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Biomedical subjects

M F Sugrue

Publications and source records attributed to M F Sugrue.

At least 73 records · Page 4Linked to original sources
PubMed1975

On the ability of prostaglandin E1, and arachidonic acid to modulate experimentally induced oedema in the rat paw.

1 Prostaglandins E1 and E2 but not prostaglandin F2alpha, arachidonic acid or linolenic acid, produced slight oedema when injected into the rat hindpaw. 2 Prostaglandin E1 potentiated hindpaw oedema produced by carrageenan, kaolin, bradykinin and trypsin but not that produced by 5-hydroxytryptamine (5-HT), histamine, dextran B or compound 48/80. Carrageenan- and bradykinin-induced paw oedemas were also potentiated by prostaglandin E2. Arachidonic acid potentiated responses to carrageenan and kaolin but not responses to bradykinin, trypsin, 5-HT, histamine, dextran B or compound 48/80. Linolenic acid did not potentiate hindpaw oedema induced by carrageenan. 3 Potentiation of carrageenan-induced oedema by prostaglandin E1 was not diminished by pretreatment with indomethacin, hydrocortisone or cyproheptadine. However, arachidonic acid potentiation of carrageenan oedema was reduced by pretreatment with non-steroidal anti-inflammatory drugs but not by anti-inflammatory steroids or by paracetamol. 4 The enhancement of the response to carrageenan and kaolin by prostaglandins E1, E2 and arachidonic acid is discussed in terms of kinin mediation.

Animals↗
PubMed1975

On the pharmacology of Org 6338 (2beta, 16beta-dipiperidino - 5alpha - androstan - 3alpha - ol acetate dimethobromide), a new steroidal neuromuscular blocking agent.

Org 6368 is a homologue of pancuronium bromide. Its interactions with other agents in the cat sciatic nerve-gastrocnemius muscle preparation revealed that paralysis was of the non-depolarizing type. This was confirmed in experiments using avian muscle. Org 6368 is a potent muscle relaxant being 2-4 times as potent as (+)-tubocurarine in the cat. Paralysis in the cat is rapid in onset and of appreciably shorter duration than that of pancuronium and (+)-tubocurarine. Repeated injections of the same dose of Org 6368 show no cumulative effect. Muscle relaxant doses generally cause a slight increase in both blood pressure and heart rate. Although its histamine-releasing capacity is greater than that of pancuronium it is less than that of (+)-tubocurarine. Org 6368 shares with pancuronium a very weak effect on both the muscarinic receptor and ganglionic transmission. Differences in the muscle relaxant profiles of Org 6368 and pancuronium are discussed.

Animals↗
PubMed1974

The effects of acutely administered analgesics on the turnover of noradrenaline and dopamine in various regions of the rat brain.

1 Noradrenaline and dopamine turnover rates were determined following blockade of synthesis by alpha-methyl-p-tyrosine. Morphine, pentazocine and methadone had no effect on steady state levels or on turnover of noradrenaline in whole brain and in the hypothalamus. Although morphine was without action on medulla-pons noradrenaline steady state levels, a drug-induced increase in turnover rate was observed which was antagonized by pretreatment with naloxone (5 mg/kg). Pentazocine and methadone failed to alter either the steady state level of noradrenaline in the medulla-pons or its turnover rate.2 Morphine accelerated the decline in striatal alpha-methyl-m-tyramine levels following subcutaneous injection of alpha-methyl-m-tyrosine 18 h previously.3 All three drugs increased the turnover of dopamine in whole brain and corpus striatum although the striatal effect was prevented by naloxone pretreatment. The minimum doses of morphine, pentazocine and methadone required to elicit a significant effect on striatal dopamine turnover were 10 mg/kg, 30 mg/kg and 10 mg/kg respectively.4 The possibility of a dopaminergic involvement in the antinociceptive effect of analgesics is discussed.

Analgesics↗
PubMed1969

A study of the role of noradrenaline in behavioral changes produced in the rat by psychotomimetic drugs.

1. LSD-25, psilocybin and JB-329 reduced the noradrenaline content of the rat hypothalamus.2. All three drugs affected the acquisition of a conditioned avoidance response, LSD-25 and psilocybin retarding and JB-329 enhancing the acquisition. With the exception of JB-329, doses affecting the acquisition of a conditioned avoidance response were lower than those required to decide hypothalamic noradrenaline concentrations. The time of peak drug effect on the acquisition of a conditioned avoidance response occurred approximately 1.5 hr after injection as opposed to 3 hr in the case of noradrenaline content.3. The amount of LSD-25, psilocybin and JB-329 necessary to elicit gross behavioural excitation was similar to the dose producing noradrenaline depletion. Here also the peak behavioural effect was detected earlier.4. Pretreatment with reserpine and alpha-MT had no effect on the intensity of gross behavioural excitation induced by LSD-25 and psilocybin but shortened the duration of the response. The excitation induced by JB-329 was abolished by reserpine pretreatment and was markedly reduced both in intensity and duration by the prior injection of alpha-MT.

Animals↗