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Biomedical subjects

S I Baskin

Publications and source records attributed to S I Baskin.

At least 37 records · Page 2Linked to original sources
PubMed1991

Ambulatory electrocardiography (Holter monitoring) in caged monkeys.

A swivel-tethering and jacket system was used in conjunction with vinyl patch electrodes and Holter recorders to obtain continuous ECG recordings in 12 rhesus monkeys on a long-term (12 day) study. Animals were custom-fitted with nylon mesh jackets that were connected to a swivel unit by a flexible, stainless steel tether. Lead wires from the chest electrodes passed through the tether to the electrical swivel apparatus located at the top of the cage. Wires from the upper part of the swivel were attached to a reel-to-reel Holter recorder. This technique was used to obtain 24-h continuous ECG recordings, which were later processed using a computer-assisted Holter analysis system.

Animals↗
PubMed1991

The effects of AF-DX 116, a cardioselective muscarinic antagonist, on the negative inotropic action of acetylcholine.

In superfused left atria from male guinea pigs, rats, and rabbits, myocardial contractility was measured before and after addition of acetylcholine (ACh) and AF-DX 116 ((11[[2-[(diethylamino)methyl]-1-piperidinyl]-acetyl]-5,11-dihydro- 6H-pyrido[2,3-b] [1,4]benzodiazepine-6-) one), a selective muscarinic antagonist. Characteristic dose-response curves for acetylcholine showing greater negative inotropic response with dose were seen. Increasing AF-DX 116 concentrations reversed the negative inotropy of acetylcholine and, in fact, increased the inotropic response approximately 100% and 50% above the baseline contractile force in a dose-dependent manner in the guinea pig and rabbit, respectively. This increase in contractility following AF-DX 116 addition was not observed in rat atria. The capacity of AF-DX 116 to produce the positive inotropic response only occurred at concentrations above 1 x 10(-5) M. The positive inotropic response of AF-DX 116 was antagonized by dl-propranolol, which suggests that the administration of AF-DX 116 at higher concentrations may unmask the effect of norepinephrine released from underlying viable adrenergic terminals which exist in the left atria.

Acetylcholine↗
PubMed1990

Formation of methemoglobin and metmyoglobin using 8-aminoquinoline derivatives or sodium nitrite and subsequent reaction with cyanide.

The kinetics of the oxidation of hemoglobin (Hb) and myoglobin (Mb) by sodium nitrite, 8-[(4-amino-1-methylbutyl)amino]-6-methoxy-quinoline diphosphate (primaquine), 6-methoxy-8-(6-diethylaminohexylamino)-4-methyl-quinoline dihydrochloride (WR6026) and 8-[(4-amino-1-methylbutyl)amino]-2,6-dimethoxy-4-methyl- 5-[(3-trifluoromethyl)phenoxy]quinoline succinate (WR238,605) were studied at pH values ranging from 7.4 to 7.6 and at 37 +/- 1 degrees C. The reaction between Hb and primaquine, WR6026 and WR238,605 resulted in precipitation, as did the reaction between Mb and WR238,605. The reaction between nitrite ion (NO2-) and Hb showed a lag period followed by an autocatalytic phase. The data in this study are consistent with and substantiate the proposed mechanism for the Hb-NO2- oxidation reaction. The reaction between Mb and NO2- at higher NO2- concentrations also showed a lag period followed by an autocatalytic period, while at lower NO2- concentrations no lag period was seen. The data suggest a shift in rate constant at these lower NO2- concentrations. The reaction between Mb and both WR6026 and primaquine followed a two-term rate law with oxidant-dependent and -independent terms. Concentration-effect curve data, along with these results, suggest the presence of a catalytic pathway. The rates of formation of cyanomethemoglobin and cyanometmyoglobin complexes from cyanide ion and methemoglobin (MHb) and metmyoglobin (MMb), respectively, were followed in the presence of the heme oxidants. The rate constants were all within a narrow range and suggest that complexation of cyanide by MHb and MMb is not affected by the presence of oxidants.

Aminoquinolines↗
PubMed1990

The effect of sodium tetrathionate on cyanide conversion to thiocyanate by enzymatic and non-enzymatic mechanisms.

Sodium tetrathionate has been proposed as a cyanide antidote despite its reported toxicology and inhibitory effect on rhodanese. We investigated the effect of tetrathionate and an analog, dithionite, on rhodanese activity because of their structural similarity to thiosulfate, a known sulfane sulfur donor for this enzyme. Rhodanese activity of guinea pig liver homogenate was assayed by measuring the formation of ferric thiocyanate complex at 460 nm. With thiosulfate as a substrate, the Km for rhodanese was 6.7 mM and the Vmax was 0.67 mumol thiocyanate min-1 mg-1 protein. The conversion of cyanide to thiocyanate by rhodanese was inhibited in the presence of tetrathionate at the millimolar concentration (e.g. 1 mM) range. Dithionite had a negligible effect on rhodanese activity. Neither thiosulfate (1-100 mM) nor dithionite produced significant amounts of thiocyanate from cyanide spontaneously (i.e. non-enzymatically). However, in the absence of rhodanese, tetrathionate (1.0, 10.0 and 100.0 mM) produced a dose-dependent increase in thiocyanate. These data suggest that tetrathionate detoxifies cyanide non-enzymatically, which may, in part, account for its antidotal effects.

Animals↗
PubMed1989

The inactivation of rhodanese by nitrite and inhibition by other anions in vitro.

Cyanide detoxification in mammals occurs, in part, by sulfur transfer by rhodanese to form the less toxic thiocyanate. Thiosulfate and nitrite are often used in combination for the treatment of cyanide intoxication. This report shows that nitrite can inhibit the rate of sulfur transfer by rhodanese in vitro. Nitrate, chloride, sulfate, and acetate were also examined as inhibitors. Inhibition by nitrite appeared to be more complex than for the other anions tested. Closer examination showed that nitrite can inactivate the sulfur-free rhodanese. Our observation leads to the suggestion that, in vivo, either rhodanese is maintained in its more stable sulfur-substituted form or cellular compartmentalization prevents inactivation by nitrite.

Animals↗
PubMed1987

The inhibition of cytochrome oxidase by diaminomaleonitrile.

Diaminomaleonitrile, a tetramer of cyanide, was examined as a possible antagonist to cyanide inhibition of cytochrome oxidase (EC 1.9.3.1). This compound was found to inhibit cytochrome oxidase in vitro; however, despite their structural similarities, diaminomaleonitrile and cyanide inhibit cytochrome oxidase by different mechanisms and bind to the enzyme at different sites. Diaminomaleonitrile inhibition of cytochrome oxidase is described in terms of a partially competitive mechanism. Biological oxidation of diaminomaleonitrile may lead to the formation of cyanide.

Animals↗
PubMed1985

The mechanisms of action of cyanide on the rabbit aorta.

Pretreatment of strips of rabbit aorta with 10(-3) M sodium cyanide reduced contractions to 10(-8) through 10(-4) M norepinephrine (NE) added cumulatively. This antagonism by cyanide was not altered by 4 X 10(-6) M ouabain or verapamil, suggesting a lack of involvement of Na+, K+ ATPase or of calcium influx in the antagonism. Cyanide potentiated contractions caused by 3 X 10(-2) M potassium, but reduced contractions induced by higher potassium concentrations. Because the antagonism of higher concentrations of potassium and NE were similar, it seems that selective actions on different calcium pools are possibly not involved in the antagonism of agonist-induced contractions. 10(-2) M cyanide contracted rabbit aorta with a mean contraction 16% of that induced by 10(-4) M NE. These contractions were potentiated by pretreatment with 4 X 10(-6) M ouabain and 4 X 10(-6) M verapamil but were unaffected by the serotonin antagonist 2-bromo lysergic acid diethylamide, 10(-4) M (2-BrLSD), the alpha adrenergic antagonist phentolamine, 4 X 10(-5) M, the H1 antihistaminic pyrilamine, 10(-5) M, or the antimuscarinic atropine, 10(-6) M. The contractions were reduced by 10(-4) M 4,4'-di-isothiocyano-2,2'-stilbene disulfonic acid (DIDS) or chlorpromazine. The reduction may be due to a blockade of anionic channel mechanisms facilitating entry of cyanide into the vascular smooth muscle cell, as both of these agents can block anionic channels in other tissues.

Animals↗
PubMed1985

The effects of cyanide and its interactions with norepinephrine on isolated aorta strips from the rabbit, dog, and ferret.

Effects of sodium cyanide on isolated strips of rabbit, dog, and ferret aorta were determined. In the rabbit aorta strip, cumulatively added cyanide caused small contractions beginning at approximately 10(-11) M cyanide and reaching a maximum response at 10(-5) M. A concentration of cyanide between 10(-5) M and 10(-3) M produced relaxation. When cyanide was cumulatively added to norepinephrine (NE)-contracted rabbit aorta strips, no contractions were observed. Cyanide concentrations above 10(-5) M produced relaxation in the NE-contracted vessels. Sensitivity of the aorta strips to NE differed among the species examined. The ED50 for contractions in the dog and ferret aorta was 4 X 10(-4) M and in the rabbit was 5 X 10(-6) M. Pretreatment with cyanide in concentrations up to 10(-2) M did not reduce contractions of dog aorta to NE, although 10(-2) M cyanide abolished contractions of rabbit aorta to NE and reversed NE-contractions of ferret aorta to relaxation. The antagonism of cyanide for NE-induced contractions was completely reversible with cyanide concentrations up to 10(-3) M. Cyanide pretreatment of strips of aorta increased the rate of contraction to NE. A concentration of 10(-2) M cyanide caused small contractions of aorta strips from each species. Thus, cyanide exerts dose and species dependent responses on vascular smooth muscle.

Animals↗
PubMed1984

Cyanide loss from tissue baths in the presence and absence of tissue.

Loss of cyanide from Krebs-Henseleit solution (KHS) was studied in aerated tissue baths at 38 degrees C in the presence and in the absence of tissue. The rate of cyanide loss was greater from 300-microM than from 30-microM solutions and still greater from 300-microM solutions in the presence of vascular tissue. Initial cyanide loss was much greater from the tissue-containing bath, and the half-time was shorter in the presence of tissue (54 min) than in its absence (98 min) in baths containing the same initial cyanide concentration (300 microM).

Animals↗
PubMed1982

Specificity of cardiac glycoside binding to membrane filters.

Two cardiac glycosides, with different physiochemical properties, were investigated to assess their binding characteristics to filters. The lipophilic cardiac glycoside, digoxin, demonstrated significant (10%) retention to certain cellulose filters. There were considerable differences in the amount of digoxin retained among the cellulose type filters. The polycarbonate type filter (10 microns thick) demonstrated less than 2% retention. This was similar in magnitude to the cellulose-acetate-nitrate ester filters (100 microns thick) which demonstrated less than 1% retention. Ouabain, the polar cardiac glycoside, appeared to have minimal (2%) retention on all filter types tested. Increasing the size of the pore from .4 microM to .8 microM resulted in a minimal decrease in retention for the Amicon filters, whereas the nucleopore polycarbonate filters demonstrated a significant reduction in retention of the lipophilic cardiac glycoside. A comparison of the 100 micron thick filters with the 10 micron thick filters suggests that there is no correlation with the thickness of the filter and the retention of the drug bound by that filter. These studies suggest that lipophilic drugs are retained on membrane filters depending on the filter's composition and that caution should be utilized with the filtration technique.

Cardiac Glycosides↗
PubMed1982

Effects of endotracheally administered distilled water and normal saline on the arterial blood gases of dogs.

The effects of endotracheally (ET) administered distilled water (DW) and normal saline solution (NSS) on the arterial blood gases of dogs were compared. When distilled water was administered endotracheally, arterial pH was depressed to 99.36% of baseline values within 5 minutes. When compared to pH changes following ET administration of NSS the depression of pH following DW administration was significant (P less than .05). Following ET injection of DW, arterial PO2 was depressed to 61% of baseline values and remained significantly depressed throughout the experiment. In comparison, following ET NSS administration, PO2 was depressed substantially less, and remained at significantly higher levels for the entire experiment. In dogs, administration of NSS by the ET route produces less detrimental effects on arterial blood gases than does the ET administration of DW. This may have implications for the choice of diluent for human drug administration using the ET route.

Analysis of Variance↗
PubMed1982

Endotracheal administration of atropine sulfate.

Atropine sulfate was successfully administered endotracheally to a 74-year-old patient suffering profound bradycardic cardiovascular collapse. Ninety seconds following endotracheal atropine administration, normal blood pressure and pulse were established. Therapeutic blood levels of atropine were documented following endotracheal administration. The endotracheal route for atropine administration appears to provide an effective alternative route of administration when intravenous access is difficult or impossible to establish rapidly.

Aged↗
PubMed1981

The action of reserpine, 6-hydroxydopamine, and bretylium on digitalis-induced cardiotoxicity.

This study determined whether the protective effect of reserpine against ouabain-induced ventricular arrhythmias in the cat is due to an action of the drug on the adrenergic nerve terminal. Reserpine (5 mg/kg i.p.) administered 24 h prior to ouabain (2 micrograms/kg per min i.v., until death) increased the dose of ouabain to produce premature ventricular contractions, ventricular tachycardia, and death from 77.3 +/- 5.2 to 105.0 +/- 6.0; 84.9 +/- 5.2 to 132.7 +/- 9.1; and 108.8 +/- 4.0 to 165.7 +/- 10.4 micrograms/kg, respectively (P less than 0.05). When 6-hydroxydopamine (6OHDA; 20 mg/kg i.v.) was given 3 days prior to the experiment, the protective effect of reserpine was not evident. When bretylium (20 mg/kg i.v., 2 h prior to ouabain) was administered to animals previously treated with reserpine, the dose of ouabain which produced premature ventricular contractions, ventricular tachycardia, and death was increased to 109.0 +/- 7.2; 146.1 +/- 12.6; and 165.8 +/- 7.6 micrograms/kg, respectively (P less than 0.05). However, the magnitude of this protective action was similar to that produced by reserpine alone. Lathers et al. (Fed. Proc. 40, 672, 1981) reported that bretylium alone provides protection of a similar order of magnitude as reserpine. Thus, the effects of reserpine and bretylium were not additive; this indicates that the two agents may be acting on the same locus or they may be acting at different sites with the action of one drug masking or blocking the action of the other. Since 6OHDA prevented the action of reserpine on ouabain-induced ventricular arrhythmia and since 6OHDA only produces degeneration of adrenergic nerve terminals, it is probable that the protective effect of both reserpine and bretylium is due to an action at the adrenergic nerve terminal. The heart rate and blood pressure were not involved in the antiarrhythmic effects of reserpine.

Animals↗