapeutic applications of these compounds. Initial clinical experience has helped to identify several unique problems, inherent to the use of peptides as CNS drugs, which must be overcome before these peptides can become useful therapeutic agents. An appreciation for the problems, as well as the promise, associated with the use of peptides is needed to assure their ultimate clinical utility.

Biological Availability↗
PubMed1983

Regional brain concentrations of neuropeptides in Huntington's chorea and schizophrenia.

To ascertain whether Huntington's chorea and schizophrenia are associated with specific regional alterations in neurotensin, somatostatin, and thyrotropin-releasing hormone, the concentrations of these putative neurotransmitters were measured by radioimmunoassay in postmortem brain samples from patients with Huntington's chorea or schizophrenia. Compared to 50 patients without psychiatric or neurological disease, the patients with Huntington's chorea showed significantly elevated concentrations of all three neuropeptides in the nucleus caudatus. In the nucleus accumbens somatostatin levels were increased threefold, while in the amygdala thyrotropin-releasing hormone levels were elevated. In contrast, the schizophrenics exhibited reduced levels of thyrotropin-releasing hormone in two frontal cortical regions, reduced somatostatin levels in one frontal cortical area, and increased neurotensin levels in one frontal cortical area. None of the differences between the diseased brains and the controls could be accounted for by differences in age, sex, or time between death and autopsy.

Brain↗
PubMed1983

Overview of clinically significant adverse reactions to bupropion.

During the clinical development of bupropion (Wellbutrin) 1,153 depressed patients and 157 normal volunteers received bupropion (doses, 15-1200 mg/day); 177 placebo-treated and 196 tricyclic-treated patients (doses, 25-300 mg/day) also participated in these trials to provide a control comparison. Safety measures during the clinical trial program included adverse event symptomatology, vital signs, clinical laboratory examinations, and EEGs. There were no bupropion-related changes in vital signs, clinical laboratory, or EEG results severe enough to warrant treatment discontinuation. The most common cause for discontinuation in the bupropion (9.1%), placebo (6.8%), and tricyclic groups (9.2%) was agitation/excitement. The only adverse experience considered of medical significance in bupropion patients was major motor seizure. The incidence of a seizure was less than 1 per 1,000 at usual outpatient doses and less than 1 per 100 at usual inpatient doses. These incidences appear to be comparable to those seen with equally therapeutic doses of tricyclic antidepressants.

Adult↗
PubMed1982

Development of a radioimmunoassay for Pro-Leu-Gly-NH2 (PLG or MIF-I): evidence that PLG is not present in rat brain.

Pro-Leu-Gly-NH2 (PLG), which is the C-terminal tripeptide tail of oxytocin, has been reported to possess melanocyte-stimulating hormone (MSH)-release-inhibiting activity. Although it has been isolated from bovine hypothalamus, little is known about the CNS distribution of this peptide in other species. In this report, we describe the development of a radioimmunoassay which can be used to measure both PLG and oxytocin following chromatographic separation by high pressure liquid chromatography (HPLC). Using this method, we are unable to demonstrate the presence of any endogenous PLG in rat hypothalamus, preoptic area, pituitary, or eye tissue. However, synthetic PLG, which is added to tissue homogenates as an internal standard, is consistently recovered from all areas. We conclude that the PLG tripeptide is not present in the rat brain and thus cannot be the physiological regulator of MSH secretion.

Animals↗
PubMed1982

Regional distribution of neurotensin in human brain.

Neurotensin (NT) is an endogenous neuropeptide that is active in many preclinical screening tests for neuroleptic drugs. Using a radioimmunoassay, we have studied the regional distribution of NT in postmortem human brain and in cerebrospinal fluid. Highest levels were present in the hypothalamus, substantia nigra, and limbic areas, whereas much lower amounts were found in the cortex and striatum. The chromatographic properties of hypothalamic immunoreactivity on ion-exchange and high pressure liquid chromatography were similar to those of the synthetic tridecapeptide. We conclude that NT is present in human brain with a distribution resembling that seen in other species, such as rat and monkey.

Adult↗
PubMed1980

Neurotensin-induced hypothermia: evidence for an interaction with dopaminergic systems and the hypothalamic--pituitary--thyroid axis.

Neurotensin (NT), an endogenous tridecapeptide, produces significant hypothermia after intracisternal (i.c.) or intracerebroventricular (i.c.v.) administration in microgram quantities in a variety of laboratory animals. The present study sought to clarify the mechanism of the hypothermic action by utilizing pharmacological treatments which alter the function of brain neurotransmitter systems. Pretreatment of rats with anti-muscarinic (atropine), anti-noradrenergic (propranolol, a beta-blocker; phenoxybenzamine, an alpha-blocker) or anti-opiate (naloxone) agents did not significantly alter NT-induced hypothermia. Similarly depletion of brain serotonin (5-HT) with parachlorophenylalanine did not affect NT-induced hypothermia. However, depletion of brain catecholamine content with 6-hydroxydopamine resulted in a significant potentiation of NT-induced hypothermia as did pretreatment with haloperidol, a dopamine (DA) receptor antagonist. Furthermore, in rats with selective depletions of brain DA, but not norepinephrine (NE), NT-induced hypothermia was significantly augmented. Thus an interaction between brain DA systems and NT appears likely. These data indicate that NT-induced hypothermia is not dependent on intact functional activity of NE, 5-HT, muscarinic ACh or endogenous opiate systems but suggests interactions between brain DA circuits and NT. In other experiments, NT-induced hypothermia was found to be antagonized significantly by i.c. injection of thyrotropin-releasing hormone (TRH), but not by pretreatment with L-triiodothyronine. Another endogenous tripeptide (Pro--Leu--Gly--NH2, MIF-I) had no effect. Thyroidectomy (THX) significantly potentiated NT-induced hypothermia; NT administered i.c. significantly reduced the high serum TSH levels of THX rats. Thus, NT and TRH, two endogenous peptides, appear to be antagonists in certain systems.

Animals↗
PubMed1979

Centrally administered neurotensin: activity in the Julou-Courvoisier muscle relaxation test in mice.

Intracisternal (IC) neurotensin (NT) produces muscle relaxation in the Julou-Courvoisier traction test, a screening procedure utilized for assessing neuroleptic drug activity. A dose-response relationship was not observed. IC administration of thyrotropin-releasing hormone (TRH) totally abolished the effects of NT. Two other peptides, substance P and bradykinin, were inactive in the traction test. These data provide further evidence for CNS effects on NT and indicate that this peptide exerts neuroleptic-like activity in a screening test for antipsychotic agents.

Animals↗
PubMed1979

Thyrotropin-releasing hormone and amphetamine: a comparison of pharmacological profiles in animals.

1. The pharmacological effects of TRH are compared to those produced by d-amphetamine in an attempt to elucidate the mechanisms underlying the activity of this endogenous peptide. 2. Although numerous amphetamine-like actions have been attributed to TRH, several differences have been noted between these compounds and are discussed. 3. At present, it is impossible to propose a single mechanism of action to explain the behavioral effects of TRH.

Amphetamine↗
PubMed1979

Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine.

The antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and beta-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas beta-endorphin was the most potent antinociceptive agent via this route of administration. Both NT, and beta-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Met]enkephalin, or [Leu]enkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studies [bradykinin, thyrotropin-releasing factor (thyroliberin), melanocyte-stimulating hormone release-inhibiting factor (melanostatin), somatostatin, [Met]enkephalin, and [Leu]enkephalin] produced any significant alterations in colonic temperature or response to a noxious stimulus with the doses tested. These data demonstrate that NT and beta-endorphin, two endogenous brain peptides, are potent in inducing hypothermia and in producing an antinociceptive state.

Animals↗