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Biomedical subjects

H R Adams

Publications and source records attributed to H R Adams.

At least 109 records · Page 6Linked to original sources
PubMed1977

Influence of mannitol on contractile responses of isolated perfused arteries.

The influence of hyperosmotic mannitol on vascular smooth muscle contractile responses was examined in isolated arterial preparations. Vasoconstrictor effects of norepinephrine (NE) and potassium chloride (K+) in the perfused central artery of the rabbit's ear and in perfused mesenteric arteries of cats were significantly inhibited by infusion with Krebs bicarbonate solution made hyperosmotic with mannitol (50-200 mosM increase). Similarly, the magnitude and duration of vasoconstrictor responses to transmural stimulation of the central ear artery of the rabbit were decreased by hyperosmotic mannitol (50 mosM). Mannitol (50 mosM) produced a decrease in perfusion pressure when perfusion pressure was maintained at an increased level by K+ (60 mM). Mannitol-induced vasodilatation was not affected by ethacrynic acid (1.5 X 10(-5) M), beta adrenergic blockade or by the development of tachyphylaxis to the vasodilator effects of nitroglycerin. The concentration of cyclic adenosine-monophosphate was not changed by mannitol. Isotonic mannitol also inhibited NE-induced contractile responses. These data indicate that hyperosmotic mannitol produces vasodilatation in isolated arterial smooth muscle by a mechanism(s) that appears dissimilar from that of several other vasodilator substances and suggest that hypertonicity may not be the only factor involved in the vasodilator effect of mannitol.

Animals↗
PubMed1977

The influence of ketamine on inotropic and chronotropic responsiveness of heart muscle.

The influence of ketamine on the inotropic and chronotropic responsiveness of heart muscle was examined in spontaneously beating right atrial preparations and in electrically driven left atrial preparations of guinea pigs. Ketamine (2.63 X 10(-5) to 4.2 X 10(-4) M) decreased heart rate of right atria and decreased contractile tension and its maximum rate of increase in both right and left atrial preparations (right atria greater than left atria). Ketamine did not prevent the heart rate increase produced by norepinephrine (NE; 1 X 10(-8) to 1 X 10(-4) M) in right atria; however, the maximum heart rate was consistently lower in ketamine-treated than in control muscles even after exposure to NE. Although contractile tension was decreased by ketamine, the maximum inotropic response to NE was consistently greater in ketamine-treated atria than in control atria. An inhibitor of the slow Ca++ current in heart muscle, D600, depressed the contractile effects of NE but did not prevent the positive inotropic interaction of ketamine and NE. Ketamine similarly enhanced the inotropic responses to norepinephrine (1 X 10(-6) M), epinephrine (1 X 10(-6) M), isoproterenol (1 X 10(-7) M) and dibutyryl cyclic adenosine 3':5'-monophosphate (AMP; 4 X 10(-3) M) in left atria electrically paced at a constant frequency of contraction of 1 Hz; however, ketamine inhibited the positive inotropic response to increased frequency of stimulation (0.1-3.0 Hz) and to ouabain (3 X 10(-7) M). These findings demonstrate that ketamine can exert a selective positive inotropic influence in heart muscle independent of heart rate or direct or reflexogenic autonomic nervous system changes, and suggest that this activity could in some way be associated with an alteration of the intracellular disposition of cyclic AMP.

Animals↗
PubMed1976

Contractile function and 45Ca movements in vascular smooth muscle of nonhuman primates: effects of aminoglycoside antibiotics.

1. The effects of 7mM neomycin, 10 mM kanamycin and 5 mM gentamicin on vascular smooth muscle contractile responses and 45Ca movements were examined in arterial preparations isolated from nonhuman primates (squirrel monkeys, capuchin monkeys and baboons). 2. Present findings demonstrate that these antibiotics inhibit contractile responses and alter 45Ca movements in monkey blood vessels, and suggest that the manner in which these agents affect vascular smooth muscle from nonhuman primates does not differ qualitatively from their effects in canine and rabbit vascular preparations.

Aminoglycosides↗
PubMed1975

Acute adverse effects of antibiotics.

A review of selected clinical reports in man and experimental studies in lower animals suggests that, under certain circumstances, several commonly used antibiotics may cause cardiovascular depression, respiratory difficulties, or alter the metabolic breakdown of other drugs. These untoward responses are believed to be due to the direct effects of antibiotics on specific physiologic functions, rather than to be related to allergic reactions or cytotoxic lesions. Severe pathologic conditions, over-dosage, or concomitant exposure to other potent drugs may predispose a patient to these acute adverse effects.

Acetylcholine↗
PubMed1975

Direct myocardial depressant effects of gentamicin.

Effects of gentamicin on myocardial contractile performance were examined in isolated, electrically driven, rat left atria. This aminoglycoside antibiotic produced a maintained and concentration-dependent (0.0156-0.25 mM) depression of myocardial contractile tension that was reversible by replacing the incubation media with gentamicin-free solution. Time to peak tension and total contraction time were not discernibly altered by gentamicin. The negative inotropic response elicited by gentamicin was antagonized in a competivitive-like manner by increasing the calcium ion (Ca2+) concentration of the bathing solution, whereas, the depressant effects of gentamicin were antagonized by norepinephrine in a non-competitive-like manner. Present findings demonstrate a direct negative inotropic effect of gentamicin and suggest that this antibiotic interferes with the participation of Ca2+ in the events leading to mecahnical activity of atrial myocardium.

Animals↗
PubMed1975

Cardiovascular depressant effects of neomycin and gentamicin in rhesus monkeys.

1. The acute cardiovascular effects of neomycin and gentamicin, representative aminoglycoside antibiotics, were examined in surgically-prepared anaesthetized rhesus monkeys. 2. Intravenous administration of 14, 28, and 56 mg/kg of neomycin consistently induced a dose-dependent depression of systemic blood pressure, cardiac output, left ventricular contractile force, maximum dF/dt of left ventricular contraction, and heart rate. Neomycin produced similar cardiovascular depressant effects when heart rate was maintained constant by electrical pacing. 3. Maximum depression of haemodynamic values usually occurred within 2 to 5 min after injection of neomycin; values then gradually returned to control levels within 20 to 30 (14 mg/kg) or 60 to 80 (56 mg/kg) minutes. 4. Injection of CaCl2 (1.35 mEq Ca2+/kg, i.v.) during the peak depressant effect of neomycin produced a rapid and maintained restoration of cardiovascular function to control levels; conversely, noradrenaline (2 mug, i.v.) of isoprenaline (0.5 mug, i.v.) produced only transient reversal of the neomycin effects. 5. Similar evidence of cardiovascular dysfunction was observed with gentamicin. 6. These findings demonstrate the direct cardiovascular depressant effects of aminoglycoside natibiotics in a higher primate species, and suggest that this adverse response is related to an alteration of calcium ion function.

Animals↗
PubMed1975

Effects of neomycin on 45Ca binding and distribution in canine arteries.

The effects of neomycin (7.0 mM) on 45Ca movements and distribution were investigated in canine aortae and in canine carotid and terminal mesenteric arteries. Uptake of 45Ca was measured in calcium-free solution; the 45Ca tissue spaces in the carotid and terminal mesenteric arteries were 2--4 times greater than those observed in the aorta. Exposure of the aortae and the terminal mesenteric arteries to 1.5 mM Ca++ during the washout elicited large increases in 45Ca efflux in both preparations (increase in terminal mesenteric greater than aorta). Moreover, in all three arterial preparations, neomycin reduced 45Ca uptake and induced a sustained increase in 45Ca efflux (effects on terminal mesenteric larger than or equal to carotid greater than aorta). The terminal mesenteric and carotid arteries may accumulate and bind 45Ca at superficial membrane sites (readily exchangeable 45Ca) to a greater degree than does the aorta. If Ca++ located at these membrane sites contributes directly to the maintenance of mechanical responsiveness, then agents which alter membrane binding of Ca++ (e.g. neomycin) may exert a stronger action on these highly reactive vessels. Thus, contractile responsiveness in peripheral arteries may depend upon depots of superficially bound Ca++ to a greater degree than in the more centrally located aorta.

Animals↗
PubMed1975

Carisoprodol-related death in a child.

A child who ingested approximately 3500 mg of carisoprodol gradually deteriorated and died within 36 h. GC analysis of serum, urine, and gastric samples indicated that meprobamate was the principal metabolite of carisoprodol.

Carisoprodol↗
PubMed1975

Differential inhibitory effect of neomycin on contractile responses of various canine arteries.

The influence of neomycin on vascular smooth muscle contractile responses was examined in different isolated arterial preparations of the dog. Prior exposure (5 minutes) to 7 mM neomycin decreased contractile responses elicited with norepinephrine (NE, 0.6 muM) or KC1 (K-+, 80 nM) in helical strips of canine aortae (Ao) and femoral (F), carotid (Cd), renal (R), superior mesenteric (Sm), terminal mesenteric (Tm) and coronary (Cr) arteries. Addition of neomycin subsequent to NE-induced contractile responses depressed tension responses of the F, Cd, R, Sm and Tm arteries but had little or no effect on the Ao. However, after contractions had been elicited with K-+, neomycin had no effect on tension responses of the Ao, F, Cd, R or Sm arteries but depressed contractions of the Cr and Tm arterial strips. Preincubation with neomycin (0.7-3.5 mM) produced a concentration-related inhibition of contractile responses elicited in Tm arterial strips by addition of calcium ions (Ca-++; 1.6 mM) to a Ca-++-free depolarizing solution; conversely, subsequent addition of neomycin had no effect on maintained Ca-++ contractures. In constant flow-perfused terminal mesenteric arterial branches, neomycin (0.5-4.0 mM) produced a concentration-related antagonism of pressor responses elicited with NE (1-8 mug) or K-+ (40 mM). The inhibitory action of neomycin on K-+-induced pressor responses was inversely related to the Ca-++ concentration of the perfusion fluid. However, inhibition of NE pressor responses by neomycin did not appear to be related to the Ca-++ concentration. The differential inhibitory action of neomycin on contractions induced by NE and K-+ in various canine arteries suggests that different vascular beds vary in the manner in which Ca-++ is bound and subsequently utilized by stimulatory agents to elicit tension changes.

Animals↗
PubMed1975

Cardiovascular depressant effects of the neomycin-streptomycin group of antibiotics.

Cardiovascular depressant effects of the neomycin-streptomycin group of antibiotics (aminoglycoside antibiotics) were examined during pentobarbital anesthesia in cats, dogs, and 4 species of nonhuman primates: owl (Aotus trivirgatus), squirrel (Saimiri sciureus), and rhesus (Macaca mulatta) monkeys, and dog-faced baboons (Papio cynocephalus). Intravenous administration of kanamycin, streptomycin, gentamicin, or neomycin produced various degrees of hypotension and relative bradycardia in all species examined. In surgically prepared (open-chest) baboons, neomycin consistently induced a dose-related depression of myocardial contractile force, maximum dF/dt of myocardial contraction, cardiac output, heart rate, and systolic and diastolic blood pressures. Maximum depression of hemodynamic values usually occurred within 2 to 5 minutes after administration of neomycin; cardiovascular function then gradually returned to control or near control levels within 30 to 60 minutes. Intravenous administration of calcium chloride rapidly reversed the neomycin-mediated alterations of cardiovascular function. Present findings indicated that aminoglycoside antibiotics altered cardiovascular dynamics in anesthetized animals, and indicated that this deleterious action(s) may be related to modification of calcium ion function.

Animals↗
PubMed1974

Alteration of contractile function and calcium ion movements in vascular smooth muscle by gentamicin and other aminoglycoside antibiotics.

Experiments were conducted to examine the effects of certain aminoglycoside antibiotics on contractile responses and related calcium ion (Ca(2+)) movements in isolated vascular smooth muscle. Gentamicin, kanamycin, and streptomycin decreased contractile responses produced by norepinephrine, histamine, and high K(+) in rabbit aortic strips. The inhibitory action of these antibiotics on mechanical function was more pronounced when the Ca(2+) concentration of the bathing solution was decreased from 1.5 mM (normal Ca(2+) solution) to 0.05 mM (low Ca(2+) solution). The uptake of radiocalcium ((45)Ca) into the isolated media-intimal layer of rabbit aortae was decreased in a maintained manner by each antibiotic. With gentamicin, the inhibitory effect on (45)Ca uptake was shown to be dependent upon the concentration of gentamicin employed and to be more evident in a 0.1 mM Ca(2+) solution than in a normal Ca(2+) solution. In addition, the rate of (45)Ca efflux from the rabbit aortic media-intimal layer was increased in a sustained manner by gentamicin, streptomycin, and kanamycin. Furthermore, contractile responses induced by high K(+) and norepinephrine in canine carotid arterial strips were inhibited by gentamicin. Present findings indicate that aminoglycoside antibiotics interfere with Ca(2+)-linked events leading to activation of the contractile mechanism of vascular smooth muscle. These in vitro findings may partially explain the occurrence of in vivo cardiovascular depression that has occasionally been observed after the administration of chemically related antimicrobial agents.

Aminoglycosides↗