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Biomedical subjects

W R Martin

Publications and source records attributed to W R Martin.

At least 199 records · Page 11Linked to original sources
PubMed1977

Actions of amphetamine and antagonists on pupil diameter in the chronic sympathectomized dog.

The left superior cervical ganglia were removed from 5 dogs. Beginning 30 days postoperatively, epinephrine (10 microgram/kg/min), norepinephrine (10 microgram/kg/min), and d-amphetamine (1.0 mg/kg) were infused i.v. for 10 min following either vehicle, phenoxybenzamine, pimozide, or haloperidol. Epinephrine and norepinephrine dilated the pupil and retracted the nictitating membrane of the denervated side, whereas amphetamine dilated both pupils and retracted both nictitating membranes. Phenoxybenzamine (4 mg/kg) constricted primarily the pupil of the innervated iris and completely antagonized the effects of the catecholamines on the irides and amphetamine on the nictitating membranes, but only partially antagonized amphetamine-induced mydriasis. Haloperidol (1.0 mg/kg) constricted both pupils, possessed only modest alpha-adrenergic blocking activity, and was as effective as phenoxybenzamine in antagonizing amphetamine-induced mydriasis. Pimozide (0.1 mg/kg) constricted both pupils, had no significant alpha-adrenergic blocking activity, and did not antagonize amphetamine-induced mydriasis. Pimozide and haloperidol, but not phenoxybenzamine, blocked amphetamine-induced stereotyped head bobbing. These results suggest that amphetamine produces mydriasis in the dog through a peripheral sympathetic action and also through a central mechanism involving inhibition of the oculomotor nucleus. However, the role of dopamine is not clear.

Animals↗
PubMed1977

The effect of the narcotic antagonists naloxone, naltrexone and nalorphine on spinal cord C-fiber reflexes evoked by electrical stimulation or radiant heat.

C-fiber reflexes were recorded from an S1 ventral root in the acute decerebrate low spinal cat following stimulation of the ipsilateral superficial peroneal nerve or application of radiant heat to the metacarpel footpad. Naloxone when administered i.v. increased the electrically evoked C-fiber reflex to 158% (+/- 23.8% S.E.M.) of control 10 min after administration; whereas, naltrexone, 0.0025 mg/kg, increased the C-fiber reflex to 206 +/- 26.1% (S.E.M.) of control. Naloxone in a dose of 0.050 mg/kg increased the radiant heat evoked ventral root reflext to 161 +/- 19.5% of control. Nalorphine, 1 mg/kg, facilitated the electrically evoked C-fiber reflex to 282 +/- 75% of control. These findings that naloxone and naltrexone facilitated these reflexes in doses too small to have non-specific excitatory effects and that nalorphine facilitated the C-fiber reflex at a dose level that is depressant to the flexor reflex in the chronic spinal dog are consistent with a hypothesis that these effects are due to antagonism of a naturally occurring opiate-like inhibitory substance.

Action Potentials↗
PubMed1977

Effect of mass transfer resistance on the Lineweaver-Burk plots for flocculating microorganisms.

It is shown that the mass transfer resistance can significantly distort the linearity of the Lineweaver-Burk plot of the kinetic data for a microbial culture which forms aggregates. For small flocs, the linearity of the Lineweaver-Burk plot is largely retained, but a different slope and intercept will be obtained compared with flocs free from mass transfer resistance. For large flocs, the Lineweaver-Burk plot shows pronounced curvature at high limiting substrate concentrations. Hence, if the true intrinsic kinetic parameters are to be extracted from a highly flocculating microbial culture, sufficient agitation has to be provided to remove the effect of mass transfer resistance. If the behavior of the flocculating microbial culture is to be explored, additional values for some physical parameters, such as the effective diffusion coefficient of the substrate in floc, the floc density, and the mean floc radius, are needed.

Bacterial Physiological Phenomena↗
PubMed1977

Transcallosally evoked potentials and the EEG in the decerebrate dog: actions of tryptaminergic, dopaminergic and adrenergic agonists.

The midpontine decerebrate dog, immobilized with gallamine, was used to determine the changes in the transcallosally evoked potential (TEP) produced by intravenous infusions of various drugs. A total of 50 TEPs, recorded from the g. ectolateralis, was computer analyzed before, during and after administration of the drugs. Changes in the TEP were also correlated with changes in the EEG recorded from the g. ectolateralis. The EEG was analyzed by inspection and amplitude integration (electrogenesis). LSD (30 microng/kg) significantly depressed the TEP, and the effect persisted for at least 80 min. DMT (1 mg/kg) caused a significant and reversible increase in the amplitude of the TEP. LSD and DMT reduced the alpha activity of the EEG and enhanced the amplitude of the low-frequency waves. DMT produced a significant and LSD a marginal increase in electrogenesis. Tryptamine (10 and 20 mg/kg), mescaline (6 mg/kg), methoxamine (0.88 mg/kg) and apomorphine (5 mg/kg) had no significant effect on the TEP or EEG. These results suggest that depression of the TEP is not related to spinal reflex facilitation in the dog or hallucinogenic activity in man.

Adrenergic Agonists↗
PubMed1976

A method for bioassay of physical dependence on sedative drugs in dog.

A method for an economical bioassay of physical dependence on sedatives is presented. Dogs maintained on sodium pentobarbital (200 mg/kg/24 h i.v.) were given periodic graded reductions in maintenance dose, and subscales for measuring signs of abstinence were developed. Using these subscales the relative potencies compared with sodium pentobarbital were determined for sodium secobarbital (RP = 0.85) and methaqualone (RP = 0.14). Sodium thiopental and methaqualone were assayed and found to be equipotent (RP = 0.96) in reducing the signs of abstinence from sodium pentobarbital. The occurrence of convulsions, during periods of complete reduction of the maintenance drug, became less frequent the longer the dogs had been maintained on a constant dose of sodium pentobarbital.

Animals↗
PubMed1976

Subjective and physiologic effects of morphine, pentobarbital, and meprobamate.

These studies extend previous observations on the effects of pentobarbital on subjective states and postrotational nystagmus in postaddict subjects. Pentobarbital (150 mg) induced a degree of liking and an elevation of the morphine-benzedrine group (MBG) scale score equivalent to 24 mg of morphine. The effects of pentobarbital and meprobamate on postrotational nystagmus were studied using electro-oculography. Both drugs increased the frequency and prolonged the duration of postrotational nystagmus in a dose-related manner. Meprobamate was about 1/15 as potent as pentobarbital in enhancing postrotational nystagmus and producing signs of sedation.

Electrooculography↗
PubMed1976

Sigma effects of nalorphine in the chronic spinal dog.

The effects of graded doses of nalorphine and morphine were studied in nondependent chronic spinal dogs. Morphine and low doses of nalorphine produced behavioral changes characterized by indifference, whereas the largest dose of nalorphine produced canine delirium indistinguishable from that produced by SKF-10, 047 or cyclazocine. Nalorphine depressed the flexor reflex; however, a plateau was observed. The data suggest that nalorphine is a partial agonist of the kappa type and a sigma agonist in addition to being a competitive antagonist at the mu receptor, and further, that the dysphoric and hallucinogenic effects of nalorphine-like drugs are due to their sigma activity.

Animals↗
PubMed1976

Naloxone.

Narcotic analgesics and related drugs act as agonists on several receptors that are responsible for their effects on pain perception, mood and feeling state, and respiration, as well as other pharmacologic actions. Naloxone is the first discovered antagonist that is devoid of agonistic activity and appears to be a competitive antagonist at several receptors. The ability of naloxone to displace or prevent the binding of agonistic narcotics is partly responsible for its antagonistic effects. The ability of naloxone to rectify narcotic-depressed homeostats and precipitate abstinence is also related to its antagonistic activity. Certain cautions and principles apply in the use of naloxone in treating narcotic overdose, reversing surgical analgesia, and the treatment of neonates and children. Unapproved uses of naloxine include reversing the psychotomimetic effects of certain agonists-antagonists, terminating narcotic-induced convulsions and coma, reversing non-narcotic depression, diagnosing physical dependence, and treating narcotic addicts.

Adult↗
PubMed1976

Actions of methoxamine and tryptamine and their interactions with cyproheptadine and phenoxybenzamine on cat spinal cord segmental reflexes.

The effects of norepinephrine, methoxamine and tryptamine were assessed on the monosynaptic and polysynaptic segmental reflexes in the unanesthetized, decerebrated acute spinal cat. Their selectivity of action was determined by studying the interactions of methoxamine and tryptamine with two antagonists, cyproheptadine and phenoxybenzamine. Potentials were evoked by stimulating either the L7 or S1 dorsal root and were recorded from the corresponding ipsilateral ventral root. Norepinephrine did not affect reflex activity, whereas methoxamine facilitated both the monosynaptic and polysynaptic potentials in a dose-related manner when infused over 20 minutes. Tryptamine facilitated both the monosynaptic and polysynaptic reflex potentials. This increase was dose related for the monosynaptic reflex but not for the polysynaptic reflex. Phenoxybenzamine blocked the facilitatory effects of methoxamine and did not antagonize the effects of tryptamine on the segmental reflex. The facilitatory effects of tryptamine were effectively blocked by cyproheptadine. Cyproheptadine failed to reduce the polysynaptic response to methoxamine, although it partially antagonized the monosynaptic facilitation. These findings demonstrate that methoxamine and tryptamine facilitate the segmental reflex by different modes of action and provide additional evidence for noradrenergic and tryptaminergic systems in the spinal cord.

Animals↗
PubMed1976

The effect of L-tryptophan on spinal cord C-fiber reflexes.

C-fiber reflex were recorded from an ipsilateral S1 ventral root in the acute decerebrate spinal (T10) cat after stimulation of the superficial peroneal nerve. L-Tryptophan, infused in a dose of 150 mg/kg, increased the C-fiber reflex to 210% (S.E.M. +/- 30.1%) of control. This effect was antagonized by cyproheptadine, 0.5 mg/kg. L-Tryptophan increased the C-fiber reflex to 176% (S.E.M. +/- 13.0%) of control after p-chlorophenylalanine pretreatment. Pretreatment of the cats with the decarboxylase inhibitor alpha-methyldopa, 100 mg/kg, 30 minutes before infusion, antagonized the facilitatory effects of L-Tryptophan. L-Tryptophan, 150 mg/kg, had no effect on the monosynaptic or short latency polysynaptic reflexes. 5-Hydroxytryptophan, 20 mg/kg, had erratic effects on the C-fiber reflex producing both facilitation and depression which were not statistically significant. The recovery of tryptamine from brain perfusates, after perfusion of the anterior cerebellum and pons, with a modified Gaddum push-pull cannula, decreased across time. L-Tryptophan caused a slight increase in tryptamine release which was not statistically significant, whereas in cats pretreated with p-chlorophenyl alanine, a significant increase in tryptamine release was seen.

5-Hydroxytryptophan↗
PubMed1976

The effects of morphine- and nalorphine- like drugs in the nondependent and morphine-dependent chronic spinal dog.

Three different syndromes produced by congeners of morphine have been identified in the nondependent chronic spinal dog. These syndromes have been attributed to interaction of agonists with three distinguishable receptors (mu, kappa and sigma). Morphine is the prototype agonist for the mu receptor, ketocyclazocine for the kappa receptor and SKF-10,047 for the sigma receptor. The morphine syndrome (mu) in the dog is characterized by miosis, bradycardia, hypothermia, a general depression of the nociceptive responses and indifference to environmental stimuli. Ketocyclazocine (kappa) constricts pupils, depresses the flexor reflex and produces sedation but does not markedly alter pulse rate or the skin twitch reflex. SKF-10,047 (sigma), in contrast to morphine and ketocyclazocine, causes mydriasis, tachypnea, tachycardia and mania. The effects of these three drugs can be antagonized by the pure antagonist naltrexone, indicating that they are agonists. Further, chronic administration of morphine, ketocyclazocine and SKF-10,047 induces tolerance to their agonistic effects. Morphine suppresses abstinence in morphine-dependent dogs while ketocyclazocine does not. Ketocyclazocine at best precipitated only a liminal abstinence syndrome in the morphine-dependent dog, indicating that it had little affinity for the morphine receptor. Ketocyclazocine thus appears to be a selective agonist at the kappa receptor. Further, it has been shown that buprenorphine is a partial agonist of the mu type which both suppressed and precipitated abstinence in the morphine-dependent dog while morphine and propoxyphene are stronger agonists. Apomorphine and SKF-10,047 produce similar pharmacologic effects suggesting that sigma activity may involve a dopaminergic mechanism.

Animals↗
PubMed1976

The effects of morphine and nalorphine-like drugs in the nondependent, morphine-dependent and cyclazocine-dependent chronic spinal dog.

A series of morphine-like and nalorphine-like drugs were studied in the nondependent, morphine-dependent and cyclazocine-dependent chronic spinal dog. In the nondependent dog, three profiles of activity were found which could be utilized to distinguish between morphine, WIN 35, 197-2 and cyclazocine. Propiram, a prototypic partial agonist of the morphine type, produced morphine-like effects in nondependent dogs and both precipitated and suppressed abstinence in cyclazocine-dependent dogs as was needed to precipitate abstinence in morphine-dependent dogs. WIN 35, 197-2, a strong agonist in the guinea-pig ileum which has been shown to be resistant to antagonism by naloxone, neither precipitated nor suppressed morphine abstinence but suppressed cyclazocine abstinence. In the nondependent dog, it depressed the flexor reflex but not skin twitch reflex. Cyclazocine altered reflex activity much like WIN 35, 197-2 but produced tachycardia, tachypnea, mydriasis and canine delirum. The morphine and cyclazocine precipitated and withdrawal abstinence syndromes were qualitatively different. Twenty times as much naltrexone was needed to precipitate abstinence in morphine-dependent dogs. Nalorphine both precipitated and suppressed cyclazocine abstinence and appeared to be a partial agonist of the nalorphine-type. Morphine suppressed the cyclazocine abstinence syndrome. Cross-tolerance was not observed in ketocyclazocine-dependent dogs. These data are consistent with the hypothesis that there are strong and partial agonists of the mu and kappa types, and further, that physical dependence on morphine and cyclazocine is mediated through different receptors. WIN 35, 197-2 appears to be a pure strong agonist of the kappa type. Cyclazocine is a mu antagonist and mixed kappa and sigma agonist.

Animals↗