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Biomedical subjects

F Urthaler

Publications and source records attributed to F Urthaler.

At least 55 records · Page 3Linked to original sources
PubMed1982

The direct negative chronotropic action of prazosin on the canine sinus node.

The direct and indirect chronotropic effects of prazosin were studied in 22 anesthetized dogs using the technique of selective perfusion of the sinus node. Concentrations of 1, 10, 50 and 100 micrograms/ml of prazosin produced cumulative, dose-related reductions in mean sinus rat of 4 +/- 2; 10 +/- 6; 15 +/- 9 and 27 +/- 15 beats/min, respectively (P less than .0001). Intranodal prazosin did not significantly alter the positive chronotropic sinus node response to norepinephrine (0.05 and 0.1 micrograms/ml) administered via the same route. Sinus rate increases during stimulus frequency response curves after right stellate stimulation were not influenced by prior administration of prazosin. Sinus bradycardia elicited by submaximal vagal stimulation also was not affected by intranodal prazosin.l In six reserpinized dogs, methoxamine (10 and 25 micrograms/ml) injected into the sinus node artery caused a sinus rate increase of 10 4/- 2 and 14 +/- 3 beats/min (P less than .001). Intranodal prazosin (50 micrograms/ml) prevented this effect. Taken together, these results indicate that prazosin exerts a direct negative chronotropic action on the canine sinus node and that this effect is at least in part mediated through interference with alpha-1 receptors located in or near the sinus node. Prazosin has little or no effect on the presynaptic alpha-2 receptors nor does it interfere with the cholinergic mechanism in the sinus node.

Animals↗
PubMed1981

Effects of selectively produced changes in cardiac rhythm or conduction upon flow in the superior vena cava.

The effects of changes in cardiac rhythm or conduction on the rate of volume flow in the superior vena cava (SVC) were studied in 25 dogs anesthetized with sodium pentobarbital. Slowing of sinus rate from 145 +/- 16 to 114 +/- 12 beats/min was achieved by selective perfusion of Ringer's solution into the sinus node artery. During sinus slowing there was a continuous change in the systolic-diastolic flow ratio measured in the SVC. At control sinus rate (net), total forward flow as 6.3 ml/beat with a systolic volume of 6.5 ml and a diastolic volume of -0.2 ml. At the slowest bradycardia, total forward flow had increased by 25%. Since there was no significant change in the systolic volume, the entire 25% increase in forward flow occurred during ventricular diastole. During atrioventricular (AV) block (second-degree or complete), achieved by selective perfusion of eserine into the AV node artery, unimpaired acceleration of flow was readily demonstrable in the SVC even in the absence of ventricular contraction. Thus systolic ventricular suction (vis a fronte) has little or no effect on right atrial filling. During high-degree AV block, the normal atrial contraction readily opened the tricuspid valve, and when both atrium and ventricle were filled to or near maximum capacity, atrial contraction was consistently vigorous enough to propel blood into the pulmonary artery. Given appropriate hemodynamic circumstances, these results confirm the remarkable effectiveness of right atrial contractile performance.

Animals↗
PubMed1980

Reflex heart block. Baroreflex, chemoreflex and bronchopulmonary reflex causes.

Reflex heart block was studied in 20 dogs anesthetized with sodium pentobarbital and in 5 trained unanesthetized dogs. Three different vagal reflexes were produced: the Marey response during hypertension caused by administering methoxamine, a cardiogenic hypertensive chemoreflex activated by injection of serotonin into the left atrium and the Hering-Breuer reflex observed during normal respiration of unanesthetized dogs. In every dog during any of the three reflexes heart block was consistently observed after the normal slowing response of the sinus node had been selectively eliminated by the direct perfusion of 10 microgram of atropine into the sinus node artery. This was a uniform response despite its being variously produced by a pressor reflex, a chemoreflex or an extracardiac bronchopulmonary reflex. Transient heart block is therefore to be anticipated during reflexes with vagal efferent components if for any reason the sinus node is incapable of slowing suitably. The possible clinical relevance of these experimental observations is discussed.

Animals↗
PubMed1980

Dilation of coronary artery stenoses after isosorbide dinitrate in man.

The effect of isosorbide dinitrate (ISDN), 5 mg sublingually, on the diameters of coronary artery stenoses (n = 27) was examined in 20 patients. Another 18 patients with angiographically normal coronary arteries received the same amount of ISDN and were used as controls. Prestenotic and stenotic diameters were measured with a vernier calliper having an accuracy of 0.05 mm. The degree of stenosis was expressed as percentage of cross-sectional area reduction. ISDN caused uniform dilatation of every normal epicardial artery; mean increase in diameter was 21 per cent (range: 17 to 26%). In 18 stenoses (28 to 95% obstruction) there was very little change after ISDN. The mean prestenotic diameter increased from 2.82 +/- 0.48 mm to 3.05 +/- 0.43 mm and the mean stenotic diameter from 1.45 +/- 0.49 mm to 1.59 +/- 0.51 mm. However, in the nine other stenoses (35 to 89% obstruction) the mean degree of obstruction decreased significantly from 68 +/- 15.6 per cent to 47 +/- 15.6 per cent after ISDN. This improvement was a result of a significant increase of the mean stenotic diameter from 1.71 +/- 0.47 mm to 2.41 +/- 0.55 mm, whereas the prestenotic diameter showed only an insignificant increase from 3.17 +/- 0.63 mm to 3.31 +/- 0.58 mm after ISDN. In four patients with two obstructions in different coronary branches ISDN dilated one without significantly affecting the other lesion. From the data we conclude that ISDN can dilate some coronary artery stenoses but that this response may vary from one site to another even in the same patient.

Coronary Disease↗
PubMed1980

Changing negative inotropic effect of acetylcholine in maturing canine cardiac muscle.

The effect of maturation on the contractile response to acetylcholine was studied in canine right atrial and right ventricular trabeculae. At any age the only inotropic response observed was negative. The decrease in contractile performance was always significantly greater in the atrial trabecula. Between 3 and 9 mo of age (12 dogs each group) there was a significant increase in the amount of negative inotropic action exerted by identical concentrations of acetylcholine. These data suggest that either the number of muscarinic receptors or the target cell response to acetylcholine increases during maturation.

Acetylcholine↗
PubMed1980

Analysis of sympathetic discharges during cardiogenic hypertensive chemoreflex.

Serotonin activates a cardiogenic hypertensive chemoreflex. During this reflex, sympathetic efferent neural discharges were examined in 10 anesthetized dogs. Thoracic nerves were identified, severed distally, and placed across electrodes. The efferent neurogram was recorded along with an electrocardiogram and blood pressure and stored on tape. Neurograms were later analyzed by a Lab 8/e computer with a Schmitt trigger. The resting tone and the elicited discharges of the multifiber preparations were plotted as poststimulus histograms. The integrals of the histograms were normalized. During the reflex, sympathetic efferent discharges averaged 4.9 (+/- 0.8) s in duration and the total discharge frequency was 199 (+/- 16)% of control tone. The evoked peak blood pressure response averaged 221/171 mmHg. Following autonomic blockade, the attenuated blood pressure response averaged 125/96 mmHg. The sympathetic efferent discharges then lasted 5.2 (+/- 0.7) s (NS). However, total discharge frequency (268 +/- 37% of control tone) was significantly greater (P less than 0.01) that before autonomic blockade. These data suggest that baroreceptors influence the rate of discharge and the total amount of neural traffic, but not the duration of the sympathetic response evoked by the cardiogenic hypertensive chemoreflex.

Animals↗
PubMed1980

Quantitative difference in "critical" stenosis between right and left coronary artery in man.

Coronary artery stenoses that limit blood flow below demand are considered critical. In this comparative study we investigated whether the same degree of stenosis in either the proximal third of the right coronary artery (RCA) or the proximal third of the left anterior descending artery (LAD) causes critical flow reduction. Lesions were quantified from 35-mm cinefilms in multiple projections using a vernier caliper. These morphometric measurements were correlated with various manifestations of critical flow reduction, such as angina pectoris, development of collateral vessels and segmental wall motion abnormalities. In 13 patients with anginal pain and isolated RCA stenosis, the mean degree of obstruction was 63% area stenosis, which was significantly lower (p < 0.05) than that measured in 17 symptomatic patients who had isolated obstructions of the LAD (77% area stenosis). In patients with an identical degree of obstruction (78%) in either the LAD or RCA, collateral vessels were angiographically demonstrable in 53% of the RCA stenoses but in only 29% of the LAD stenoses. Furthermore, when the stenoses were less than 63% in the RCA and LAD, regional wall motion abnormalities were more frequently (p < 0.05) associated with RCA than with LAD stenoses. These observations indicate that a significantly smaller percent area of stenosis is critical in the RCA than in the LAD.

Arterial Occlusive Diseases↗
PubMed1980

Selective effects of clonidine on the canine sinus node.

The direct and indirect chronotropic effects of clonidine (0.001--10 micrograms/ml) were studied by selective perfusion of the sinus node artery of 20 pentobarbital anesthetized dogs. Concentrations of 0.1, 1.0 and 10 migrograms/ml produced dose-related reductions in sinus rate of 3.7 +/- 0.9 (P less than .005), 6.9 +/- 1.8 (P less than .005) and 15.8 +/- 2.3 (P less than .0001) beats/min, respectivel. Sinus acceleration after right stellate ganglion stimulation at 16 and 32 Hz was significantly (P less than .05) inhibited by intranodal clonidine (0.1 microgram/ml). The positive chronotropic effect of norepinephrine (0.1 microgram/ml, sinus node artery) was not significantly affected by prior administration of clonidine. Atropine (1 mg/kg i.v. or 10 micrograms/ml, selectively perfused into the sinus node artery) had no effect on the sinus slowing produced by clonidine. Clonidine had an inconsistent effect on the response to vagal stimulation. Clonidine had an inconsistent effect on the response to vagal stimulation. Clonidine inhibits the heart rate increase after sympathetic nerve stimulation without affecting the heart rate response to norepinephrine infusion. The findings are consistent with previous observations that clonidine can inhibit norephinephrine release and demonstrate that this mechanism of action may occur within the sinus node.

Animals↗
PubMed1979

Experimental studies on the pathogenesis of asystole after verapamil in the dog.

The effect of verapamil on automaticity and conduction in the atrioventricular (A-V) junctional region was studied in anesthetized dogs. In five normal dogs verapamil, 10 microgram/ml, was selectively perfused into the A-V nodal artery and caused first degree heart block, which progressed to second degree heart block in three of the five. Higher concentrations of verapamil, 25 microgram/ml, caused complete heart block in three of five other dogs, but no episodes of asystole (defined as a ventricular pause of 10 or more seconds). In six other dogs after beta receptor blockade with propranolol, 20 microgram/ml, perfused into the A-V nodal artery, verapamil, 10 microgram/ml, regularly caused second degree heart block; in four of the six dogs there was a transient episode of third degree A-V block, and in two of these there was a period of asystole. In each of the 10 dogs pretreated with reserpine, verapamil, 10 microgram/ml, caused third degree A-V block; in seven of these there was a period of asystole with ventricular standstill up to 30 seconds. Concentrations of verapamil that do not produce high grade heart block in the normal heart thus readily cause both high grade block and prolonged ventricular standstill after elimination of adrenergic influences in the A-V junction.

Adrenergic beta-Antagonists↗
PubMed1979

Correlative electrophysiological and anatomical studies concerning the site of origin of escape rhythm during complete atrioventricular block in the dog.

Complete heart block was produced in eight dogs by the selective perfusion of physostigmine or neostigm into the atrioventricular (AV) node artery. A characteristic escape AV junctional rhythm emerged in each dog. After reversal of the cholinesterase paralysis with atropine, in each dog partial heart block was produced by an incision into the AV nodal region. In three of these eight dogs, a second incision placed slightly more anteriorly produced complete AV block which was followed by the emergence of an escape AV junctional rhythm similar to the one produced pharmacologically. Hearts of these three dogs were examined histologically with serial sections to determine the exact location of the incisions and their relationship to the AV node and His bundle. In each dog the incision that produced complete heart block passed directly through the junction of AV node with His bundle. In this region previous studies had demonstrated numerous P cells, which are thought to be the site of origin of normal cardiac automaticity. In each of the three hearts there were abundant P cells in continuity with the His bundle distal to the cut producing heart block. Significance of these findings is discussed relative to the locus of action of acetylcholine within the AV junction, the site of origin of AV junctional rhythm, and sme aspects of the experimental and therapeutic production of heart block.

Animals↗