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Biomedical subjects

J Gero

Publications and source records attributed to J Gero.

At least 19 recordsLinked to original sources
PubMed1992

Heterogeneity in geometrical alterations of main branches of left coronary artery induced by increase in ventricle volume.

With the use of ultrasound technique, segment length and diameter of ramus circumflexus (RC) and ramus interventricularis anterior (RIA) in the dog heart, placed in a bath, were monitored under constant pressure. When the left and/or right ventricular volume was increased by 150% of the normal diastolic filling, segment length of RC increased by 2.54 +/- 0.17 and 2.15 +/- 0.06%, respectively, and diameter of RC decreased by 4.72 +/- 0.20% and by 4.60 +/- 0.20%, respectively. The same filling of the left and/or right ventricle induced in the proximal third of RIA an increase in segment length by 11.40 +/- 0.55 and 12.2 +/- 0.42%, respectively, and a decrease in diameter by 9.41 +/- 0.42% and by 10.01 +/- 0.31%, respectively. The latter values of RIA were significantly higher (P less than 0.001) than those registered in RC. The deformations of RIA decreased toward the periphery of the vessel. By the fact that conduit coronary artery tracks instantaneously the increase of the volume of the left and right ventricle, its contribution to the total coronary resistance increases dynamically. With the ventricular volume increased by 150%, the RC contributes to the total coronary resistance by 14% and RIA in the proximal part contributes by 23%, with values significantly higher than control (10%) (Malindzak, G. S. In: The Coronary Artery. London: Croom Helm, 1982, p. 241-267). The results imply a methodical consequence, namely that the diameter of the respective coronary artery is an index of smooth muscle activity only if both perfusion pressure and volume of the heart are maintained constant.

Animals↗
PubMed1983

Dilatation of conduit coronary artery induced by high blood flow.

The ramus interventricularis ventralis (RIV) of the dog heart was perfused with donor blood from the femoral artery. The inflow and outflow pressure, the blood flow and the diameter of the RIV were recorded. An increase in the blood flow from 11.3 +/- 0.3 to 81.4 +/- 6.2 ml/min induced, in 24.4 +/- 1.7 s a gradual increase in RIV diameter which became stabilized in 90-120 s and amounted to 80.87 +/- 11.68 microns, i.e. to 3.37 +/- 0.70% of the resting diameter. Since the mean pressure at the site where the diameter was recorded was maintained constant, relaxation of RIV smooth muscle has been assumed to have occurred. Dilation could not be evoked after RIV had been dilated by papaverine. Any interference by changes in pressure amplitude accompanying the increase in blood flow was precluded by using non-pulsating perfusion of the RIV. An increase in the non-pulsating blood flow from 12.11 +/- 2.20 to 90.33 +/- 11.30 ml/min likewise--in 19.50 +/- 1.83 s--produced an increase in RIV diameter of 1.8%. Blood flow is being suggested as one factor regulating the tone of the smooth muscle of the major coronary artery. This mechanism is supposed to counteract sympathetic constriction of the major coronary artery.

Animals↗
PubMed1980

Factors determining post-stimulation dilatation.

Post-stimulation dilatation (PSD) of the femoral artery and vein after cessation of postganglionic sympathetic stimulation were related to the frequency and pulse number of the preceding stimulation. It was found that: 1) A minimum number of pulses (MNP) is needed to evoke PSD. MNP is inversely related to the stimulation frequency. A marked PSD develops after stimulation at 1 Hz when only 100 pulses were applied, whereas, if stimulated at 4 Hz or at higher frequencies, even 2,000 pulses fail to induce PSD. 2) The maximum value, the maximum rate and the overall diameter change of PSD (expressed either in absolute values or in relation to the preceding contraction) are a) directly related to the number of pulses at a constant stimulation frequency, b) for a constant number of pulses the above values are inversely related to the stimulation frequency. 3) The relation of PSD values to the stimulation parameters contradict the assumption that PSD is elicited either by a neurogenic transmitter released by the stimulation, or by an extraneuronal transmitter whose release is associated with the release of noradrenaline. PSD is suggested to be due to a decreased noradrenaline level within the synaptic cleft due to persistence of the reuptake after the release of noradrenaline had ceased.

Adrenergic Fibers↗
PubMed1980

The contribution of the left and right sympathetic trunk to control of the diameter of the femoral artery and the consecutive resistant bed.

Laterality of sympathetic control of the diameter of the femoral artery (using an inductive transformer) and the blood flow in its consecutive bed (using a Stattham flowmeter) was studied at the postganglionic level. The fibres leaving LG3, LG4 and LG5 were stimulated. Stimulation of the left sympathetic trunk (ST) evoked 88.33 +/- 0.98% of maximum sympathetic constriction of the ipsilateral and 15.0 +/- 1.1% of the contralateral femoral artery (P less than 0.001). Stimulation of the right ST evoked 86.38 +/- 0.90% of maximum constriction of the ipsilateral and 11.95 +/- 0.99% of the contralateral femoral artery (P less than 0..001). Vasomotor fibres contained in the femoral nerve exert only 23.5 +/- 3.3% (P less than 0.01), while fibres from other sources (probably including the aortic plexus) were responsible for 74.1 +/- 5.2% (P less than 0.001) of maximum constriction. The blood flow in the resistant bed consecutive to the left and right femoral artery is controlled solely by postganglionic fibres of the ipsilateral lumbar ganglia. The results indicate the variability of lateralization of the sympathetic control of the individual segments of the vascular tree.

Animals↗
PubMed1980

Monoaminergic pathways to the coronary arteries and to the myocardium.

The monoaminergic innervation of the coronary vessels and of the myocardium in dogs was examined by means of degenerative techniques: (i) local perivascular neurotomy was performed at the origin of the left coronary artery; (ii) the stellate ganglion was removed bilaterally. Evaluation of the neural degeneration pattern led the suggestion that three types of neurons at least exist within the heart: (i) neurons innervating the coronary vessels both in the ventricles and in the atria; (ii) neurons innervating the ventricular myocardium, and (iii) neurons innervating the atrial myocardium. The post-ganglionic fibres of the stellate ganglion innervate the vessels of the whole heart. Their contribution to the innervation of the ventricular myocardium represents about 30%.

Animals↗
PubMed1979

Sympathetic control of major coronary artery diameter in the dog.

The diameter of a major coronary artery, the ramus interventricularis ventralis (RIV), was measured in dogs with arrested hearts perfused by an extracorporeal circulation. The resting diastolic diameter was 1.78 +/- 0.07 mm (mean +/- SE) at a diastolic pressure of 74.2 +/- 3.4 mm Hg. Bilateral supramaximal stimulation of fibers leaving the cranial pole of the stellate ganglion decreased the diameter by 71.2 +/- 8.9 micrometer, i.e., 4.0 +/- 0.5% of the resting diameter. Stimulation of the left stellate ganglion contributed 59.8 +/- 5.7% of the maximum response; that of the right contributed 40.3 +/- 5.5%. Stimulation of the thoracic ganglia (T2-4) resulted in a 1.2 +/- 0.4% decrease in coronary vessel diameter. RIV failed to respond to bilateral caudal cervical ganglion stimulation. After iv administration of phentolamine, 1-2 mg/kg, no response to sympathetic stimulation could be elicited. Therefore, it appears that alpha-receptors are activated by the release of the sympathetic neurotransmitter to sympathetic stimulation and that beta-receptors are not involved in the response of RIV to sympathetic stimulation.

Animals↗
PubMed1979

Role of the vagus in control of the major conduit coronary artery in the dog.

Using El Badawi and Schenk's modification of Karnovski's method for the demonstration of acetylcholinesterase, the authors found cholinergic fibres both in the perivascular connective tissue and directly in the wall (in the adventitia) of the major coronary arteries; the fibres were distributed regularly around the circumference of the arteries. In the case of the smaller intramyocardial arteries, the cholinergic fibres were concentrated at two poles of the blood vessel; none were present in the wall of the veins. The shape and topography of the coronary cholinergic arterial plexus resemble the shape and topography of the coronary sympathetic adrenergic system. In apparent contradiction of this finding, stimulation of the cervical vagus did not affect the diameter of the large coronary arteries. Since acetylcholine (6--10 micrograms/kg i.v.) produced a mean 7.4% increase in the diameter of the ramus interventricularis ventralis, we concluded that there are no postgangliar cholinergic fibres of vasomotor significance for the large coronary arteries in the cervical vagus. The specific acetylcholinesterase activity found in the wall of these vessels belongs either to cholinergic terminals whose ganglion cells are not located in the vagal ganglion, or to cholinergic axones terminating outside the wall of the large coronary arteries.

Acetylcholinesterase↗
PubMed1978

Mechanisms underlying overshoot dilation after sympathetic denervation.

(1) 30--60 sec after transection of the sympathetic chain, the diameter of both femoral artery and vein dilates to approximately 120% of the control diameter ('overshoot dilation'). Vessel diameter subsequently decreases and stabilizes with 5--10 min at a value of 108% of the original ('stabilized dilation'). (2) After treatment with norepinephrine-uptake-blocking drugs (cocaine, imipramine), the transient overshoot dilation is abolished and the diameter 1 min after denervation is identical to that at stabilized dilation. (3) It is proposed that (a) the stabilized rather than the transient overshoot dilation represents the loss of sympathetic control following following denervation and (b) the overshoot dilation reflects a transient decrease in transmitter concentration within the vessel wall, associated with a temporarily undiminished rate of neural reuptake activity persisting even in the absence of transmitter release.

Animals↗
PubMed1978

Adrenergic innervation of the coronary arteries and the myocardium.

The monoaminergic innervation of the coronary vessels and myocardium in the dog was studied by means of the histochemical fluorescence method. The distribution of monoaminergic terminals in the arterial wall depends on the diameter of the artery. In large arteries, the terminals are regularly distributed around the entire circumference, the fibres being situated between the elastic lamellae of the adventitia. The terminals within the media could not be detected. In small arteries, the sympathetic ground plexus aggregates in two parallel strands, the artery being between them. In arterioles, two thick fibres only accompany the vellel. The myocardium is innervated by means of a three-dimensional sympathetic ground plexus distributed between the myocardial cells independently of vessels. No difference in density of innervation was found between the right and left heart. The point-counting method, on the other hand, has revealed that the density of innervation in the left auricle is nearly twice as dense as in the left ventricle. The terminals innervating the myocardium are markedly thinner than the fibres innervating the arteries. Two-dimensional plexuses innervate the epicardium, endocardium and valves.

Adrenergic Fibers↗