bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reducing Heart Rate of the Dog by Electrical Stimulation
Authors: LOPEZ JOSE F. , EDELIST ARYEH , KATZ LOUIS N. , Boyd Eugene 
Published: June 2012

1) The frequency of effective ventricular contractions could be reduced by almost 50% in dogs by stimulating the ventricles (or atria) with electrical impulses of long duration (2 volts, 200 to 350 msec).
2) A similar result was obtained when pairs of impulses (2 volts), each 3 msec in duration, were used, with the time interval between the two impulses of the pair similar to that between the make and break of the long impulses (noted above).
3) The dogs were under general anesthesia and positive pressure breathing was maintained. After thoracotomy, platinum electrodes were implanted in the epicardial surface of the right ventricle or atrium. Pressures were measured in all heart chambers and the unipolar electrocardiogram was recorded from the right atrium with a catheter electrode. Several frequencies of stimulation, below the inherent sinus rate, were tested and at each frequency the time interval between pairs of stimuli was progressively increased from 100 to 350 msec.

4) In all dogs reduction of the frequency of the effective ventricular contractions could be obtained with pairs of stimuli 200 and 350 msec apart. Only the make of the long impulse or the first of the pair of short impulses produced an
effective
ventricular contraction, while the break of the long impulse or the second short impulse stimulated the ventricles so early in the cycle that no effective mechanical contraction followed. However, the refractory period produced by the break prevented the sinus impulse from reaching the ventricles. The several mechanisms involved are discussed.

5) In one dog the reduction of the frequency of the effective ventricular contractions could be maintained during the 24 hours of survival.
6) The method was applied to a patient being treated for Stokes-Adams attacks. Right atrial stimulation produced a noticeable reduction in ventricular frequency. This involved a reduction in the frequency of electrical responses of the ventricles as well, ensuring a reduction of the per minute energy cost and oxygen consumption of the heart. Such a reduction of the frequency of electrical responses of the ventricles could not be accomplished, so far, in the dog by atrial stimulation.
7) Reduction of the frequency of effective ventricular responses was obtained in one dog with induced atrial flutter and in another with a pacemaker induced "parasystolic" ventricular tachycardia by employing an artificial ventricular pacemaker similar to that used with sinus rhythm.
8) The significance of the findings is discussed. This experimental approach suggests a possible method of slowing the heart rate in clinical cases of ventricular or atrial tachycardia refractory to other methods of treatment.
9) Finally, this approach offers a means of studying certain properties of the heart in the dog which may give insight into the mechanisms involved in some of the more complex arrhythmias encountered in man.
Coronary Inflow and Oxygen Usage Following Cardiac Sympathetic Nerve Stimulation in Unanesthetized Dogs
Authors: GRANATA LINO , OLSSON RAY A. , HUVOS ANDREW , GREGG DONALD E. 
Published: June 2012

The effects of cardiac sympathetic nerve stimulation on coronary inflow were studied in previously operated conscious dogs, using electromagnetic flowmeters. Stimulation caused an increase of coronary inflow which was due mainly to an augmentation of flow during diastole. In systole, inflow changes were smaller and variable according to the strength of stimulation. The data presented indicate that an arteriolar dilatation may play a role in augmenting coronary inflow.
In several instances, the increase of coronary inflow was preceded by a phase of reduction which suggested the possibility of coronary vasoconstriction as a primary direct effect of cardiac sympathetic activation.
Transfer of Carbon Monoxide and Nitrous Oxide in the Artificially Perfused Sheep Placenta
Authors: METCALFE JAMES , MOLL WALDEMAR , BARTELS HEINZ , HILPERT PETER , PARER JULIAN T. 
Published: June 2012

1. The sheep placenta was perfused in situ through the umbilical circulation with a dextran solution containing carbon monoxide and nitrous oxide.
2. The concentration of carbon monoxide in the perfusion fluid after passage through the umbilical circulation was found to be 19±3% of its concentration in the entering perfusion fluid. This represents "shunted umbilical flow," the percentage of the perfusion fluid (and presumably of the fetal blood) which does not exchange substances with the maternal blood.
3. The concentration of nitrous oxide in the perfusion fluid after passing the placental membrane and before admixture of shunted perfusion fluid was found to be 14±4% of its original concentration in the perfusion fluid when the maternal arterial concentration was zero. This leads us to the conclusion that the perfusion fluid did not at any time reach the maternal arterial concentration and that no functionally effective countercurrent flow pattern exists in the sheep placenta.

4. Reversal of the flow direction in the fetal umbilical vessels resulted in a slight increase of the N
2
O concentration in the perfusion fluid after passing the placental membrane and before admixture of the shunted perfusion fluid.

5. We suggest that the placenta contains a mixture of countercurrent and concurrent flow units. Diffusion of gases along the capillaries within the comparatively thick placental membrane of the sheep is also presented as a possibility.
Oxygen Consumption of Arterioles and Venules as Studied in the Cartesian Diver
Authors: HOWARD RUFUS O. , RICHARDSON DAVID W. , SMITH MORRIS H. , PATTERSON JOHN L. 
Published: June 2012

1. The Cartesian diver microrespirometer has been applied to the measurement of oxygen consumption by mesenteric arterioles and venules from hamsters and human beings. Oxygen consumption by the smallest arterial vessels, less than 150 µ in diameter, averaged 1.05 µliter/mg/hr, in contrast to only 0.58 µliter/mg/hr for arteries 250 to 400 µ in diameter. Hamster venules consumed oxygen at an average rate of 0.53 µliter/mg/hr, nearly equal to the largest arteries studied. Venous oxygen consumption did not vary with vessel diameter.

2. Both arterioles and venules were highly resistant to hypoxia, maintaining normal rates of oxygen uptake at environmental oxygen tensions as low as 12 mm Hg, but not at 5 or 2 mm Hg. Veins consumed less oxygen at an environmental
p
O
2
of 150 mm Hg than at 57, 28, or 12 mm Hg, whereas arterial
Q

O

O
2

was unchanged between 12 and 150 mm Hg.

3. Ten human mesenteric arteries, 65 to 175 µ in diameter, and 10 human veins, 130 to 450 µ in vitro, had average rates of oxygen consumption of 0.35 and 0.25 µliter/mg/hr, significantly lower than hamster vessels.
4. Vessels from hamsters sacrificed without anesthesia consumed oxygen at rates similar to arterioles and venules removed from animals under pentobarbital anesthesia.
Hemodynamic Effects of Hyperbaric Oxygenation in Experimental Acute Myocardial Infarction
Authors: KUHN LESLIE A. , KLINE HOWARD J. , WANG MICHAEL , YAMAKI TAKASHI , JACOBSON JULIUS H. 
Published: June 2012

The hemodynamic effects of hyperbaric oxygenation were investigated in anesthetized dogs with acute myocardial embolism and infarction produced by injecting plastic spheres 325 micra in diameter. In 50 "control" animals with acute myocardial infarction induced while breathing either air at one atmosphere, 100% oxygen at one atmosphere or 7% oxygen at three atmospheres, 24-hour mortality was 85 to 90%. In 23 animals that received the same dose of microspheres and breathed 95 to 100% oxygen at three atmospheres for two hours following embolization, there was significantly less 24-hour mortality (30%), less ventricular fibrillation, and less advanced atrioventricular block. Hyperbaric oxygenation afforded protection against immediate mortality from ventricular fibrillation and also against later death, in shock, occurring within 24 hours of coronary embolization but after the immediate postembolization period had passed. In the animals exposed to hyperbaric oxygenation, declines of cardiac output and of central aortic pressure occurring 60 and 90 minutes after coronary embolization were significantly less than in the other animals.
In normal animals, hyperbaric oxygenation reduced cardiac output moderately, increased systemic vascular resistance, and elevated aortic pressure slightly.
The anatomic extent of the infarction did not differ detectably between the "control" animals and those treated with hyperbaric oxygenation.
It is concluded that hyperbaric oxygenation provides protection against mortality in the early period after coronary embolization by preventing ventricular fibrillation. In addition, prevention of major declines in aortic pressure and cardiac output during the later postembolization period in the group with hyperbaric oxygenation was associated with diminished rates of late mortality.
Some Characteristics of Ventricular Echoes
Authors: MENDEZ CARLOS , HAN JAOK , DE JALON P. D. , MOE G. K. 
Published: June 2012

Reciprocal responses (ventricular "echoes") were initiated by premature stimuli applied directly to the bundle of His in dog hearts perfused from donor animals. The time relations of the responses in the His bundle and at the atrial margin of the exposed A-V node were studied under a number of conditions. It was found that:
1. The earliest premature response that can be induced in the His bundle is not propagated back to the atrium and does not lead to an echo.

2. There is, in most hearts, a continuous range of H
1
H
2
intervals (the echo "zone") within which reciprocal responses of the His bundle occur.

3. The earliest effective H
2
propagates slowly to the atrium, and the echo returns quickly.

4. The latest effective H
2
responses propagate more quickly to the atria, but return more slowly.

5. The atrium is an essential link in the echo pathway; i.e., the H
2
response must reach and activate the atrium before a return is possible.

6. Direct stimulation of the atrium in advance of the expected arrival of the A
2
response propagated from the His bundle can initiate a response which propagates
to
the bundle; i.e., two responses can travel in opposite directions on a collision course, yet one of them can complete its journey.

7. The limiting parameter of the return pathway is the refractory period of that portion of the lower node which must fire twice in the echo circuit.
8. The limiting element is not the bundle of His.

9. The limiting element can be discharged by early H
2
responses which fail to reach the atrium.

10. The refractory period of the limiting element is a function of the preceding cycle length.

It was also demonstrated that the echo "zone" is shifted to a range of longer H
1
H
2
intervals when the basic driving frequency is increased, or when the vagi are stimulated. Epinephrine shifts the echo zone to a range of briefer H
1
H
2
intervals.

It is suggested that echo responses occur when a retrograde impulse is arrested at one site within the node and continues to propagate to the atrium through collateral pathways. If the retrograde propagation time is long enough to permit the recovery of the lower elements of the node, an echo response reaches the His bundle. It was concluded that a self-sustained repetitive circuit may be possible when the round-trip conduction time exceeds the refractory period of the limiting tissue in the node.
Metabolism of Atherosclerotic Tissue of Rabbit and Dog, with Special Reference to Esterase and Lipase
Authors: MAIER NELICIA , HAIMOVICI HENRY 
Published: June 2012

Esterase and lipase were studied in the aorta, liver, and serum of dogs and rabbits on an atherogenic diet. With the exception of dog serum, lipase was not present in any of the tissues studied.
At a relatively early stage the atherosclerotic intima-media layer, separated at the cleavage plane, showed increased esterase activity in both animals. At later stages, a reverse trend was noted in the rabbit, whereas in the dog, the esterase activity remained markedly increased. No pre-atherosclerotic enzymatic changes were noted.
The liver of both species showed increased esterase activity first and reversal to normal values later. In contrast, rabbit serum displayed no change for several months and decreased activity subsequently whereas in the dog, decreased esterase activity was noted throughout the administration of the atherogenic diet. Lipase activity in dog serum, which was unaffected for several months, decreased later.
Our results expand previous findings with other arterial enzymes and indicate further that metabolic alterations of the arterial wall are associated with the development of atherosclerosis.
In Vitro Demonstration of Vascular Hyper-responsiveness in Experimental Hypertension
Authors: HINKE JOSEPH A. M. , Simpson Patricia A. 
Published: June 2012

The ventral caudal artery from DCA hypertensive and control rats was excised, mounted in a plastic chamber, and perfused with Krebs-Henseleit solution. Diameter of the artery and flow through the artery were measured at perfusion pressures ranging from 0 to 150 mm Hg. During these perfusions, constriction of the arterial segment was produced by adding norepinephrine, vasopressin, angiotensin II or rat serum in concentrations known to produce submaximal contractions.
Samples of each experimental artery before and after artificial perfusion were fixed, sectioned, and stained. The tunica media of hypertensive arteries was thickened. Also, degenerative changes were observed in the internal elastic lamina and adjacent tunica media. Structural thickening of the tunica media was due primarily to expansion of the extracellular space and also due possibly to muscle fibre hypertrophy.
In the absence of contraction, flow through the hypertensive artery was moderately reduced at all pressures because its lumen was narrowed by the thickened wall.
Total wall tension, muscle tension, and elastic tension of the artery were estimated from the pressure-flow-radius data. Strength of muscular contraction was then measured in terms of work performed during contraction at a constant pressure. From this analysis, the muscle fibres in hypertensive arteries were found to be unequivocally hyper-responsive to norepinephrine, vasopressin, and rat serum. The possible cause of this hyper-responsive property is discussed.

Serum was collected both from normotensive and from hypertensive donor rats and its pressor activity tested on the
in vitro
preparation. The pressor activity in hypertensive serum was found to be significantly elevated.

The elasticity of the hypertensive artery was increased in the absence of contraction and unchanged during contraction. No hypertensive artery was found to be stiffer than normotensive arteries. These changes are probably related to degeneration of elastin.
Factors Controlling Pacemaker Action in Cells of the Sinoatrial Node
Authors: LU HSIN-HSIANG , LANGE GERTRUDE , McC. BROOKS CHANDLER 
Published: June 2012

Rapid drive of isolated pacemaker tissues from cats resulted in a post-drive depression followed by a late acceleration to supernormal rates of pacemaker activity. These effects were similar to those occurring after drive of the pacemaker
in situ
. Lower SA nodal pacemakers discharged more slowly and irregularly than did upper SA nodal pacemaker cells. They were more readily depressed by rapid imposed drive. The balance between depression and acceleration varied in different preparations. Drive at only slightly above the intrinsic rate resulted frequently in acceleration not preceded by depression. Within limits, the greater the frequency and duration of drive, the greater the intensity and duration of both the depression and the late acceleration.

Prostigmin augmented and atropine reduced post-drive depression. Cocaine potentiated the late acceleration. Excess potassium reduced post-drive depression and, in concentrations used, caused some acceleration.
Pacemaker cells could be driven less rapidly than could other SA nodal cells. Drive generally shifted pacemaker action to a distant site; the first post-drive propagated responses originated from other pacemaker cells and dominance by the original unit was reestablished slowly. Rapid drive reduced amplitudes of action potentials and prepotentials. It also raised threshold potentials and during the post-drive period the durations of pacemaker cell action potentials were temporarily prolonged. In some preparations membrane potentials remained at a subnormal value after drive. Subthreshold potentials occurred at a somewhat subnormal rhythm but gradually developed an effective amplitude.
Conduction block was observed in isolated SA nodal tissue. This was augmented during the post-drive period of depression.

This work lends support to the hypothesis
1
that dominating action by pacemaker cells influences the pacemaker activity in other potential pacemaker tissues.
Fibrinolytic Activity in Thrombosed Veins
Authors: KWAAN HAU C. , ASTRUP TAGE 
Published: June 2012

Thrombosis of the femoral vein in rats was produced by the injection of thrombin, serum, or sodium morrhuate into ligated venous segments. The histologic effects were followed during resolution or organization of the thrombus and were correlated with the appearance and localization of fibrinolytic activity as assayed histochemically.
Lysis of the venous thrombus began immediately when thrombin or serum had been used. Sites of thrombolysis were related to the presence of endothelial cells of venous origin and containing plasminogen activator. Sodium morrhuate destroyed the fibrinolytically active endothelial cells thus delaying thrombolysis. Recanalization was associated with the presence locally of active endothelial cells, originating presumably in the adjacent normal venous endothelium.
These results support previous observations on the vascular origin of the plasminogen activator. They elucidate the role played by the fibrinolytically active endothelium in the resolution of venous thrombi. They also confirm and extend previous observations on the role of fibrinolytic activity in tissue repair.
Left Ventricular Performance During By-Pass or Distension of the Right Ventricle
Authors: MOULOPOULOS SPYRIDON D. , SARCAS ARIS , STAMATELOPOULOS STAMATOS , AREALIS EVANGELOS 
Published: June 2012

A dog heart preparation was used to investigate the direct or mechanical effects of a right ventricular by-pass and of right ventricular distension on the performance of the left ventricle. Several other factors known to affect left ventricular performance were eliminated.
The data obtained indicate impairment of left ventricular function either by right ventricular by-pass or by right ventricular distension. It is suggested that this impairment may be due to a direct effect of the volume of blood contained in the right ventricle and of right ventricular function on the common muscle bundles that encircle both ventricles.
Pressure-Volume Correlates of Left Ventricular Oxygen Consumption in the Hypervolemic Dog
Authors: ROLETT ELLIS L. , YURCHAK PETER M. , HOOD WILLIAM B. , GORLIN RICHARD 
Published: June 2012

Volume changes in the intact functioning canine left ventricle were induced by whole blood infusion and were measured by the thermodilution technic. Multiple regression analyses were performed to detect significant correlations between hemodynamic variables and left ventricular oxygen consumption. Hemodynamic variables, in addition to the pressure-time integral, ventricular volume, and ventricular work, included estimates of myocardial stress, force, and shortening. The most significant individual correlates of oxygen consumption were the pressure-time integral (
r
=0.91) and ventricular end systolic volume (
r
=0.81), whereas the interaction of volume with pressure-time, thus approximating wall stress and force, was the most significant variable overall (r=0.93). A number of multiple linear regression models were tested for the prediction of ventricular oxygen consumption. The equation (model E) with the greatest multiple regression coefficient (R=0.947) included heart rate, pressure-time per beat, pressure-time per minute, end systolic volume, and (end systolic volume)
2/3
as independent variables. A less elaborate regression equation including only pressure-time per minute and end systolic volume as independent variables was, however, nearly as accurate as model E in the prediction of oxygen consumption. The addition of estimates of left ventricular work and shortening to these regression models did not further improve the ability to predict oxygen consumption accurately.

The relationships between these hemodynamic variables and ventricular oxygen consumption were not altered by pericardiotomy or catecholamine depletion. In the hypervolumic heart acute ventricular dilatation did not occur following pericardiotomy.
The results of this study confirm the postulate that an increase in ventricular volume, as well as pressure, will be accompanied by an increase in ventricular oxygen consumption. This in turn implies a relationship between the wall stress or force generated by the myocardium and the energy requirement of contraction.
Ventricular Conduction and Refractoriness During Hypothermia
Authors: Torres Joseph C. , Warschaw Rachelle , Chase Patricia 
Published: June 2012

The effect of hypothermia on ventricular conduction was determined with a multi-terminal electrode sutured to the epicardial surface. Measurements of conduction intervals revealed average increases of 95% at 22°C in 13 dogs and 148% at 20°C in seven dogs that survived to this temperature. The mean conduction velocity estimated at 0.55 m/sec at 37°C diminished to 0.29 m/sec and 0.19 m/sec respectively at 22° and 20°C. An apparent overall exponential relationship between conduction velocity and temperature was observed, although below 30°C the rate of conduction decreased almost linearly with a Q
10
, of 1.6 to 1.8.

Individual measurements along both rows of intersecting electrode terminals revealed slightly different rates of conduction. However, within the entire group the direction of relatively faster conduction was inconsistent and, furthermore, the changes of conduction velocity with hypothermia were practically identical for the two recording alignments in all instances.
During cooling to 22°C the absolute and the relative phases of ventricular refractoriness both increased by more than 200% of the control values observed at 37°C. This threefold effect on recovery of excitability was in contrast to the twofold slowing of conduction at the same temperature.
It is concluded that the occurrence of ventricular fibrillation during hypothermia cannot be explained adequately by assuming a greater slowing of conduction relative to prolongation of refractoriness.