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Biomedical subjects

J G Papp

Publications and source records attributed to J G Papp.

131 records · Page 8Linked to original sources
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Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes.

Distinct differences exist in action potentials and ionic currents between rabbit, rat, and guinea pig ventricular myocytes. Data obtained at room temperature indicate that about half of the rabbit myocytes show prominent phase 1 repolarization and transient outward current. Action potentials in guinea pig ventricular myocytes resemble those from rabbit myocytes not exhibiting phase 1 repolarization; and guinea pig myocytes do not develop transient outward current. Rat ventricular action potentials are significantly shorter than those from rabbit and guinea pig ventricular myocytes. Unlike rabbit and guinea pig myocytes, rat ventricular myocytes also exhibit a prominent phase 1 and lack a well defined plateau phase during repolarization. All rat ventricular myocytes exhibit a transient outward current which can be best fitted by a double exponential relation. There are no significant differences between the amplitude, voltage dependence and inactivation kinetics of the inward calcium currents observed in rabbit, rat and guinea pig. The steady-state current-voltage relations between -120 mV and -20 mV, which mostly represent the inward rectifier potassium current are similar in rabbit and guinea pig. The amplitude of this current is significantly less in rat ventricular myocytes. The outward currents activated upon depolarization to between -10 and +50 mV are different in the three species. Only a negligible, or absent, delayed rectifier outward current has been observed in rabbit and rat; however, a relatively large delayed rectifier current has been found in guinea pig. These large interspecies variations in outward membrane currents help explain the differences in action potential configurations observed in rabbit, rat, and guinea pig.

Action Potentials↗
PubMedDate not supplied

Autonomic responses and neurohumoral control in the human early antenatal heart.

Previous sporadic findings and the results of recent, more systematic studies now permit us to make an attempt to outline the contribution of the sympathetic and parasympathetic system to the control of the human early antenatal cardiac function. In the developing heart of man, only acetylcholine and catecholamines have so far been proven to act as true autonomic transmitters. Muscarinic-cholinergic responses to acetylcholine and related agents can be detected from the 4th postconception week onwards, i.e. soon after the initiation of the first heartbeats. The same applies to the beta-adrenergic responsiveness to noradrenaline, adrenaline and other adrenergic stimulants in a somewhat later period, commencing at week 5 after conception. The maximum cardiac response to all these agonists becomes stronger as development continues. Evidence is accumulating to suggest that prostaglandins and triiodothyronine might modulate the regulatory function of autonomic transmitters in the human early antenatal heart. Morphological and functional establishment of the autonomic innervation occurs in the human heart well after the appearance of the reactivity to autonomic transmitters. Under 'in vitro' conditions, muscarinic-cholinergic neuro-effector transmission can be demonstrated in 10-12 week-old hearts, and cardiac beta-adrenergic transmission can first be detected in weeks 13-14. From these observations and from the appearance of the 'in utero' fetal tachycardiac response to atropine in weeks 15-17 and the bradycardiac response to beta-blockers in weeks 23-28, it seems that the parasympathetic-cholinergic control of the developing human heart becomes functional and can play a role in the overall regulation of the antenatal cardiac function earlier than the sympathetic-adrenergic neural control.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

Cardiac responses to drugs at the extremes of age.

Although current knowledge concerning drug responsiveness in the human heart is still deficient at both extremes of age, i.e. in the fetus and the elderly, new information is beginning to emerge. Pharmacodynamic studies have provided a fairly comprehensive picture of the appearance and maturation of the automatic receptors, and also of the emergence and development of sympathetic-adrenergic and parasympathetic-cholinergic mechanisms in the prenatal human heart. A timetable can now be drawn up for the earliest detection of intrinsic responsiveness to numerous adrenergic and cholinergic agonists and antagonists, and to inotropic and antiarrhythmic drugs in the human embryonic and fetal heart. Information on the antenatal cardiac pharmacodynamics of antiarrhythmics and inotropic drugs is mostly confined to some of the classical remedies, so that a systematic study of the effects of the various newer drugs is warranted. As legal abortions yield prenatal hearts only in very limited numbers, human embryonic and fetal cardiac tissue and cell cultures could also be used for such research under both physiological and pathological conditions, such as hypoxia or simulated ischemia. Since the sporadic data available on the transplacental efficacy of maternally administered cardioactive agents are encouraging, extensive clinical investigation into the pharmacological control of intrauterine cardiac arrhythmias and heart failure, based on new, high-resolution fetal echocardiographic techniques to monitor the success of drug therapy at the various stages of prenatal development, is also a stimulating challenge. In the elderly human heart, pharmacodynamically-based alterations in responsiveness to drugs have so far been conclusively proven for adrenergic agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Agonists↗