bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reactive Hyperemia in Legs of Dogs:
Authors: BACHE ROBERT J. , EDERSTROM H. E. 
Published: June 2012

1. In normal dogs 5- and 10-minute occlusions of the femoral artery were followed by periods of reactive hyperemia (RH) whose duration closely approximated the length of occlusion. The resulting vasodilatation repaid about 50% of the blood flow debt, which was calculated from the flow rate measured just prior to occlusion.
2. When the animal's body temperature was lowered to 32°C, the duration and percentage blood flow debt repaid decreased to about one-half and one-third, respectively, of that found at 40°C. Observations of RH during rewarming revealed progressive increases in debt repayment and duration of the hyperemic period. The temperature characteristics of RH suggested that thermolabile factors were responsible for the vasodilatation that resulted from arterial occlusion.
3. Venous occlusion was followed by RH that was considerably reduced, resulting in a debt repayment of about one-fourth of that attained after arterial occlusion. The possibility that high transmural pressure might be a factor in reducing the intensity of RH that followed venous blockage was investigated. However, when a pressure equivalent to that in the carotid artery was maintained in the vasculature by pumping venous blood into the leg with its artery and vein clamped, the RH following restoration of blood flow closely resembled that induced by arterial clamping only. When arterial blood was infused, RH was reduced to the level seen after simple venous occlusion. It was concluded from these results that during venous occlusion some arterial blood entered the vascular bed, and brought with it chemical factors that reduced the degree of vasodilatation. Since total absence of arterial blood inflow was required to cause maximal dilatation, it may be that oxygen lack was involved in relaxation of the vascular wall, as has been implied by the work of investigators using other techniques.
Action of Lobeline on Pulmonary Artery Mechanoreceptors of the Cat
Authors: BEVAN JOHN A. , KINNISON GERALD L. 
Published: June 2012

1. The effects of lobeline (15 to 45 µg/kg) and of local changes of pulmonary artery pressure on the afferent activity of single neurone preparations of pulmonary artery mechanoreceptors have been studied in the intact cat. Pulmonary artery pressure was monitored via a double lumen balloon catheter passed into the pulmonary artery.
2. Pulmonary artery mechanoreceptors were distinguished from systemic mechanoreceptors by applying two simple tests to all mechanoreceptors found by random selection of single fibers from the right cervical vagus. The afferent activity of pulmonary mechanoreceptors closely followed induced changes of pulmonary artery pressure, whereas other arterial mechanoreceptors did not. Pulmonary artery pressure was increased by the rapid injection of 2 ml dextran into the right atrium and was reduced by inflation of the intravascular balloon.
3. In the absence of a rise in pulmonary artery pressure, lobeline increased the afferent activity in two phases. The early response, which was seen in 17 of the 18 fibers studied, occurred within one to two seconds after injection and was characteristically a variable and moderate response. This effect is caused probably by the diffusion of lobeline to sensory endings within the pulmonary artery wall. The delayed response occurred about eight to ten seconds later. The activity of afferent fibers was intensified conspicuously and frequencies up to 300/sec were recorded. It is probable that this is due to the action of lobeline carried by the vasa vasorum to the intramural receptors.
4. By combining the results following balloon inflation and dextran injection, the relationship between impulses per heart beat and mean pulmonary artery pressure was established for a number of pulmonary artery mechanoreceptors in the intact animal.
5. Pulmonary artery mechanoreceptors were insensitive to doses of veratridine and relatively insensitive to doses of phenyldiguanide which, in the intact cat, produce equivalent reflexogenic responses as lobeline (45 µg/kg).
6. Other intrathoracic sensory endings studied, including atrial and ventricular stretch receptors, Hering-Breuer receptors, and systemic mechanoreceptors, were completely insensitive to the doses of lobeline used in these experiments.
7. These results support earlier experiments which suggested that when lobeline is injected, its reflex effect from the pulmonary vascular bed, namely depression of ventilation, is due to its action on a pressure- or stretch-sensitive area in the region of the bifurcation of the pulmonary artery.
Renal Vein Renin and Juxtaglomerular Activity in Sodium-Depleted Subjects
Authors: AJZEN HORACIO , SIMMONS JOHN L. , WOODS JAMES W. 
Published: June 2012

Ten patients requiring surgery for renal cysts or calculi and having no evidence of secondary hyperaldosteronism were divided, as volunteers for special study, into experimental and control groups. After base line studies, the experimental group was given a diet containing 87 mEq of sodium and 1.0 g of chlorothiazide daily for ten days. Control subjects ate a normal diet. At operation, samples of peripheral and renal venous blood were obtained for measurement of renin activity and renal biopsy was taken for determination of the juxtaglomerular index.
Increased renin in renal venous plasma and hypergranularity of the juxtaglomerular apparatus were found in sodium-depleted subjects but not in control subjects. These findings confirm results previously found in animals.
Reflex Effects of Cephalic Hypoxia, Hypercapnia, and Ischemia Upon Ventricular Contractility
Authors: DEGEEST HILAIRE , LEVY MATTHEW N. , ZIESKE HARRISON , Nelson Geraldine , Rogoff Thomas 
Published: June 2012

The effects of brief periods of cephalic hypoxia, hypercapnia, and ischemia upon the contractility of the normally oxygenated ventricular myocardium were studied in an innervated, isovolumetric, canine left ventricle preparation. The majority of responses to cephalic hypoxia were of two types in preparations with vagi and carotid sinus nerves still intact. (a) More frequently, peak left ventricular pressure changed in biphasic fashion, consisting of an initial depression of contractility followed by subsequent augmentation. (b) Less frequently, a monophasic enhancement of contractility appeared. After transection of either the vagi or the carotid sinus nerves, a monophasic facilitation of contractility was usually evoked by cephalic hypoxia. From these data, it was concluded that two opposing influences act simultaneously upon the ventricular myocardium during cephalic hypoxia in preparations with intact vagi and carotid sinus nerves. Central nervous system hypoxia enhances myocardial contractility; its effect is mediated principally via sympathetic pathways. Hypoxia at the level of the carotid chemoreceptors depresses contractility reflexly; the efferent limb of this reflex is mediated chiefly via the vagi. At any moment in time, the effect upon ventricular contractility is the result of these opposing influences.
Cephalic hypercapnia produced effects similar to those of hypoxia. Cephalic ischemia always evoked a marked, positive inotropic effect upon the ventricles.
Optimal Parameters of Electrical Impulses for Defibrillation by Condenser Discharges
Authors: Peleška Bohumil , Blažek Z. , Rábl M. , Sládkovaá E. , Roth Z. 
Published: June 2012

The defibrillation threshold for various wave forms of condenser discharge, using capacitors from 4 to 200 µF, has been measured. Condenser discharge alone was used, or condenser discharge 0.25 henry (20 ohms) with an iron core series inductance, or condenser discharge, 0.29 henry (27 ohms) inductance, but without the iron core. Statistical analysis of the results showed that the last of these three circuits gave the lowest threshold voltage values. Optimal parameters of inductance-altered discharges are obtained with values of 24, 32, and 50 µF.
Detailed analysis of the separate physical parameters of the discharge show that optimal pulse duration is 8.5 to 16.6 msec. Further increase of duration does not decrease the voltage or current for threshold shocks, but merely increases the energy delivered. Pulse duration appears to be one of the more important parameters for successful defibrillation, and for this reason, a series inductance is also important.
Reactivity of the Vessels of Collapsed and Ventilated Lungs to Drugs and Hypoxia
Authors: Barer Gwenda R. 
Published: June 2012

1. In anaesthetised cats the left lung was collapsed by obstructing a ventilating tube which had been wedged into the left bronchus. If the cat had been ventilated with oxygen beforehand, the lung became gas-free in one to five minutes.
2. Blood flow to the left lung diminished rapidly as the lung collapsed and in about ten minutes was reduced by about 65%. Pulmonary vascular resistance increased greatly and these changes persisted after denervation of the lungs.
3. Vascular resistance of collapsed lungs could be reduced substantially by several drugs (acetylcholine, small doses of histamine, theophylline ethylenediamine, isopropylnoradrenaline, adrenaline) so that it must depend to some extent on increased vascular tone.
4. Vessels of collapsed lungs constricted when the oxygen saturation of the blood reaching them was reduced. This was demonstrated in vivo both before and after denervation of the lungs and after adrenalectomy and also in isolated perfused lungs. This effect is large enough to account for the changes in the pulmonary circulation which follow collapse of a lung. The time course and magnitude of the pulmonary vasoconstriction which took place during hypoxia were similar in collapsed and ventilated lungs.
5. The effects of a number of naturally occurring vasoconstrictor substances on the pulmonary circulation were compared with the effect of hypoxia. Noradrenaline caused weak but definite vasoconstriction of the pulmonary vessels, in a majority of cats; dopamine and tyramine had a more powerful constrictor effect and 5-hydroxytryptamine a much more powerful effect. Doses of histamine also usually caused pulmonary vasoconstriction.
6. Dibenamine and phenoxybenzamine reduced greatly or abolished the pulmonary vasoconstriction which accompanies hypoxia in collapsed or ventilated lungs. Guanethidine sometimes reduced or abolished it. Dibenamine and phenoxybenzamine reduced pulmonary vascular resistance. Pulmonary vasoconstriction during hypoxia was less frequently observed in cats treated with reserpine than in normal cats.
7. Lysergic acid diethylamide did not alter the pulmonary vasoconstrictor effect of hypoxia in doses which reversed the pulmonary vasoconstrictor action of 5-hydroxytryptamine. Mepyramine did not abolish (but may have sometimes diminished) the effect of hypoxia on the pulmonary vessels, in doses which reversed or abolished the pulmonary vasoconstrictor effect of histamine.
Pulsatile Flow Patterns in Distensible Tubes
Authors: Attinger E. O. , Sugawara H. , Navarro A. , Anné A. 
Published: June 2012

Pulsatile flow patterns in polyvinyl tubes were visualized by means of streaming birefringence and compared with those obtained using an electromagnetic flowmeter.
At low flow rates the frequency spectrum of the birefringence pattern is similar to that of volume flow. As the flow rates are progressively increased, irregular eddies appear, particularly during deceleration of flow, first in the central core and later spreading into the peripheral sleeve. They are characterized by a wide frequency spectrum.
The concepts of laminar and turbulent flow are reviewed and evidence is presented which indicates that the power losses associated with the observed eddies are negligible with respect to the losses due to the average flow and its pulsatile components of low frequency.
Flow disturbances observed in the arterial tree appear to be similar in character to those found in the present study. It is unlikely that they can account for significant discrepancies between experimental and theoretically predicted pressure-flow relations.
Failure of D- and L-Thyroxine to Protect Cholesterol and Oil Fed Cockerels Against Coronary Atherogenesis
Authors: Jain Savitri , Pick Ruth , Johnson Philip J. , Katz Louis N. 
Published: June 2012

In cockerels, L-thyroxine was significantly more active biologically than an equivalent dose of D-thyroxine, or even four times the dose, as demonstrated by the effects on body weights, organ weights and comb index.
In cockerels fed an atherogenic diet, the plasma cholesterol concentrations in all the thyroxine-treated groups were significantly lower than in the control groups.
No consistent effect of D-thyroxine on thoracic aorta atherosclerosis was observed. However, L-thyroxine had some protective action in the one experiment done.
Despite suppression of hypercholester-olemia, no protection against coronary atherosclerosis was seen with the administration of either L- or D-thyroxine. In fact, with an increase in dose of D-thyroxine to 4 mg, there developed actually an increase in the percentage of coronary vessels showing atherosclerosis.
These observations confirm once again the importance of avoiding reliance exclusively on blood cholesterol levels when judging the effects of hormones on atherogenesis.
Errors in the Processing of Dye Dilution Curves
Authors: Kelman G. Richard 
Published: June 2012

Errors of two kinds occur in the processing of dye dilution curves:
1) Individual estimates of the decay constant of a dye curve are subject to random errors causing a variability of up to 10% in the calculated cardiac output, and of up to 4% in the estimated vascular volume.
2) The use of an inappropriate numerical integration formula can cause an additional error of up to 5% in the calculated cardiac output. This may be avoided by using either the trapezoid rule or Simpson's rule. The planimeter measures areas with sufficient accuracy for routine determination of cardiac output.
Hemodynamic Effects of Dopamine in the Dog Before and After Alpha Adrenergic Blockade
Authors: MCNOY JOHN L. , GOLDBERG LEON I. 
Published: June 2012

Dopamine reacts with blood vessel receptors, causing both dilatation and constriction. In the dog the vasodilator receptors are presentin the renal and mesenteric vascular beds but absent from the vascular beds of the limb. The vasoconstrictor receptors, alpha adrenergic in type, are present in both somatic and visceral regions. The net effect of intravenously administered dopamine on regional flows will depend on the relative intensity of these opposing effects and on changes in blood pressure. The present study was an attempt to evaluate the significance of the vasoconstrictor action of dopamine infused at nonpressor doses, i.e., 3 to 6 µg/kg/min. Renal and femoral blood flows were measured simultaneously, and systemic hemodynamics were evaluated before and after administration of the alpha adrenergic antagonists, phentolamine and phenoxybenzamine.
The results indicate that the vasoconstrictor property of dopamine is masking a mild depressor effect, ranging in magnitude from 10 to 25 mm Hg. Dopamine increases cardiac output independently of its alpha adrenergic properties. Dopamine causes an increase in renal blood flow of equal magnitude before and after alpha adrenergic block but reduces renal vascular resistance to a lower level after alpha block, reflecting the depression in blood pressure. Dopamine does not alter femoral vascular resistance either before or after alpha adrenergic block. However, femoral blood flow is decreased by dopamine after alpha block, secondary to the depression of blood pressure. It is concluded that under the conditions of these studies, alpha adrenergic block enhances the vasodepressor property of dopamine and does not appreciably modify its ability to increase cardiac output and redistribute peripheral blood flow.
Reflex Vasoconstrictor and Vasodilator Responses in Man
Authors: ABBOUD FRANCOIS M. , ECKSTEIN JOHN W. 
Published: June 2012

The application of ice to the forehead and the Valsalva maneuver are known to cause reflex vasoconstriction by stimulation of adrenergic pathways of the sympathetic nervous system. In the experiments reported here, the effects of these stimuli on blood flow to the forearm of man were studied after intra-arterial injection of adrenergic blocking drugs. Changes in flow were measured with water plethysmographs applied to both forearms. One forearm served as "control," and the other forearm, into which the drugs were injected, was the "experimental" one.
The stimuli caused a consistent reduction of flow to the control forearm, but after the intra-arterial infusion of small doses of guanethidine there was increased flow to the experimental arm simultaneous with decreased flow to the control arm. The increased flow in response to the stimuli was accentuated after phentolamine and reduced after atropine.
The results indicate that the application of ice to the forehead and the Valsalva maneuver stimulate adrenergic vasoconstrictor pathways and cholinergic vasodilator pathways simultaneously. The vasoconstrictor response predominates, and the vasodilator effect is unmasked only after adrenergic blockade. It appears, therefore, that mental stresses are not the only stimuli which can cause reflex cholinergic vasodilatation in the forearm of man. Work by others would suggest that leg exercise may also cause cholinergic dilatation after adrenolytic agents. It is possible that cholinergic vasodilatation may play a role in the severe orthostatic fall in blood pressure, as well as in the exercise hypotension, observed in patients treated with guanethidine.
Increased Susceptibility of the Heart to Ventricular Fibrillation During Metabolic Acidosis
Authors: GERST PAUL H. , FLEMING WILLIAM H. , MALM JAMES R. 
Published: June 2012

Alterations of acid-base balance, clearly defined as metabolic or respiratory in origin, were produced in anesthetized dogs; ventricular fibrillation thresholds were determined during these conditions. During metabolic acidosis, we found that the heart became more susceptible to ventricular fibrillation, as indicated by a decrease in the ventricular fibrillation threshold value. During metabolic alkalosis, the threshold to ventricular fibrillation increased. In contrast, similar variations in pH owing to respiratory acidosis and alkalosis did not affect the ventricular fibrillation threshold. Hyperventilation in dogs with metabolic acidosis, even though resulting in alkaline arterial blood pH, did not protect the hearts from the increased susceptibility to ventricular fibrillation which existed as long as a base deficit was present.
These results indicate that the heart is more susceptible to ventricular fibrillation during acidosis caused by metabolic factors and that primary variations in carbon dioxide tension have no such effect. Our study on dogs, under controlled conditions, provides experimental evidence in support of clinical experience which suggests that metabolic acidosis predisposes the heart to ventricular fibrillation.
Wave Propagation in the Pulmonary Circulation
Authors: WIENER FRED , MORKIN EUGENE , SKALAK RICHARD , FISHMAN ALFRED P. 
Published: June 2012

A mathematical model of the entire pulmonary circulation of the dog, based on branching elastic tubes, is shown to yield a useful description of the propagation of pulmonary vascular pressure and flow waves. The pressure and flow pulses throughout the model are computed from the pressures measured at the arterial and venous ends of the system. Computed flow pulses at each end of the system agree with experimental findings.
Contour changes in the pressure and flow pulses are shown to be primarily due to dispersion and amplitude changes associated with reflected waves. Wave reflections are distributed throughout the model, and no specific site can be designated as the major source for reflections.
Blood pressure and flow computed from the model remain pulsatile in the microcirculation; pressure pulses are attenuated but flow pulses pass essentially unchanged through the microcirculation.
The computed results support the conclusion previously drawn from experimental evidence that pressure and flow pulses in the pulmonary veins originate primarily in the right ventricle and are propagated through the pulmonary capillary bed. A retrograde pulse, resulting from pressure fluctuations in the left atrium, is also present in both arteries and veins, but has only a secondary effect on the contours of pulmonary vascular pressures and flows.
Direct Positive Inotropic Effect of Acetylcholine on Myocardium
Authors: BUCCINO ROBERT A. , SONNENBLICK EDMUND H. , COOPER THEODORE , BRAUNWALD EUGENE 
Published: June 2012

The effects of acetylcholine and nicotine on isometric tension, in the presence and absence of atropine, hexamethonium, and endogenous norepinephrine stores, were examined in isolated cat atria and papillary muscles. Acetylcholine exerted a negative inotropic effect, competitively inhibited by atropine, in atrial and papillary muscle; in higher concentrations in papillary muscles, it produced a positive inotropic effect that was independent of cardiac norepinephrine stores and that was not blocked by atropine or hexamethonium. Nicotine, in addition to releasing norepinephrine, was found to exert, in higher concentrations, a direct positive inotropic effect, not antagonized by hexamethonium.
These data are compatible with the existence of two distinct cholinergic receptors in the myocardium: a muscarinic receptor intimately associated with vagal nerve endings; and a spatially separate receptor, whose stimulation produces responses similar to those produced by nicotine. This hypothesis allows for the reconciliation of much apparently contradictory data concerning acetylcholine and parasympathetic control of the heart; it accounts for the opposite inotropic effects of acetylcholine on atria (negative) and ventricles (positive) and for the opposite effects of vagal nerve stimulation (negative) and exogenous acetylcholine (positive) on ventricular myocardium.
Microelectrode Studies on Retrograde Concealment of Multiple Premature Ventricular Responses
Authors: MOORE E. NEIL 
Published: June 2012

Retrograde concealment of serially evoked premature ventricular responses was studied in an isolated preparation of rabbit atria and ventricles. Transmembrane potentials were recorded simultaneously from single cells within the atrioventricular (A-V) node and ventricular specialized conduction system, together with atrial and ventricular bipolar electrograms. In these experiments, retrograde conduction delays and block occurred within the ventricles, between ventricular muscle and the Purkinje-bundle branch system, between the bundle branch and His bundle, and within the A-V node.
The ventricular specialized conduction system was found to be a major location of retrograde conduction delays and block. Many examples of retrograde concealment and block, previously interpreted as due to A-V nodal mechanisms, almost certainly result instead from mechanisms operating within the ventricular specialized conduction system.
Antegrade and retrograde block of sequentially evoked premature responses occurred within the A-V node. Reentry "echo" responses occurred in many experiments following premature stimulation of the atria, the ventricles, or both.