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Biomedical subjects

I W Waters

Publications and source records attributed to I W Waters.

At least 37 records · Page 2Linked to original sources
PubMed1978

Effect of 1-alpha-acetylmethadol (LAAM) on various physiological parameters in the conscious dog.

LAAM was administered intravenously to conscious dogs at doses of either 0.1, 0.3 or 1.0 mg/kg. Cardiopulmonary responses were measured prior to drug administration, 0.5 hr post-drug and hourly thereafter. All doses produced a sleep-like state which was dose-related in duration (3-14 hr). Cardiac output, heart rate, respiratory rate and minute volume were decreased below mean pre-drug control values after drug administration in the two higher dosage groups; cardiac output in both groups failed to return to pre-drug control levels. Additionally, total peripheral resistance was elevated in these dosage groups although mean arterial pressure remained stable. Arterial pCO2 increased and arterial pH decreased as respiratory rate and minute volume decreased. Depression of rectal temperature occurred only in response to the highest dose.

Animals↗
PubMed1978

Interactions of catecholaminergic receptor blockers with lethal doses of amphetamine or substituted amphetamines in mice.

Lethality to both isolated and aggregated mice was determined for graded i.p. doses of d-amphetamine, dl-4-methoxyamphetamine (PMA), dl-2,5-dimethoxyamphetamine (DMA), dl-2,5-dimethoxy-4-bromoamphetamine (DOB), dl-2,5-dimethoxy-4-methylamphetamine (DOM) and d1-3,4-methylenedioxyamphetamine (MDA). Haloperidol (2.0 mg/kg), propranolol (10 mg/kg) and phenoxybenzamine (30 mg/kg) were tested for ability to antagonize the lethal effects of amphetamine and its derivatives. Considerable protection against amphetamine lethality was produced by haloperidol in both isolated and aggregated mice and by phenoxybenzamine in isolated mice, but propranolol was ineffective. An equivalent degree of protection was not achieved by use of any of the three agents before PMA, DMA or DOB. Protection against DOM was achieved only with phenoxybenzamine and only for isolated mice. Extensive protection against MDA was supplied by both phenoxybenzamine and propranolol for either condition of housing. Despite close structural relationships between the toxicants, the antidotal effectiveness of the receptor-blocking agents seemed quite limited and specific, and did not support any generalizations.

Amphetamines↗
PubMed1978

Acute cocaine intoxication in the conscious dog: pathophysiologic profile of acute lethality.

Cocaine HCl was infused intravenously to conscious mongrel dogs until death (0.5 mg/kg/min; 0.82 ml/min). All animals convulsed (mean convulsive dose: 12 +/- 1 mg/kg) and died approximately 42 min after the beginning of cocaine infusion (mean lethal dose: 21 +/- 2 mg/kg). All animals exhibited significant increases in arterial systolic and diastolic pressures, left ventricular pressure, cardiac output, heart rate, respiratory rate, minute volume, tidal volume, oxygen uptake, plasma glucose, blood lactate and body temperature. Statistically significant reductions from pre-drug control levels were observed in total peripheral resistance, arterial pH, and arterial pO2.

Alanine Transaminase↗
PubMed1977

Conformational analogues of antihypertensive agents related to guanethidine.

In an effort to clarify the conformational requirements, if any, of agents producing adrenergic neuronal blockade through mechanisms similar to guanethidine, the synthesis and pharmacological evaluation of 15 analogues of cinnamylguanidine are described. These analogues represent derivatives in which the distance between the center of the ring system and the guanidinium nitrogen atom varies from 3.9 to 6.2 A. While conformational relationships could not be defined in this study, three analogues (3, 4, and 5) were apparently more potent than guanethidine in the in vitro assay employed.

Adrenergic Agents↗
PubMed1975

Effect of acylation with eleostearic acids on the monoamine oxidase inhibitory potency of some hydrazine antidepressants in mice.

The effect of incorporation of an eleostearoyl group into molecules of aralkylhydrazines on their monoamine oxidase inhibitory potency was investigated in vitro and in vivo. The results showed that on a molar basis the hydrazides possessed an in vitro potency lower than and an in vivo potency and acute toxicity comparable to those of the corresponding aralkylhydrazines. The sequence of the relative potency of aralkylhydrazines and their hydrazides was similar. The overall pharmacological profile indicated that these aralkylhydrazines retained their monoamine oxidase inhibitory properties when the free hydrazine nitrogen was acylated with an eleostearoyl group.

Acylation↗
PubMed1975

Interactions of tricyclic antidepressants and barbiturates in barbiturate-tolerant and nontolerant rats.

Pretreatment of rats with tricyclic antidepressants, imipramine, desipramine, amitriptyline and nortriptyline, at two doses (5 and 25 mg/kg) 20 minutes before administration of barbiturate markedly reduced the latent period of the response to barbital and prolonged the sleeping time induced by pentobarbital (PB) and barbital. The effects were dose-dependent. The prolonged sleeping time produced by PB was associated with decreases in the rates of disappearance of PB from the brain and plasma. The effect of tricyclic antidepressants on PB hypnosis in PB-tolerant and nontolerant rats was apparently not related to change in central nervous system (CNS) sensitivity to PB, since at the time of awakening there were no significant differences in the concentrations of unmetabolized PB in either the plasma or brain of tricyclic antidepressant-treated animals as compared to controls. As barbital is not metabolized, potentiation of barbital hypnosis by tricyclic antidepressants must be attributable to a direct effect on CNS rather than on liver microsomal enzymes. Direct evidence was provided by the findings that amitriptyline accelerated the brain uptake of barbital and that amitriptyline-treated animals lost and recovered the righting reflex at brain barbital levels lower than those of controls. Rats made tolerant to the hypnotic effect of barbital also became tolerant, in varying degrees, to the hyposis-prolonging properties of tricyclic antidepressants. It is concluded that tricyclic antidepressants prolong PB sleeping time in PB-tolerant and nontolerant rats by inhibiting its biotransformation in the liver. The action of tricyclic antidepressants to prolong the hypnotic action of barbital in normal rats is related to their direct effects on CNS sensitivity to barbital, but such effects are makedly diminished after animals become tolerant to barbital.

Amitriptyline↗