摘要:

Major branches from right and left sympathetic ganglia were electrically stimulated while force of contraction was recorded from multiple areas of the right and left ventricles. Stimulation of the stellate ganglia generally elicited alterations in force of contraction from all test segments, but excitation of selected nerve trunks induced responses in highly localized regions of the heart. Ablation of narrow strips of epicardium resulted in obliteration of contractile responses in specific, highly localized regions of the heart; thus a major fraction of the sympathetic innervation of the ventricular chambers is by way of the epicardial plexus. The anterior surface of the right ventricle is supplied by projection pathways arising within the immediately subepicardial regions of the right A-V groove and, to a lesser extent, from the tissues immediately adjacent to the left anterior descending artery. The left ventricle receives minor projections from the right A-V groove with major projections from subepicardial tissues along the left anterior descending artery. In some animals there also exists a definite left ventricular supply from the region of the left A-V groove. Whereas the thoracic vagi send dense projections to the atria, and particularly to nodal tissue, they also supply both ventricles with inhibitory and augmentor fibers. Although isolated cardiac nerves may carry predominantly sympathetic or parasympathetic fibers, many show rich intermingling of these fibers in trunks distal to the caudal cervical ganglion.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

Isolated cat lungs perfused at constant flow (75 ml/min per kg total body weight) were ventilated with gases of varying CO2content (0 to 10%), 20% O2, and the balance N2. Tidal volume was constant, and airway pressure did not change. Left atrial pressure was held constant, and changes in pulmonary artery pressure (PPA) were taken to reflect changes in pulmonary vascular resistance. Progressive hypercapnia (Pco2= 0 to 60 mm Hg) resulted in an increase in PPA as pH decreased. Equivalent degrees of acidosis, produced by the infusion of 0.3 N lactic acid, resulted in a higher PPA. Changes in PPA produced by lactic acid were reversible with 0.89 M sodium bicarbonate. With Pco2constant, and pH changed by lactic acid or sodium bicarbonate infusion, PPA was higher in lungs ventilated with room air (Pco2= 0) than in those ventilated with 5 or 10% CO2(Pco2= 30 or 60 mm Hg) at the same hydrogen ion concentration of the perfusate. These findings can be explained by two opposing actions of CO2on pulmonary vessels: a dilator action due to the direct effect of CO2and a constrictor action caused by the increase in hydrogen ion concentration.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

Left ventricular performance in the isolated dog heart was observed in a preparation in which left ventricular pressure and volume could be monitored continuously while the ventricle contracted isobarically by compressing air into a large chamber. By suddenly reducing the orifice connecting the ventricle to the chamber a constant load was imposed on the ventricle, abruptly forcing it to develop pressure in systole. This pressure increased over the ensuing 3 minutes while both the load and the end-diastolic pressure remained constant, implying that the sudden development of pressure by the ventricle was attended by a positive inotropic effect, otherwise known as homeometric autoregulation. Further studies showed this positive inotropic effect to be a function of the magnitude of the abrupt increase in systolic pressure and the time course of the experiment. β-adrenergic receptor blockade with propranolol decreased but did not abolish this effect. Infusion of norepinephrine did not enhance it. Increases in ventricular compliance that accompanied loading could not fully account for it. Evidence is presented that this positive inotropic effect may in part be mediated through the release of intrinsic catecholamines when the ventricle is forced to increase its systolic pressure.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

The adrenergic innervation of the canine kidney was studied with the fluorescence histochemical method of Falck and Hillarp in conjunction with chemical assays for catecholamines in specific portions of the kidney. Adrenergic nerve fibers were seen traveling along the interlobar, arcuate, and interlobular arteries and along the afferent arterioles. The vasa recta of the outer medulla also received adrenergic innervation. Adrenergic nerve fibers were never seen in association with the glomerulus, the efferent arteriole, or the tubules. The distribution of the nerve fibers agreed with the distribution of norepinephrine. After administration of reserpine or denervation of the kidney, no adrenergic nerve fibers were seen, and the norepinephrine level in all portions of the kidney fell to negligible levels. Accumulation of norepinephrine in the nerve fibers was observed after kidney slices had been exposed to solutions of norepinephrine. On the basis of these experiments, it was concluded that the fibers visualized with the fluorescence histochemical method were adrenergic nerve fibers. The possible physiologic role of the adrenergic innervation of the canine kidney is discussed.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

Reciprocal beats between sinus node and atrium were studied in isolated rabbit heart tissue by microelectrode techniques. Early premature atrial responses which entered the sinus node frequently emerged to re-excite the atrium as “echoes.” When the premature atrial beats discharged some but not all nodal areas, the atrial echoes, in turn, appeared to re-enter the sinus node. Repetitive reciprocation involving the sino-atrial circuit was occasionally observed. Anatomic and temporal patterns of excitation at multiple recording sites suggest that “entrance” block and slow conduction of premature impulses within the sinus node may explain the observed reciprocation. The results support the hypothesis that self-sustained reciprocation in a sino-atrial circuit might be responsible for some cases of paroxysmal atrial tachycardia.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

A supernormal phase of conduction between right and left atria was observed in the exposed hearts of anesthetized dogs. Interatrial conduction time of premature atrial responses was reduced by as much as 17% during the early phase of diastole, relative to the conduction interval of basic driven responses. The supernormal phase lasted from 60 to 140 msec and was greater at slower basic driving frequencies. A brief phase of supernormal excitability was also found in the specialized cells of Bachmann's bundle from puppy hearts in vitro. Supernormal conduction was not observed within the atrial appendages (i.e., in areas not supplied by specialized conducting bands); supernormal excitability was not demonstrable in cells of ordinary atrial myocardium. Although vagal stimulation abbreviated transatrial conduction time, atropine did not abolish the phase of supernormality.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

Pharmacological agents that block or potentiate the effects of naturally occurring vasoactive substances were used to try to determine which substance, if any, mediates the vasoconstrictor response to acute alveolar hypoxia in isolated rat lungs. Isolated and ventilated lungs of rats were perfused at 37°C with homologous blood at constant-volume, pulsatile inflow, and pressor responses to brief periods of ventilation hypoxia (2% O2) were recorded (control, 21% O2). Antihistamines of four different chemical classes in concentrations of 70 to 140 μg/ml abolished all pressor responses to alveolar hypoxia without interfering with the effects of injected bradykinin, ATP, or serotonin. A histaminase-inhibiting compound, semicarbazide, potentiated the hypoxic pressor response. The hypoxic pressor response could not be abolished by α-receptor-, serotonin-, or ATP-blocking agents. The results suggest that endogenous histamine in the lung is involved in the vasoconstrictor response to acute alveolar hypoxia.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID

摘要:

The present investigation was undertaken to see if any of the naturally occurring vasoactive substances was likely to act as a mediator for the pulmonary vasoconstrictor response to acute alveolar hypoxia. Rats were treated with agents that deplete local stores of vasoactive amines or inhibit their synthesis. Lungs from these animals were isolated, ventilated, and perfused with homologous blood at constant volume inflow. Their pressor responses to 2- to 3-minute periods of ventilation hypoxia (2% O2) were observed.The histamine-releasing agent 48/80 or the histidine decarboxylase inhibitor NSD 1055, or both, depleted 73% of the histamine in the lung but had no consistent effect on the pressor responses to hypoxia. When 48/80 (0.2 to 1 mg) was given in vitro, histamine in the lung was reduced to 10% of normal, or less, and the pressor response to alveolar hypoxia was completely abolished.Reserpine, guanethidine, or alpha-methyl-tyrosine reduced catecholamine stores in heart tissue (as an index of general tissue changes) by a maximum of 90% and reserpine decreased serotonin in the lung by 93% without inhibiting the hypoxic pressor responses. The findings strengthen the concept that histamine mediates the pressor response to acute alveolar hypoxia in the rat.

ISSN:0009-7330    

出版商:OVID    

年代:1968

数据来源: OVID