PubMed Health⌕ Search

Biomedical subjects

J L Matheny

Publications and source records attributed to J L Matheny.

At least 37 records · Page 2Linked to original sources
PubMed1976

Role of neuronal and extraneuronal factors in temperature mediated responsiveness of adrenoceptors.

Changes in bath temperature caused changes in the adrenergic responsiveness of rabbit iris dilator muscle as indicated by shifts in dose-response curves along the log axis and changes in maximum responses. Responses of control tissues to an alpha agonist (norepinephrine) were increased at lower temperatures and responses to a beta agonist (isoprenaline) were increased at higher temperatures. Responses of control tissues were compared with responses of tissues pretreated with cocaine or with responses of adrenergically denervated tissues (chemical and surgical). Changes in ED50 values with temperature change are similar in control, cocaine pretreated or denervated muscles. In contrast, changes in maximum response with temperature change are reversed by cocaine pretreatment or denervation. Pretreatment of tissues with an inhibitor of catechol-o-methyl transferase (tropolone) or an inhibitor of monoamine oxidase (iproniazid) did not affect the temperature sensitivity of adrenoceptors. Also, responses to terbutaline, a beta agonist not susceptible to catechol-o-methyl transferase, changed with temperature. These data indicate that for rabbit iris dilator muscle both a neuronal and an extraneuronal component are involved in adrenoceptor response changes induced by temperature change and that changes in rates of activity of metabolizing enzymes are not involved.

Animals↗
PubMed1976

Myocardial function during hypoxia in the presence of different buffers.

Electrically driven rabbit left atria were exposed to 20 min periods of either hypoxia or anoxia in the presence of a bicarbonate-phosphate buffer, a Tris buffer [tris (hydroxymethyl) aminomethane hydrochloride] or combination of both. The bicarbonate-phosphate buffer system was shown to be important for tissue survival during hypoxia or anoxia whereas recovery was diminished in the presence of Tris only. Stimulus threshold and arrhythmias were shown to increase for atria in Tris. Oxygen consumption determinations on both spontaneously beating right atria and quiescent left atria showed no difference between pre- and post-hypoxia or between different buffers. Tris was shown to elicit a positive inotropic effect without an increase in O2 consumption.

Animals↗
PubMed1976

Cardiac chronotropic mechanisms of dimethyl sulphoxide: inhibition of acetylcholinesterase and antagonism of negative chronotropy by atropine.

The chronotropic effects of dimethyl sulphoxide (DMSO) were studied in spontaneously beating rabbit atria. Low concentrations of DMSO (0.14, 0.42 M) produced slight positive chronotropic (+C) responses; 0.84 and 1.41 M DMSO caused significant negative chronotropic (--C) responses. All concentrations decreased contractile strength. Atropine sulphate (10)-7) to 10(-5) M) antagonized the chronotropic effects, but not the inotropic effects. In the presence of atropine all DMSO concentrations produced significant +C responses. Reserpine pretreatment or propranolol did not affect contractile responses to DMSO in the absence or presence of atropine. DMSO produced concentration-dependent inhibition of acetylcholinesterase (AChE) activity of atrial homogenates. The results indicate that the --C responses are due specifically to AChE inhibition by DMSO and resulting cholinergic influences on the atrial pacemaker. Adrenergic mechanisms do not appear to mediate the +C responses. Data presented here provide evidence that a cardioactive effect of DMSO is mediated by a well-defined receptor-linked mechanism, and that this effect can be modified by a specific receptor blocking agent.

Animals↗
PubMed1975

Adrenergic drug-receptor interaction in the presence of strontium (Sr++) in mammalian myocardium.

The specificity of Ca++ for the interaction of beta adrenergic agonists with their receptors in rabbit right atrial muscle was evaluated. This was accomplished by substituting Ca++ by an equimolar concentration of Sr++. Dose-response curves which demonstrate the effect of norepinephrine and isoproterenol on the rate of electrical activity in the presence of Ca++ or Sr++ were made. In addition, the antagonistic action of propranolol (1 X 10(-7) M) in a Ca++-containing or Sr++-containing medium was determined. The results clearly demonstrate that Sr++ can effectively substitute for Ca++ in maintaining electrical and mechanical activity in cardiac muscle. Also, norepinephrine and isoproterenol can increase the rate of electrical activity in a Ca++ or Sr++-containing medium. This effect of these beta agonists is mediated through the beta-receptors since propranolol effectively blocked their action. It appears that Ca++ per se is not required for beta agonist or antagonist-receptor interaction in cardiac muscle. The results are discussed in relation to the dependency on extracellular Ca++ for beta agonists to cause a change in the rate of electrical activity after receptor occupancy.

Adrenergic beta-Agonists↗
PubMed1975

Metabolic inhibition and adrenoceptor interconversion.

The adrenergic receptor responses of isolated strips of iris dilator muscle from rabbits were studied. An alpha agonist, norepinephrine and a beta agonist, isoprenaline, were used to assess adrenergic sensitivity before and after pretreatment of tissues with metabolic inhibitors at 22, 29 and 37 degrees C. The metabolic inhibitors used were iodoacetic acid and dinitrophenol. Temperature change altered adrenoceptor sensitivity in the same manner before and after metabolic inhibition. Iodoacetic acid (10.4 mug/ml) pretreatment increased both alpha and beta responses. Dinitrophenol (1.8 mug/ml) pretreatment increased alpha and decreased beta responsiveness. The results obtained indicate that some metabolic process altered by dinitrophenol may be involved in this adrenoceptor interconversion seen when temperature is changed. This supports the theory that local environment determines the drug sensitivity (alpha or beta) of a single adrenergic receptor.

Adrenergic alpha-Agonists↗
PubMed1975

Myocardial function during hypoxia: protective effect of dimethyl sulfoxide (DMSO).

Electrically driven rabbit left atria were exposed to 20 min periods of hypoxia in the presence and absence of dimethyl sulfoxide (DMSO) or sucrose. Contractile strength declined significantly less than control when tissues were exposed to DMSO during hypoxia. On reoxygenation tissues treated with DMSO recovered pre-hypoxia contractile strength more slowly. Sucrose did not protect tissues during hypoxia. Comparison of results with DMSO and sucrose indicated that tissue depression prior to hypoxia could not explain the action of DMSO. Kinetic analysis performed on tension decline which occurred during hypoxia showed that two components were involved; rate of tension loss in both components was decreased by DMSO and there was a shift in the percentage of decline to the slower component. These data indicate that DMSO may increase energy availability, increase efficiency of energy utilization, or possibly affect the shift from aerobic to anaerobic metabolism during hypoxia, but not during the post-hypoxic recovery period.

Animals↗
PubMedDate not supplied

Macro- and microvascular effects of nitrous oxide in the rat.

The aims of this study were: (1) to determine the macro- and microvascular actions of nitrous oxide (N2O) in the rat, and (2) to determine whether the vascular actions of N2O involved specific interaction with alpha-adrenergic receptors or opioid receptors. Systolic blood pressure, heart rat, total tail blood flow, blood cell velocity in subepidermal capillaries of the tail, and percentage of capillaries exhibiting flow were monitored in conscious rats during the administration of N2O before and after administration of clonidine (an alpha 2-adrenergic agonist), prazosin (an alpha 1-adrenergic antagonist) or naloxone (an opioid antagonist). Total tail blood flow increased significantly in a dose-dependent manner with N2O at 20% and 40% with oxygen. This action of N2O was not blocked by clonidine, prazosin, or naloxone. Capillary flow velocity increased during 20% and 40% N2O compared to 100% O2, but the changes were not statistically significant nor did they correlate with the changes in tail blood flow. These data suggest that the peripheral vascular action of N2O does not involve specific actions at alpha-adrenergic receptors or opioid receptors and may be the result of direct actions on the peripheral vasculature.

Analysis of Variance↗
PubMedDate not supplied

The effects of nitrous oxide administration in the healthy elderly: N2O elimination and alveolar CO2.

Healthy young and elderly males were administered sedative concentrations of nitrous oxide/oxygen (N(2)O/O(2)) under a protocol designed to mimic that used in a dental operatory. Samples of end-tidal expired gas were taken at the end of 30-minutes inhalation of, and periodically for 70 minutes after withdrawal from, nitrous oxide/oxygen. Samples were analyzed to monitor the decline of alveolar nitrous oxide levels and any changes in alveolar carbon dioxide levels, to determine if there were any age-related differences. The fall in alveolar N(2)O following cessation of administration was rapid, and in a double-exponental manner as was expected. No age-related difference in N(2)O decline was observed. Alveolar carbon dioxide (CO(2)) levels were lower and more variable in the elderly group. Both groups exhibited elevated CO(2) levels at the end of the N(2)O period, and an unexplained rise in CO(2) at approximately 30 min post N(2)O.

Adult↗
PubMedDate not supplied

Effect of age on the digit blood flow response to sedative concentrations of nitrous oxide.

Twenty healthy male subjects [11 young, x̄ = 25.4 ± 0.8 (SEM) years old; 9 elderly, x̄ = 64.5 ± 0.7 years] volunteered for a study designed to investigate the effect of age on several cardiovascular parameters to inhaled N(2)O-O(2). The protocol was designed to mimic the administration of N(2)O-O(2) for sedation in the dental office, although no dental treatment was performed. Clinical criteria were used to judge the appropriate sedative level for each subject; no attempt was made to establish doseresponse relationships. Digit blood flow was measured by strain-gauge plethysmography, and heart rate, arterial blood pressure, respiratory rate, and skin temperature were monitored and recorded. N(2)O and CO(2) levels were monitored in end-tidal gas samples by gas chromatography; machine gauge readings were calibrated against known gas mixtures by the same technique.Under the conditions of this experiment both healthy young and healthy elderly subjects experienced a marked (200-300%) increase in digit blood flow during N(2)O inhalation, compared to that during air and 100% O(2) inhalation. There was no significant difference in the degree of flow increase between young and elderly subjects. Also, there were no significant differences in the response of these healthy young and healthy elderly subjects to sedative concentrations of N(2)O with regard to heart rate, arterial blood pressure, respiratory rate, skin temperature, or mean end-tidal CO(2) levels. The data indicate that N(2)O, in the concentrations routinely administered in the dental office for sedation, does not have a differential effect on the measured parameters in healthy elderly and healthy young males.

Adult↗