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Biomedical subjects

J G Mill

Publications and source records attributed to J G Mill.

At least 73 records · Page 4Linked to original sources
PubMed1987

Electrophysiological effects of labetalol on canine atrial, cardiac Purkinje fibres and ventricular muscle.

1. Using conventional microelectrode techniques for the intracellular recordings of the membrane potential, the effects of labetalol were studied on cardiac Purkinje, atrial and ventricular muscle fibres of the dog. 2. Labetalol (1-10 microM) reduced, in a concentration-dependent manner, the action potential amplitude (APA) and the maximum rate of rise of the action potential (Vmax) in Purkinje fibres. 3. The action potential duration (APD) was decreased in Purkinje fibres but significantly increased in ventricular fibres after small concentrations of labetalol (1-3 microM). The atrial fibres were not very sensitive to labetalol. 4. Depolarization of the cardiac Purkinje fibres by increasing the external potassium concentration (8-12 mM), potentiated the labetalol effects on APA and Vmax but blocked its effects on the APD. 5. The effects of labetalol on Vmax of Purkinje fibres were dependent on the frequency of stimulation. 6. The ratio of the effective refractory period to the APD was increased both in normally polarized and depolarized Purkinje fibres after treatment with labetalol (10 microM). 7. Labetalol (10 microM) shifted the membrane responsiveness curve of Purkinje fibres by about 10 mV in the hyperpolarizing direction. 8. The slow response obtained in K-depolarized, Ba-treated Purkinje fibres was not significantly affected by labetalol (10-100 microM). 9. It is suggested that labetalol can exert Class I and Class III antiarrhythmic actions in cardiac muscle of the dog in vitro.

Action Potentials↗
PubMed1987

The Na+-Ca2+ exchange mechanism as a regulator of post rest contractions in cardiac muscle.

The effects of external Na+ concentration and stimulation rate changes on the post rest contractions of rat myocardium were studied. An increase in external Na+ concentration or in stimulation rate causes relative potentiation of the post rest contractions, suggesting that the sarcolemmal Na+-Ca2+ exchange mechanism affects the magnitude of the potentiation of post rest contractions.

Animals↗
PubMed1986

Characteristics of myocardial contractions activated under depolarizing conditions.

Guinea pig papillary muscles were used to study the activation of myocardial contractions under depolarizing conditions. Depolarization promoted by TKBa (normal Tyrode solution containing KCl and BaCl2) and TKAdr (normal Tyrode solution containing KCl and adrenaline) inactivates the fast Na current and under these conditions only slow responses are available to activate contractions. Since the slow response is sensitive to changes in rate and rhythm, we searched for mechanical correlates using isometrically contracting preparations to study the force-frequency relationship as well as rest potentiation. We also investigated if contractions are dependent only on the slow response or if the complete action potential plays a special role in the activation of contractions. We conclude that the slow response is the main mechanism for the activation of myocardial contraction, because complete mechanical activation was observed under depolarizing conditions. However, the electrical behavior of the slow response is reflected in the mechanical behavior of the depolarized preparations. At high rates, disturbances of excitation occur in depolarized cells and contractions appear to be bigeminal or with 2:1 block. Furthermore, after long pauses, post-rest contractions are depressed and increase progressively with repetitive stimulation, probably due to changes in the latency and threshold of the slow response. The complete action potential also plays a role in the activation of myocardial contractions which is necessary for the resting potentiation phenomena and also to avoid the larger depression of the rest contractions that can be seen in depolarized muscles when the pause is prolonged. This behavior seems to be related to the decrease of intracellular Na concentration produced by the inhibition of the fast inward Na-current.

Action Potentials↗
PubMed1984

Effects of verapamil on blood pressure and heart rate in neurogenic hypertensive rats.

The effects of verapamil (220 micrograms/kg per min i.v.) on blood pressure and heart rate were studied in sinoaortic baroreceptor denervated and sham-operated rats. In the conscious animals the verapamil-induced hypotension was accompanied by a significant heart rate increase in the first group (from 352 +/- 7 to 422 +/- 10 beats/min) and a decrease in the second group (from 485 +/- 13 to 400 +/- 9 beats/min). The verapamil-induced tachycardia observed in sham-operated rats was prevented by atropine plus propranolol but not by adrenal demedullation. Tachycardia was present in urethane-anesthetized sham-operated rats, similar to the sinoaortic baroreceptor-denervated rats. After verapamil a significant heart rate reduction was observed in sham-operated but not in sinoaortic baroreceptor-denervated rats. The results in conscious rats suggest that the direct inhibitory action of this drug on sinus node automaticity is suppressed by baroreflex tachycardia and that anesthesia masks this response.

Anesthesia↗
PubMed1983

Ventricular hypertrophy in sinoaortic denervated rats.

Sinoaortic denervation (SAD) induced a significant increase in mean arterial pressure in male (122 +/- 3 mmHg) and female (126 +/- 3 mmHg) rats compared to male (103 +/- 2 mmHg) and female (106 +/- 3 mmHg) sham-operated (SO) controls (P less than 0.05). A significant increase of the weight of the left ventricle (LV) (11.5%, P less than 0.001) was observed 15 days after surgery in male, but not in female, SAD hypertensive rats compared to pair-fed SO controls. The data suggest that hormonal factors contribute to rapid LV hypertrophy in male SAD hypertensive rats.

Animals↗
PubMed1982

Length-dependent inotropic changes in cardiac muscle.

1. Length-dependent changes of the inotropic state of rabbit atrial strips were studied using inotropic interventions. Increases in extracellular calcium and adrenaline were used as positive inotropic agents, whereas acetylcholine and verapamil were the negative inotropic agents. Length-tension curves were normalized with respect to maximal developed tension and length. 2. The expected length-tension relations were obtained when plotted in a conventional manner. However, when length-tension curves were normalized with respect to maximal developed tension and length, a length-dependent activation was indicated by the separation of the curves. 3. These results suggest that length-dependent activation altered the inotropic state of cardiac muscle when length changed.

Acetylcholine↗
PubMed1978

Effect of uranyl ions on isometric contractions in rabbit atria.

The effects of uranyl ions on isometric contractions of atrial strips of rabbit heart were studied. It was observed that uranyl ions, in a concentration of 1.1 X 10(-5) M, do not alter isometric contraction; 2.2 X 10(-5) M concentration produced a small positive inotropic effect that was magnified at a 4.5 X 10(-5) M concentration; concentrations greater than 1.8 X 10(-5) M produced a negative inotropic effect. There is evidence that the positive inotropic effect is mediated by catecholamine release, in a similar manner to the action of uranyl ions on intestinal smooth muscle preparations. This response was blocked by propranolol and also after tyramine treatment of the preparation. The negative inotropic effect seems to be mediated by a blocking effect on calcium entry through the sarcolemma during activation. Indirect evidence supporting this hypothesis was the observation of a decrease of action of uranyl ions in the presence of isoproterenol and of increased extracellular calcium concentration.

Animals↗
PubMed1978

[Characteristics of the isometric myocardial contractions during its activation by the slow response (author's transl)].

The characteristics of the isometric contractions of rabbit's left atria were studied during its activation by the slow response of the cardiac action potential. When compared to the conditions where activation occurs with normal action potentials it verifies that contraction amplitude decreases, becoming slowly and larger. Positive inotropic effects that enhance calcium entrance through the membrane (Ca and IPA), during action potential, increase contraction amplitude. Negative inotropic effects that depress the slow response (Ach and verapamil) also depress the contractions. Staircase becomes reversed, with contraction strength decreasing with increase in rate of beating. It was seen that adequate conduction is an important factor for the normality of contractions, and the importance of the fast component of the cardiac action potential, for this occurrence, was remembered.

Acetylcholine↗
PubMedDate not supplied

Activation of the Langendorff perfused rat heart depolarized by increased external potassium concentration.

Myocardial activation under depolarized conditions was studied in spontaneously beating Langendorff perfused hearts from albino rats. Depolarization was obtained by increasing external potassium concentration in steps (5.4, 7.4, 10, 10.5, 11 and 11.5 mM) in the perfusing solution with or without adrenaline (Adr). Left ventricle isovolumic systolic pressure and coronary flow did not change as external potassium increased, albeit being larger with Adr in the perfusing solution. Atrial and ventricular rates decreased, the latter showing a larger decline. The same behaviour was displayed by perfused hearts, with higher rates being developed by the group with Adr. PR interval and QRS complex duration increased as a function of external potassium. PR intervals were the same in both groups but QRS duration was larger in the Adr group, indicating that AV conduction was not changed in presence of Adr but intraventricular conduction was delayed in that situation. It was also observed that in the great majority of perfused hearts, differing from isolated preparations, ventricular mechanical activity ceased at around 11.5 mM external potassium.

Action Potentials↗