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Biomedical subjects

H R Adams

Publications and source records attributed to H R Adams.

At least 91 records · Page 5Linked to original sources
PubMed1981

Contractile dysfunction of atrial myocardium from endotoxin-shocked guinea pigs.

Atrial muscle isolated from guinea pigs subjected to Escherichia coli endotoxin shock was used to study the myocardial changes associated with this experimental disease state. Isometric contractile tension and its first derivative (dT/dt) consistently were depressed by about 45% in muscle from the shock group (P less than 0.001), but contraction time intervals of the shock tissues were not significantly altered. The inotropic deficit of shock was completely antagonized by high concentrations of Ca2+ (greater than 4.5 mM). However, the maximal positive inotropic response to increased frequency of stimulation (0.1-2.2 Hz) only partially antagonized shock-induced cardiac depression. Heart muscle from shocked animals exhibited increased sensitivity to the negative inotropic effects of Mn2+, low Ca2+, and gentamicin; recovery from the depressant actions of these agents was prolonged 3.6- to 4.8-fold in shock. However, the negative inotropic potency of slow Ca2+ channel blockers, D 600 and nifedipine, was unaffected by shock. Similarly, studies with an isoproterenol-activated slow Ca2+ channel technique demonstrated equivalent inotropic responses of shock and control heart muscle. Present data provide evidence for a disruption of myocardial Ca2+ metabolism associated with endotoxin-induced inotropic depression of the heart but suggest that slow Ca2+ channels of the sarcolemma remain functional in this disease state.

Anaerobiosis↗
PubMed1981

Adverse cardiovascular effects of oxytetracycline preparations and vehicles in intact awake calves.

Comparisons were made of cardiovascular effects in intact, awake, previously instrumented calves given the following oxytetracycline (OXY) preparations and components: polyvinylpyrrolidine vehicle (PVP), OXY HCl in PVP (OXY-PVP), OXY HCl (USP) in saline solution, propylene glycol, 77.8% (PG), propylene glycol vehicle (PGV), and OXY HCl in PGV (OXY-PGV). The 3 preparations containing PG caused significant increases in pulmonary arterial pressures and significant decreases in cardiac output and stroke volume. Aortic pressures were significantly decreased, as were heart rates. Both pulmonic and systemic resistances were significantly increased. There were no direct effects measured on left ventricular contractility. The aqueous OXY caused no significant changes. The PVP preparation and vehicle caused no changes in pulmonary pressures, pulmonary resistance, cardiac output, or stroke volume. Significant increases were observed in aortic pressure, heart rate, and systemic resistance. Left ventricular contractility was not changed. Seemingly, the PG-induced changes were a result of histamine release which did not appear to be dependent on prior sensitization of the calves.

Animals↗
PubMed1981

Development of acute burn shock in unresuscitated guinea pigs.

Conscious guinea pigs were used to study the development of burn shock as a function of the size of thermal injury to the body surface. Scale burns equivalent to 0 (control, n = 18), 15.7 +/- 0.8% (n = 11), 24.6 +/- 0.5% (n = 10), and 43.4 +/- 1.5% (n = 10) of total body surface area were obtained by use of a template device, while the animals were deeply anesthetized with methoxyflurane. Circulatory function was assessed without further anesthetic restraint before and at 1, 2, 4, 6, 8, and 24 hr after burn. Values from control guinea pigs varied little during the observation period. Hemodynamic functions of burned guinea pigs were abnormal, and both the magnitude and duration of dysfunction generally depended upon the size of injury. Burn shock was characterized by hemo-concentration, hypothermia, tachycardia (bradycardia in the 43.4% group), minimal adjustments in systemic blood pressure, hyperkalemia, normonatremia (hyponatremia in the 43.4% group) arterial acidemia, and decreased respiratory rate. Circulatory functions of the 15.7% and 24.6% groups returned toward control levels during 8 hr after burn. Severe shock persisted in the 43.4% group, which experienced 70% mortality by 24 hr. These experiments characterize the guinea pig as a reproducible small animal model for studying different severities of burn shock unencumbered by secondary influences associated with general anesthesia.

Animals↗
PubMed1980

A comparison of the influence of La3+, D600 and gentamicin on frequency-force relationships in isolated myocardium.

The capability of heart muscle to respond mechanically to changes in frequency of stimulation was studied in the absence and in the presence of La3+, D600 and gentamicin using left atrial preparations of guniea pigs. L3+ (0.5 x 10(-3) M) and gentamicin (1 x 10(-3) M) depressed the basal contractile state at 1.0 Hz by about 90% (EC90), and inhibited the positive inotropic response to increased driving rate throughout the frequency range that was studied (0.1--2.2 Hz). In contrast, a comparable concentration of D600 (1.05 x 10(-6) M) reduced inotropic responses to high rates of stimulation (> 1.4 Hz) more than responses to low rates (< 0.8 Hz). Muscles exposed briefly (20 min) to an EC90 of La3+ or D600 failed to regain 50% of basal inotropy after one h rinse in normal medium; whereas, muscle exposed to gentamicin recovered 50% inotropy in approximately 5 min. Effects of D600 and La3+ on the frequency-force relationship were not abolished after 1.5--2 h recovery of the muscles in normal solution, but the effects of gentamicin were easily removed by the same recovery procedures. These data indicate that: (1) the cardiodepressant actions of La3+ and D600 were poorly reversible after in vitro treatment, and these actions were manifested at cellular loci essential for normal contractile responses to changes in heart rate, and (2) the cardiac actions of gentamicin were reversible and could be differentiated from the more complex actions of both D600 and La3+.

Animals↗
PubMed1979

Pharmacologic management of circulatory shock: cardiovascular drugs and corticosteroids.

Effective use of cardiovascular drugs in the management of circulatory shock requires knowledge of the pathophysiologic changes occurring in the different types and stages of shock and an understanding of the specific hemodynamic actions of drugs used to correct shock. Objectives of therapy are to: (1) restore circulating blood volume, (2) ensure of increase perfusion of critical organs by selectively reducing arteriolar resistance, (3) augment cardiac output, and (4) increase perfusion pressure. If blood volume is not restored, drugs may be ineffective and can even induce deleterious effects. If reflex sympathetic discharge has induced generalized vasoconstriction, it is irrational to expect beneficial results from administration of exogenous vasconstrictor agents. Instead, selective vasodilatation of vascular beds in critical tissues (eg, myocardium, intestines, and kidneys) accompanied by increased perfusion pressure and cardiac output can prove useful. Large doses of adrenocorticosteroids are used commonly in the therapy of different shock conditions, based primary on empiric tests of efficacy. Although such steroids may not influence the course of shock by direct cardiovascular effects, beneficial actions may result from mechanisms such as protection of cell membrane integrity and stabilization of lysosomes.

Adrenal Cortex Hormones↗
PubMed1979

Inotropic responsiveness of atrial myocardium bathed in Tris- or bicarbonate-buffered solutions.

Atrial muscle of guinea pigs was used to study the inotropic influences of substituting a tris(hydroxymethyl)-aminomethane-buffered solution aerated with 100% O2 for a bicarbonate-buffered solution aerated with 95% O2-5% CO2 under otherwise equivalent in vitro conditions. Basal values of isometric contractile tension and its first derivative (dT/dt) were smaller and time to peak tension and time to 90% relaxation were longer in Tris- than in bicarbonate-bathed muscles. Both groups responded similarly to changes in stimulation frequently (0.1--2.2 Hz) and Ca2+ concentration (1.0--7.0 mM); however, maximal inotropic responses to these variables were smaller in the Tris-bathed atria. The negative inotropic effects of D600 and gentamicin were greater in the Tris group. Tris-bathed atria developed pulsus alternans when exposed to Mn2+ or a reduced Ca2+ concentration, whereas pulsus alternans did not occur in the bicarbonate group. A transient increase in contractility occurred in bicarbonate-bathed atria after treatment with 0.125 mM Mn2+, but only a negative response occurred in the Tris group. Thus important, and seemingly Ca2+-dependent, differences exist between the inotropic influences of Tris and bicarbonate solutions that may affect the utility of Tris-buffered (and/or bicarbonate deprived) heart muscle for studying certain inotropic interventions.

Animals↗
PubMed1979

Cardiovascular manifestations of acute antibiotic toxicity during E coli endotoxin shock in anesthetized dogs.

Surgically instrumented, pentobarbital-anesthetized dogs were used to examine the acute cardiovascular activities of gentamicin, tobramycin, sodium penicillin-G, and sodium cephalothin during a control state and during experimental circulatory shock induced by E coli endotoxin. Intravenous administration of 2.5, 5, 10, and 20 mg/kg gentamicin or tobramycin resulted in a transient (5--20-minute) state of cardiovascular depression, as reflected by dose-related decreases of systemic blood pressure, cardiac output, left ventricular pressure, dP/dt max, left ventricular contractile force, and dF/dt max; heart rate was affected little. Endotoxin produced a persistent state of circulatory depression characterized by hypotension, decreased cardiac output, arterial acidemia, and reduced indices of cardiac function. During endotoxin shock, the cardiovascular effects of gentamicin and tobramycin were relatively more pronounced (sometimes more than doubled) than effects observed during the control state. Equally large doses of penicillin or cephalothin, however, had no discernible circulatory effects in either control dogs or dogs subjected to endotoxin shock. Present data indicate that the cardiovascular toxicities of the aminoglycoside antibiotics gentamicin and tobramycin were augmented during experimental circulatory shock, and suggest the need for specific hemodynamic surveillance when intravenous administration of cardioactive antibiotics is required in patients with pre-existing circulatory dysfunction.

Animals↗
PubMed1979

Myocardial effects of endotoxin shock: characterization of an isolated heart muscle model.

Atrial myocardium of guinea pigs was used to study effects of Escherichia coli endotoxin shock on inotropic characteristics of heart muscle free from noncardiac influences of the in vivo shock state. In vitro exposure of atrial muscle to large concentrations of endotoxin (10-1,000 microgram/ml, final concentration) for a prolonged period (90 minutes) had no effect on myocardial contractility. However, atrial muscle isolated from endotoxin-shocked guinea pigs exhibited clear evidence of mechanical depression, as reflected by markedly low values for both isometric contractile tension and maximal rate of tension development (dT/dt). Also, since systolic and diastolic time intervals of myocardial contractions were not discernibly affected by shock, the contractile deficit represented a true inotropic dys-function and was not due simply to a temporal change in the active state of the muscle. The shock-induced inotropic disorder was permanent enough to persist in vitro for several hours of observation. However, if the Ca++ concentration of the bathing medium was increased from 2.5 mM to maximally effective concentrations ( greater than 4.5 mM), contractile strength of heart muscle from the shocked group was equal to corresponding responses of control muscles. Present findings verify myocardial contractile dysfunction associated with in vivo endotoxin administration and provide characterization of a test system that should prove useful for further study of functional changes occurring to the heart in shock.

Animals↗
PubMed1979

Cardiovascular effects of intravenous administration of propylene glycol and of oxytetracycline in propylene glycol in calves.

Comparisons were made of the acute cardiovascular effects of oxytetracycline, oxytetracycline in propylene glycol, and propylene glycol alone given to conscious dairy calves. The calves were chronically instrumented with intravascular catheters and electromagnetic flowmeter transducers in and on the pulmonary and renal arteries. Injection (IV) of aqueous preparations of oxytetracycline produced no statistically significant (P greater than 0.05) cardiocirculatory changes in these calves. Oxytetracycline in propylene glycol and propylene glycol alone both produced transient (1 to 4 minute) periods of cardiovascular depression characterized by cardiac asystole, systemic hypotension, and decreased pulmonary and renal arterial blood flow. The two preparations, in equivalent doses and volumes, produced statistically similar hemodynamic changes in the calves. The data from this study support the conclusion that the monitored cardiovascular effects of the commercially available oxytetracycline in propylene glycol in the intact, awake calves were due to the solvent propylene glycol. This conclusion is consistent with reports of other injectable products containing the same solvent.

Animals↗
PubMed1979

Lactose and casein content of nonpuerperal breast secretion.

Twenty-seven patients with nonpuerperal breast secretion were evaluated for the presence of casein and lactose in the secretions. Only two of seven patients with brownish or greenish secretions were positive for both lactose and casein although an additional six patients were positive for casein alone. Two patients with clear breast secretions were positive for both casein and lactose. However, 16 of 17 patients with milky or white secretions were positive for both casein and lactose. Although casein and lactose are more likely to be present in white breast secretions, other types of breast secretions may also contain these constituents.

Adolescent↗
PubMed1978

Inhibitory effect of hypertonic mannitol on vasoconstrictor and vasodilator responses of isolated coronary arteries.

The effect of hypertonic mannitol on pressor responses to vasoactive agents was studied in isolated canine coronary arteries perfused with physiologic salt solution at a constant flow. When perfusion pressure was increased with 60 mM KCl, mannitol (50 mosM) consistently caused a decrease in perfusion pressure that lasted for at least 1 h. Withdrawal of mannitol from the perfusion media was associated with a vasoconstrictor response that was not prevented by alpha- or beta-adrenoceptor blockade or by the presence of either nitroglycerin or norepinephrine. Hypertonic mannitol also reduced the responsiveness of the isolated smooth muscle preparations to several different mechanistically unrelated vasodilator agents. The mechanism(s) responsible for the paradoxical ability of hypertonic mannitol to reduce vascular responsiveness to both vasoconstrictor and vasodilator interventions in isolated canine coronary arteries is not known, but future studies should be directed at elucidating it as well as determining whether similar phenomena occur in vivo.

Animals↗
PubMed1978

Gentamicin blockade of slow Ca++ channels in atrial myocardium of guinea pigs.

Cardiac dysfunction is occasionally detected in patients undergoing treatment with amino-glycoside antibiotics, however, the mechanism responsible for the negative inotropic effect of these agents has not been identified. In the present investigation electrically driven left atria of guinea pigs were used to study the effects of gentamicin on calcium ion (Ca++)-dependent contractile events in heart muscle isolated from in vivo influences. When atria were first inactivated by excess potassium ion (K+; 22mM) and contractions were then restored by isoproterenol (an experimental model that accentuates the contractile dependence of myocardial fibers on influx of Ca++ through specific "slow channels" of the sarcolemma), the cardiac depressant activity of gentamicin (0.1 mM) was profoundly augmented. Conversely, the negative inotropic effect of tetrodotoxin (23.5 micron) was abolished by the same experimental conditions. Also, gentamicin (1 mM) and La+++ (0.5 mM) markedly decreased the positive inotropic response to increased frequency of stimulation; whereas, D600 (1.05 micron) converted the positive frequency-force relationship to a negative relationship. Present data indicate a direct cardiac depressant action of gentamicin, and suggest that this antibiotic adversely affects either the transport system responsible for Ca++ movement through slow channels of the sarcolemma, the availability of Ca++ for translocation to these sites, or both.

Animals↗
PubMed1978

Cardiac toxicities of antibiotics.

Isolated heart muscle preparations are useful in the study of cardiac toxicities of drugs and environmental chemicals: such tissues allow assessment of chemical effects on heart muscle that is free from indirect in vivo influences that can mask or even accentuate cardiac responses measured in the intact animal. In the present study, left atria of guinea pigs were used to demonstrate a direct cardiac depressant effect of greater-than-therapeutic concentrations of several aminoglycoside antibiotics. The toxic effect of these antibiotics seems to be a calcium-dependent event, and may prove useful to characterize contractile responses of the heart. Other antibiotic agents can also depress cardiovascular function, as summarized in this report, but mechanisms of action have not been clearly defined.

Aminoglycosides↗
PubMed1978

The influence of chemical restraining agents on cardiovascular function: a review.

A review of selected experimental reports indicated that chemical restraining agents commonly used in experimental animals affected basal cardiovascular function and could influence the response of the cardiovascular system to physiologic-pharmacologic stimuli. Drugs that were considered included pentobarbital, halothane, alpha-chloralose, droperidol, fentanyl, and ketamine. In relation to effects on hemodynamics, anesthetic restraint produced by one drug was not necessarily equivalent to that produced by another.

Anesthetics↗