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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Cardiovascular depressant effects of neomycin and gentamicin in rhesus monkeys. 80 79

The significance of calcium soap formation in the inhibition of calcium absorption has been studied in rats. 47Ca labelled soaps of fatty acids were introduced into the duodenum and the absorption of calcium measured after four hours in a whole body counter. The absorption of calcium was inversely correlated with the chain length of the fatty acid varying from 1% for Ca-stearate to 60% for Ca-hexanoate. Increasing the degree of unsaturation of the fatty acid was accompanied by increased calcium absorption. The availability of calcium for absorption from the soaps was correlated with their solubility in 1% aqueous Na-tauroglycocholate. The percentages of calcium as soap in the small intestine and the faeces after intragastric administration of calcium and fats were similar, which suggests that the faecal content of calcium soaps is an index of intestinal soap formation. Soap formation was negligible when CaCl2 was given with tristearate, triolaeate, or tridecanoate and no depression of calcium absorption was observed. Calcium absorption was markedly impaired by the addition of phosphates at a Ca/P ratio of 1:1 irrespective of the presence of neutral fats. Stearic acid resulted in significant soap formation and reduced calcium absorption. The degree of Ca-soap formation and the inhibition of calcium absorption were well correlated. The results suggest that, although calcium soap formation may markedly depress calcium absorption in the rat, no significant soap formation takes place when fats are given in the form of triglycerides.
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PMID:Significance of Ca-soap formation for calcium absorption in the rat. 83 5

Calcium chloride is frequently administered to patients immediately after separation from cardiopulmonary bypass to improve the contractile state of the myocardium. Animal studies suggest that calcium chloride may produce increases in pulmonary vascular resistance, which can precipitate right ventricular failure. In an attempt to determine the effect of calcium chloride administration after cardiopulmonary bypass on right ventricular function, this study was designed to evaluate patients with normal and elevated pulmonary vascular resistance. Fifty patients scheduled for elective cardiac surgery were prospectively studied for changes in ionized calcium levels before and after bypass. The impact of calcium administration on right ventricular function was assessed by a pulmonary artery catheter modified for the measurement of right ventricular ejection fraction. In all patients the level of ionized calcium decreased during bypass from a mean of 4.91 to 4.29 mg.dl-1. However, the infusion of calcium chloride (10 mg.kg-1) after bypass resulted in increasing the ionized calcium levels to prebypass levels. Administration of calcium chloride after bypass to patients with normal right ventricular function resulted in a transient increase in both cardiac output and right ventricular ejection fraction without any change in pulmonary vascular resistance. Eight patients with both elevated pulmonary vascular resistance and depressed right ventricular function were evaluated to determine the effect of calcium chloride after bypass on pulmonary vascular resistance and right ventricular ejection fraction. Administration of calcium chloride (10 mg.dl-1) to these patients did not result in any significant increase in pulmonary vascular resistance or depression of right ventricular performance. More important, in these patients, right ventricular ejection fraction and cardiac output were significantly increased after calcium chloride administration. In summary, the results of this study fail to demonstrate any increase in pulmonary vascular resistance or deterioration of right ventricular function with the administration of calcium chloride (10 mg.kg-1) after bypass in patients with elevated pulmonary vascular resistance.
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PMID:The effect of calcium on pulmonary vascular resistance and right ventricular function. 149 94

The effect of a new carbanilate derivative BK 129, 1-methoxymethyl-2(1-perhydroazepinyl)ethyl ester 2-(n)-pentyloxycarbanilic acid hydrochloride, was tested on preparations of canine dorsal pedal and coronary artery in vitro. The drug produced relaxation of arterial rings both under resting conditions and under precontraction with KCl. BK 129, at a concentration of 10(-5) mol/l, produced a shift to the right of the concentration-response curve of phenylephrine, with a decrease in the slope and a depression of the maximal response. BK 129 inhibited the response to norepinephrine and blocked histamine- and norepinephrine-induced contractions in Ca(2+)-free physiological salt solution. The electrical stimulation-induced contractions of arterial preparation were also inhibited. BK 129 shifted the concentration-response curve of CaCl2 in Ca(2+)-free depolarizing solution to the right in a non-competitive manner. It may be concluded that BK 129 is a local anesthetic which possesses relaxant properties. It appears to inhibit Ca2+ entry into the smooth muscle cell and Ca2+ release from sarcoplasmic reticulum.
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PMID:Effect of a new antiarrhythmic BK 129 on canine vascular smooth muscle in vitro. 162 1

The vasorelaxing and dihydropyridine receptor binding properties of NZ-105, a new dihydropyridine derivative, were studied using isolated rabbit aorta, and compared with those of nicardipine, nifedipine and diltiazem. NZ-105 (3 x 10(-10)-3 x 10(-9) M), nicardipine (3 x 10(-10), 10(-9) M), and diltiazem (3 x 10(-7), 10(-6) M) selectively relaxed aortic strips precontracted with high-K+ solution (50 mM) with little effect on strips precontracted with phenylephrine (10(-5) M) or clonidine (10(-6) M). The relaxation produced by NZ-105 was of very slow onset, and no recovery was observed after a 2 hr washout with high-K+ or normal bathing solution. NZ-105 (3 x 10(-10)-3 x 10(-9) M) caused a non-parallel depression of the concentration-response curve for the CaCl2-induced contraction in high-K(+)-depolarized rabbit aorta, whereas nicardipine (10(-10), 3 x 10(-10) M), nifedipine (10(-9), 3 x 10(-9) M) and diltiazem (10(-7), 3 x 10(-7) M) all produced a concentration-related rightward displacement of the curve. The depression induced by NZ-105, but not by nicardipine, became greater as the period of preincubation with the drug was prolonged. NZ-105, nicardipine and diltiazem, at the very high concentration of 10(-6) M, caused a slight and noncompetitive inhibition of the concentration-response curves for norepinephrine, prostaglandin F2 alpha, angiotensin II and 5-hydroxytryptamine. NZ-105 displaced 3H-nitrendipine binding to rabbit aortic membranes in a manner similar to that of nicardipine and nifedipine, and this was also incubation time-dependent. These results indicate that NZ-105 possesses selective calcium antagonist properties, with respect to the rabbit isolated vascular smooth muscle, which are of very slow onset and long-lasting. The slow onset of the vasorelaxation may be due to a slow association rate to dihydropyridine receptors. These pharmacological properties of NZ-105 may, at least in part, be responsible for the slow onset and long duration of its antihypertensive action in vivo.
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PMID:Vasorelaxing and receptor binding properties of NZ-105, a novel dihydropyridine derivative, in isolated rabbit aorta. 166 36

The cardiovascular selectivity of NZ-105, a novel dihydropyridine derivative, was studied in vitro in comparison with nicardipine and other calcium antagonists. NZ-105 and nicardipine (10(-9), 10(-8) M) decreased the spontaneous contraction rate of the isolated guinea-pig right atrium. On the other hand, NZ-105, even at concentrations as high as 10(-6) M, slightly diminished the contractile force of the electrically driven left atrium, while nicardipine strongly and dose-dependently decreased the contractile force at a concentration of 10(-7) M by 39.9% and at 10(-6) M by 72.1%. NZ-105, nicardipine and diltiazem, at concentrations below 10(-6) M, caused no or only a slight depression of isoproterenol-induced increases in the contractile force of the driven left atrium. In left atrium partially depolarized with high K+ (22 mM) in the presence of 10(-6) M of isoproterenol, NZ-105 (10(-8)-10(-6) M), nicardipine (10(-9)-10(-7) M) and diltiazem (10(-7), 10(-6) M) produced both a concentration-related displacement of the concentration-response curves for CaCl2 to the right and a depression of the maximum response to CaCl2. In various rabbit blood vessels depolarized with high K+ (100 mM) (coronary, superior mesenteric, renal and femoral arteries and saphenous vein). NZ-105 (3 x 10(-10)-10(-8) M) caused a non-parallel depression of the concentration-response curves for CaCl2-induced contractions. The calcium-antagonizing effect of NZ-105 was strongest in the basilar artery. NZ-105 displaced the [3H]-nitrendipine binding to rabbit cardiac and aortic membranes in a manner similar to nicardipine and nifedipine. The Ki values of these compounds, with respect to cardiac membranes, were several times larger than in the case of aortic membranes. The Ki value of NZ-105, but not of nicardipine, grew smaller as the preincubation period with the drug increased. These findings indicate that NZ-105 possesses selective calcium-antagonizing properties in vascular smooth muscle, especially in the basilar artery, when compared with cardiac muscle. The negative chronotropic action of NZ-105 was more potent than its inotropic action. On the basis of these pharmacological properties, NZ-105 is considered to be a useful drug for the treatment of cardiovascular disorders.
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PMID:Cardiac and vascular effects of NZ-105, a novel dihydropyridine derivative, in vitro. 166 4

The current study was designed to analyse the mechanisms which are impaired in the vascular hyporeactivity to contractile agents induced by E. coli lipopolysaccharide endotoxin (LPS). Endothelium-denuded aortic rings were prepared from thoracic aorta removed from control and LPS-pretreated rats (20 mg/kg i.p., 4 h before the experiment). In order to determine whether LPS treatment altered the contractile components that depend on intracellular calcium release and extracellular calcium entry to the same extent, rings were contracted under various experimental conditions. The responses elicited by indanidine, phenylephrine (without and with nitrendipine 1 microM), (-) Bay K 8644, (+) S 202-791 and the calcium ionophore calimycin in the presence of 1.25 mM external CaCl2 were all impaired by LPS pretreatment (maximal contractions 19, 63, 44, 28, 22 and 22% of controls, respectively). Concentration-effect curves for CaCl2 made in depolarizing medium (KCl 40 and 100 mM) and in the presence of calimycin (3 microM) were shifted to the right in rings from LPS-pretreated rats. However, the LPS-induced depression of contraction was overcome by the addition of CaCl2 (up to 30 mM). Additionally, in the absence of external CaCl2, the contraction induced by caffeine (50 mM) was not significantly altered by LPS treatment. It is concluded that LPS treatment does not reduce the ability of aortic smooth muscle cells to contract. The results suggest that LPS treatment impairs mechanisms involved in calcium handling within smooth muscle cells after stimulation of calcium entry through different pathways and activation of intracellular calcium release by alpha 1-adrenoceptor agonists.
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PMID:Endotoxin-induced impairment of vascular smooth muscle contractions elicited by different mechanisms. 170 72

The effects of calcium chloride administered at low infusion rates on the cardiovascular depression and the blood calcium balance were studied during a constant halothane anaesthesia in dorsally recumbent ventilated ponies. A pronounced cardiopulmonary depression characterized by decreases of all cardiac parameters and lowering of the mean arterial blood pressure was observed after the initial anaesthetic stabilization period of 30 minutes in the ponies. A significant decrease in the total calcium plasma concentration together with a constant ionized and complexed calcium fraction was present after the stabilization period. Calcium chloride administration at different infusion rates (0.1, 0.2 and 0.3 mg/kg/min) induced a dose-dependent increase in mean systemic blood pressure, probably due to the observed increase in total peripheral resistance. A dose-dependent gradual decrease in heart rate, probably mediated by the increased vagal activity, was observed after the calcium infusions. The stroke volume increased also in a dose-dependent way. Cardiac output, arterial blood gases or packed cell volume were not influenced by the exogenous calcium infusions. The observed increases in mean pulmonary artery pressure and total pulmonary resistance were probably time-related responses. Overall, only the effects of the exogenous calcium on the peripheral vasculature, namely a vasoconstriction leading to an increase in blood pressure, were present in this study. Although LV dP/dt max was not measured in this study, minor positive inotropic effects of the exogenous calcium infusions might nevertheless be possible since the observed increase in stroke volume could be an indication of an increase in the ventricular contractility function. The different fractions of the calcium in the plasma (total and ionized & complexed calcium) increased during the exogenous calcium infusions but the proportion of the fractions remained always constant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular effects of low dose calcium chloride infusions during halothane anaesthesia in dorsally recumbent ventilated ponies. 179 75

This study describes the effects of some anthracyclines (adriamycin, 4-epiadriamycin and esorubicin) on isolated, electrically driven left guinea pig atrium in normodynamic or hypodynamic (Tyrode solution with 0.1 g/1 CaCl2) conditions. Exposure for 60' to the anthracyclines caused a depression of contractile force and of maximal rate of tension development (df/dt). The statistical analysis of data showed an equivalent inhibitory effect between adriamycin and esorubicin, whereas 4-epiadriamycin has in normodynamic conditions greater negative inotropic effects significantly different from that of the two other drugs. Thus the lower toxicity of 4-epiadriamycin observed in vivo by other authors may probably be imputed to a lower concentration of the drug in the heart. The cardiac depressant effects induced by anthracyclines in vitro, as previously reported, are antagonized by new cardiotonic agents whose mechanism of action can be related to an increase in calcium activity in myocardial tissue.
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PMID:Cardiotoxicity of anthracyclines. 193 27

To study the cardiovascular effects of low blood ionized calcium ion concentrations [Ca2+] induced by citrate infusion followed by high [Ca2+], induced by CaCl2 infusion awake and during enflurane (2.5% ET), halothane (1.2% ET), and isoflurane (1.6% ET) anesthesia, dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) blood pressures, and cardiac output. In conscious dogs low [Ca2+] (decreased 0.35 mM); increased heart rate (HR) and mean aortic pressure (MAP) and decreased stroke volume (SV) and LV dP/dtmax. Low [Ca2+] increased HR during all three anesthetics and decreased LV dP/dtmax except during isoflurane anesthesia. Low [Ca2+] produced more hemodynamic depression during enflurane anesthesia than during anesthesia with halothane or isoflurane increasing left atrial pressure and decreasing MAP and SV. The differences seen were partially related to decreased systemic vascular resistance during halothane and isoflurane anesthesia. In conscious dogs following high [Ca2+] (increased 0.37 mM); only MAP and LV dP/dtmax increased. LVdP/dtmax was also increased by high [Ca2+] during all three anesthetics without a change in MAP. Cardiac output increased during halothane and isoflurane anesthesia but was unchanged during enflurane. It would appear that the hemodynamic sensitivity for the effects of changing [Ca2+] was enflurane greater than halothane greater than isoflurane greater than awake. The results suggest that the effects of changes in [Ca2+] induced by citrate and CaCl2 infusion are modified by the three volatile anesthetics.
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PMID:Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in chronically instrumented dogs, conscious and during enflurane, halothane, and isoflurane anesthesia. 229 13


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