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Biomedical subjects

R Mantin

Publications and source records attributed to R Mantin.

5 recordsLinked to original sources
PubMed1996

Ketorolac and propofol anesthesia in a patient taking chronic monoamine oxidase inhibitors.

There is continued controversy regarding the concurrent use of monoamine oxidase inhibitors (MAOIs) and opioids in anesthesia. MAOIs are being used in both psychiatry and also in the treatment of Parkinson's disease. The adverse interaction of meperidine with MAOIs is well described in the literature. Several other opioids used in anesthesia have been reported as potentially safe and also implicated in interaction with MAOIs. We present a case report using ketorolac as a nonopioid analgesic during a general anesthesia combined with midazolam and propofol in a successful approach in a patient continuing MAOI therapy.

Analgesics, Non-Narcotic↗
PubMed1993

Massive cisplatin overdose by accidental substitution for carboplatin. Toxicity and management.

BACKGROUND: Unlike the related drug carboplatin, cisplatin is highly nephrotoxic and must be given with vigorous intravenous hydration at a much lower dose. As the result of an accidental substitution of cisplatin for carboplatin, a 68-year-old woman received a massive overdose of cisplatin without intravenous hydration. METHODS: Laboratory documentation included measurements of platinum concentrations by atomic absorption spectroscopy and of xeroderma pigmentosum group E (XPE) binding factor, a protein that is involved in the recognition step of DNA repair. RESULTS: Toxicities included severe emesis, myelosuppression, renal failure, and deafness, which are well known. Other toxicities were seizures, hallucinations, loss of vision, and hepatic toxicity, which were unusual and may have been caused by the magnitude of the overdose. As late as day 19, there was a continued cellular response from cisplatin, as evidenced by decreased levels of XPE binding factor in extracts from the patient's peripheral blood lymphocytes. Plasmapheresis was effective in lowering the platinum concentration from greater than 2900 ng/ml to 200 ng/ml and appeared to be of clinical benefit. Even after the onset of renal failure, hydration to increase urine volume resulted in increased urinary excretion of platinum. Granulocyte-macrophage colony-stimulating factor (GM-CSF) was used to ameliorate myelosuppression. The patient received a transplanted kidney from her monozygotic twin sister and survived with no clinically significant deficit except for deafness. CONCLUSION: No previous reports exist of survival after such a high dose of cisplatin without intravenous hydration. In the future, patients may benefit from similar management and heightened awareness of the possibility of accidental substitution.

Aged↗
PubMed1990

Frontal cortex as the site of action of physostigmine in nbM-lesioned rats.

The administration of a variety of cholinomimetic agents to nucleus basalis of Meynert-lesioned rats has been shown to alleviate their lesion-induced memory deficits. This experiment attempted to determine whether the frontal cortex was the site of the memory enhancing action of the cholinomimetic physostigmine. Different groups of rats received excitotoxic lesions of the basal forebrain, the frontal cortex or both. Immediately after one trial passive avoidance training, these rats were injected with either saline or a 0.06 mg/kg dose of physostigmine. Physostigmine enhanced the 72-hour retention test performance of sham-operated and basal forebrain-lesioned rats, but failed to affect the performance of rats with cortical lesions. These data were interpreted as consistent with the hypothesis that the memory-enhancing effects of physostigmine are at least partially mediated by the frontal cortex.

Acetylcholinesterase↗
PubMed1987

Cysteamine-induced depletion of central somatostatin-like immunoactivity: effects on behavior, learning, memory and brain neurochemistry.

The effects of a wide range of doses of systemically administered cysteamine were studied on locomotor behavior, passive avoidance memory, cortical and cerebrospinal fluid somatostatin-like immunoactivity and cortical levels of dopamine and norepinephrine. High doses of cysteamine (200 and 250 mg/kg s.c.) led to sustained locomotor activation. Doses of 150 mg/kg and above resulted in head and neck tremor and increased defecation. When cysteamine was administered immediately following the acquisition of a passive avoidance response, doses of 50 mg/kg and above resulted in significant attenuation of passive avoidance retention test performance. Cysteamine in doses of 50 mg/kg and above depleted cortical somatostatin-like immunoactivity by approximately 50%. The depletion of cortical somatostatin-like immunoactivity was accompanied by a rapid rise in somatostatin-like immunoactivity in cerebrospinal fluid. In addition to the depletion of somatostatin-like immunoactivity, high doses of cysteamine (150 mg/kg and above) produced changes in cortical levels of norepinephrine and dopamine, reminiscent of dopamine-beta-hydroxylase inhibition. The results of this series of experiments suggest that somatostatin, in addition to its effects on hormonal regulation, may play an important role in behavior and passive avoidance learning and memory. It is possible that the amnesia produced by cysteamine may have been due to the release of somatostatin into CSF from tissue stores, rather than somatostatin depletion per se. It is also possible that the catecholaminergic effects of high doses of cysteamine contribute to the behavioral deficits observed.

Animals↗