bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiopulmonary Effects of Pulmonary Venous Hypertension with Special Reference to Pulmonary Lymphatic Flow
Authors: RABIN ERWIN R. , MEYER EDWARD C. 
Published: June 2012

Acute elevation of left atrial pressure could be precisely controlled at any desired level up to a mean of 60 mm. Hg in dogs with an intact thorax. The following observations were made in a series of 15 dogs. Right lymphatic duct flow did not increase at acutely elevated left atrial mean pressure below 25 mm. Hg, whereas flow increased 3- to 4-fold at mean pressure above 25 mm. Hg. The total amount of lymph at maximum flow, however, was only 0.3 ml./min. Lymph flow remained elevated for as long as 1 hour after left atrial pressure was restored to normal. Elevation of left atrial pressure did not affect lymph flow in the thoracic duct. Pulmonary edema did not occur readily at left atrial mean pressure elevated only slightly above plasma oncotic pressure. The production of pulmonary edema was observed only after a considerable elevation of left atrial pressure above plasma oncotic pressure was maintained for a period of one half hour or more in an otherwise normal dog. The hematocrit increased significantly after a 10-minute period of high left atrial pressure. Pulmonary vascular resistance decreased sharply as left atrial mean pressure was raised from 0 to 15 mm. Hg. The resistance gradually rose as left atrial pressure was raised to between 15 and 30 mm. Hg. Pulmonary arterial pressure uniformly rose and cardiac output uniformly declined with increasing left atrial pressure.
Chronic elevation of left atrial pressure was achieved in 15 dogs. Left atrial mean pressure varied from 10 to 23 mm. Hg. These dogs were followed up to 10 months and the following observations were made. Right lymphatic duct flow did not increase at chronically elevated left atrial mean pressure below 25 mm. Hg. Flow was not studied at higher pressures since we were unable to sustain left atrial mean pressure above 25 mm. Hg in any dog in our chronic group. The animals that were brought to left atrial mean pressure between 30 and 40 mm. Hg and in whom these high levels were presumably maintained were found dead in their cages with pulmonary edema 1 to 2 days after tightening the snare. Many of the usual functional and structural changes often found in lungs of patients with mitral stenosis, except for hemosiderosis, were not observed in our experimental animals although the extent of the supravalvular stenosis produced was marked. Pulmonary arterial pressure rose slightly and cardiac output declined slightly. No change was noted in pulmonary vascular resistance. Ascites and other signs of right sided failure were not encountered.
Relative Effect of Chronic Ischemia and a Myocardial Revascularization Procedure on the Ventricular Fibrillation Threshold
Authors: MACLEAN LLOYD D. , PHIBBS CLIFFORD M. 
Published: June 2012

Since ventricular fibrillation is the predominate cause of death following experimental coronary occlusion, measurement of the ventricular fibrillation threshold is recommended to assess the value of cardiac revascularization procedures. This determination is quantitative, precise and permits measurement under controlled circumstances. It was dissatisfaction with measurement of mortality rate following coronary occlusion in control and experimental animals (bioassay technic) that led to the adoption of the present more exact method.
Acute ligation of the anterior descending branch of the left coronary artery causes an immediate drop in the fibrillation threshold to one-fifth of normal. This is not changed if one releases the artery and retests the animal with occlusion 5 to 6 months later. Implantation of the internal mammary artery into the myocardium of the left ventricle creates a greater resistance to ventricular fibrillation after coronary occlusion. In animals in which the internal mammary artery remained patent, the fibrillation threshold remained after coronary occlusion at 85 per cent (mean) of control without coronary occlusion. This was highly significant. If the internal mammary artery was thrombosed, as demonstrated by vinyl plastic injection technics, the fibrillation threshold dropped markedly after coronary occlusion and did not vary significantly from the controls. When the anterior descending branch of the left coronary artery was permanently ligated in 1 group of dogs, the expected decline of fibrillation threshold occurred. When the survivals from this group were retested 5 to 6 months later, the fibrillation threshold had increased slightly (not statistically significant) but remained below 50 per cent of control without coronary occlusion and significantly different from the threshold of animals with patent internal mammary artery implants.
The results of this investigation suggest that a greater resistance to ventricular fibrillation associated with coronary occlusion can be achieved by operative means than by either mild or severe ischemia alone.
Influence of Cholesterol Feeding on Phospholipid Metabolism of Connective Tissue
Authors: McCANDLESS ESTHER L. , BAILEY ROBERT E. , ZILVERSMIT D. B. 
Published: June 2012

Subcutaneous injection of carrageenan, a sulfated polygalactose extracted from the red algae
Chondrus crispus
, stimulated the production of fibrous connective tissue in the rabbit. Animals fed cholesterol for 3 and 5 weeks had significantly higher phospholipid concentrations in this connective tissue than did control rabbits, but no alteration in phospholipid specific activity. These results are similar to those obtained in preliminary studies of connective tissue cultured by the sponge implantation technic.

Significant increases occurred in cephalin, lecithin, and sphingomyelin concentrations in tissue proliferated after cearrageenan injection. The cholesterol content of connective tissue was increased 7- to 8-fold.
Histologically, the tissue taken after 3 weeks of cholesterol feeding could not be distinguished from that of control animals. At 5 weeks, connective tissue from cholesterol-fed rabbits contained mature fat cells and macrophages resembling foam cells, in addition to the fibroblasts and collagen present in control tissue. Development of collagenous fibers and alterations in lipids were not found to be directly related. It is suggested that the elaboration of collagen and the accumulation of phospholipid, both of which occur in experimental atheromatosis, represent independent processes of connective tissue cells.
Ability of Serotonin and Norepinephrine to Mimic the Central Effects of Reserpine on Vasomotor Activity
Authors: McCUBBIN J. W. , KANEKO Y. , PAGE IRVINE H. 
Published: June 2012

Reserpine, serotonin, norepinephrine, 5-hydroxytryptophan and 3,4-dihydroxyphenylalanine had qualitatively the same cardiovascular effects when they were injected into a lateral ventricle or into the cisterna magna. All lowered arterial pressure, usually caused bradycardia despite prior section of the vagus nerves, and caused marked inhibition of the pressor response to occlusion of the common carotid arteries. Essentially the same results were obtained in unanesthetized as in anesthetized dogs. On a weight basis, norepinephrine was the more active amine tested and 5-hydroxytryptophan was more active than serotonin and 3,4 dihydroxyphenylalanine. Reserpine injected centrally had an effect equivalent to that of 20 or more times larger dosage given intravenously. All drugs were more active against the response to carotid occlusion than against the reflex pressor response to stimulation of a cut central end of a sciatic or vagus nerve. Decreased afferent electric activity of the carotid sinus nerve accompanied lowering of arterial pressure following central injection of small dosage, or intravenous injection of large dosage, of 5-hydroxytryptophan, indicating that the cardiovascular effects are not due to a direct action of 5-hydroxytryptophan on carotid sinus baroceptors.
Central injection of an amine oxidase inhibitor, beta-phenylisopropylhydrazine, markedly augmented and prolonged the cardiovascular effects of the amines and of reserpine as well.
These results are all consistent with, though they do not validate, the premise that the acute cardiovascular effects of reserpine are mediated centrally by serotonin and/or norepinephrine, either released from a bound and inactive to a free and active form, or formed by decarboxylation of their respective amino acids.
Effect of Various Adrenal Steroids on the Electrocardiogram of Adrenalectomized Dogs
Authors: DAVANZO JOHN P. , CROSSFIELD H. C. , SWINGLE W. W. 
Published: June 2012

The effects of large amounts of various adrenal steroids on the electrocardiogram of the adrenalectomized dog are described. The changes which occurred most frequently fell into 2 major groups: (1) those following excess of mineralo-corticoids, e.g., desoxycorticosterone and aldosterone, and (2) those appearing after gluco-corticoid administration. A characteristic type of diphasic T wave frequently followed treatment with hydrocortisone and its analogs, and its correction was hastened by substituting mineralo-corticoid therapy.
The 3 analogs of hydrocortisone (dexamethasone, prednisolone and triam$$$inolone) induce similar electrocardiographic patterns and after prolonged administration alter the P-Q interval in varying degrees, but more frequently produce a diphasic T. Dexamethasone preserves the normal pattern longer than the other steroids tested.
Interpretation of the Appearances of the Small Pulmonary Blood Vessels in Animals
Authors: BEST P. V. , HEATH D. 
Published: June 2012

A study was made of the histology of the small pulmonary blood vessels in uninflated postmortem specimens from the monkey, dog, fox, mouse, rat, rabbit, squirrel, sheep, pig, cow, seal, kitten, eivet, and guinea pig. The small pulmonary arteries appeared unusually muscular compared to those of man, and the increased medial thickness was reminiscent of the medial hypertrophy found as an early change in the human lung in diseases asso ciated with pulmonary arterial hypertension.
This suggests to us that the histological cri teria usually employed for grade 1 hyperten sive pulmonary vascular disease in man are invalid when applied to lung biopsies from animals used for experiments on the pulmo nary circulation. There is a sphincter-like arrangement of the muscle of the media of the muscular pulmonary arteries of the guinea pig. In the rat, mouse, and squirrel there is an extension of cardiac muscle along the larger intrapulmonary veins. Fibromuscu Ear prominences project into the vein lumen iii the cow and the pig.
Site of Action of Hypertonic Saline in the Pulmonary Circulation
Authors: ELIAKIM M. , STERN S. , NATHAN H. 
Published: June 2012

The effect of intravenous injections of 20 per cent saline on the pulmonary circulation was examined in 19 dogs. A marked rise of pulmonary arterial pressure was recorded in all cases. The pressure changes in the pulmonary veins depended largely on the choice of the vein for pressure measurements. A hypertensive response was usually recorded in the superior vein, while in the inferior vein no change or a slight fall in pressure was the rule. Left atrial pressure either did not change or fell.
A difference in the anatomical structure of the muscle sphincter around the superior and inferior pulmonary veins is described. A potent sphincter surrounds the superior veins and infiltrates within their walls some-times as far as the border of the lung. The sphincter around the inferior veins is rudimentary and inconspicuous.
Evidence is brought that hypertonic saline acts both on the pulmonary veins close to the left atrium and at the pulmonary arteriolar level.
Carotid Pulses and Peripheral Plethysmograms at Rest
Authors: DONTAS A. S. , SIMONSON ERNST 
Published: June 2012

In 75 healthy men and 47 men with previous coronary occlusion (mean age for both groups 60.0 years), the right carotid pulses and an impedance plethysmogram of the forehead were recorded. There were no significant differences between the major items of the carotid pulse in the two groups, but the absolute and relative peak times of the forehead plethysmograms of the coronary group were shorter than those of the normal group of the same age, and more similar to the pulse contours in healthy younger population.
The correlation between the carotid pulse and the forehead impedance plethysmograms was highly significant for most items in the healthy group, whereas in the coronary group only the ratio of initial anacrotic break height to maximal pulse height was significantly correlated in the two pulses.
The results suggest a compensatory reaction of peripheral circulation in patients with previous coronary occlusion, and the possible mechanism is discussed.
Observations on the Pathogenesis of Spontaneous Inherited Hypertension and Constricted Renal-Artery Hypertension in Rats
Authors: LAVERTY RICHARD , SMIRK F. HORACE 
Published: June 2012

A preparation is described in which blood is taken alternately from a pair of donor rats and perfused at constant rate through the same vascularly isolated, denervated recipient rat hind limb. The preparation, though sensitive to the vasoconstrictor agent released in acute renal hypertension, fails to detect any vasoconstrictor substance either in the blood of rats bred to develop hyper-tension spontaneously or in the blood of rats with chronic renal hypertension.
To study nervous tone in limb blood vessels, an innervated rat hind limb was perfused through a femoral artery with blood taken from the opposite femoral artery. After administration of hexamethonium, weight-corrected hind-limb perfusion pressures of spontaneous hypertensive (B), chronic renal hypertensive (CR), and control (C) rats (all series included) fall to the same average level. Hence, the component of the hind-limb peripheral resistance which is not neurogenically maintained must be of the same order of magnitude in all three groups. In B, CR, and C rats, the perfusion pressure falls after hexamethonium ; all have the same relationship to the height of the blood pressure at the time the perfusion pressure is measured, high blood pressures being associated with high perfusion pressures and low blood pressures with low perfusion pressures. Therefore, since the differences between the hind-limb peripheral resistances of B, CR, and C rats, as measured by the perfusion pressure, are removed by administration of hexamethonium, it follows that they depend upon differences in the neurogenically maintained component of the peripheral resistance. After hexamethonium the blood pressures of B and C rats fall to the same average level.
Peripheral Venous and Arteriolar Responses to Infusions of Angiotensin in Normal and Hypertensive Subjects
Authors: WOOD J. EDWIN 
Published: June 2012

The distensibility of the peripheral veins of the hypertensive subject is normal, that is, there is no evidence of peripheral venoconstriction, despite the excessive arteriolar constriction. The forearm veins of hypertensive patients respond to pooling of blood in the upright position to a lesser degree than do veins of normotensive individuals, indicating a lesser degree of smypathetic nervous activity in response to this stimulus. The peripheral veins of hypertensive subjects constrict normally in response to an infusion of norepinephrine, indicating that failure of venoconstriction in any circumstance cannot be attributed to failure of the smooth muscle of the veins.
Infusions of angiotensin produce constriction of the veins as well as the arterioles in normotensive individuals thus failing to mimic the naturally occurring state of essential hypertension. Infusions of angiotensin in hypertensive patients result in further arteriolar constriction and hypertension without concomitant venoconstriction. The results of these experiments suggest that peripheral venous responses of hypertensive subjects to angiotensin infusions may have been modified by previous exposure of these vessels to a material at least similar to angiotensin.
A Method for Electrocardiogram Wave-Pattern Estimation
Authors: CADY LEE D. , WOODBURY MAX A. , TICK LEO J. , GERTLER MENARD M. 
Published: June 2012

Canine antisera to rabbit and hog renin were coupled to several fluorescein dyes. The antiserum was immunologically adsorbed once each with rabbit-liver and with bone-marrow powder, thereby removing excess dye and eliminating nonspecific staining. Mounted frozen-dried sections of kidneys from sodium- deficient rabbits (in which hyperplasia and hypergranulation of juxtaglomerular [JG] cells were present), from control rabbits, from a sodium-deficient dog, and from sodium-deficient rats were treated with the adsorbed labeled antiserum. Ultraviolet microscopy (direct technique) revealed an intense yel low-green fluorescence sharply limited to the granules of the juxtagloinerular cells in all sections studied from kidneys of rabbit and dog. JG granules in rats did not fluoresce, an observation in accord with the species spe cificity of renin.
The indirect ("sandwich") method was also employed (with adsorbed, labeled, rabbit antiserum to canine globulin), and although slight staining of gloinerular epithelium resulted, that in the JG granules was far more intense. In our hands, the faint glornerular staining was not blocked by prior treatment with unlabeled renin. Staining of JG granules in any kidney paralleled the intensity of JG granulation by light microscopy and the amount of extractable renin in the same kidney. JG-granule staining (direct and indirect techniques) was blocked by neutralization of the antirenin with renin. Heterogenous anti sera (to insulin; to human gamma globulin) failed to stain. Other rabbit tissues (heart, lung, liver) similarly treated with labeled antirenin never stained.
If this work can be repeated with immunologically pure renin, the evidence presented here, together with previously published studies from this and other laboratories, will establish beyond any reasonable doubt that the source of renin in the kidney is the juxtaglomerular cell, as postulated first by Goormagh tigh nearly a quarter of a century ago.
Role of Intrarenal Venous Pressure in the Regulation of Renal Vascular Resistance
Authors: HINSHAW LERNER B. , WORTHEN DAVID M. 
Published: June 2012

A series of eighteen experiments have been carried out on the heart-lung perfused dog kidney, and the results have defined the role of the intrarenal veins in the autoregulation phenomenon. It was found that there are a variety of intrarenal venous pressures which differ greatly according to (a) anatomical location and (b) the prevailing renal-artery pressure.
Findings have pointed out the importance of correct techniques in establishing the changes occurring in the intrarenal venous segment in response to an increase in renal artery pressure.
An increase in ureteral pressure results in a significant decrease in renal blood flow and an increase in overall renal vascular resistance, which further supports the role of extra-vascular pressure increases in renal-flow regulation.
The findings of the present study corroborate previous reports from this laboratory indicating that autoregulation is primarily accounted for on the basis of changes in renal extravascular pressure. Evidence has been provided for the absence of the "myogenie reflex" as a causal factor in autoregulation.
Action of Ryanodine on Mammalian Cardiac Muscle
Authors: AMORIM DALMO DES. , MARSHALL HIRAM W. , DONALD DAVID E. , WOOD EARL H. 
Published: June 2012

Systemic and pulmonary blood flows and pressures were determined in anesthetized closed-chest dogs with chronic atrial septal defects and in dogs with intact cardiac septa. In the former animals, graded obstruction of the main pulmonary artery associated with right ventricular systolic pressures of more than 80 mm. Hg was produced without evidence of failure of the right side of the heart. A considerable decrease in the magnitude of the left-to-right shunts and an increase in the size of the right-to-left shunts occurred; these changes were associated with only minor changes in filling pressure of the right ventricle, and systematic changes in systemic arterial pressure did not appear. Analysis of right atrial pressure pulses suggested the development of an increased force of contraction of the right atrium and no evidence of tricuspid regurgitation under these circumstances.
In contrast, partial obstruction of the main pulmonary artery in the dogs with intact cardiac septa, so as to increase the right ventricular systolic pressure to more than 60 mm. ITg, was associated with pronounced increases in mean right atrial pressure and striking decreases in cardiac output and systemic arterial pressure. The pressure recordings from the right atrium and indicator-dilution curves demonstrated the development of significant tricuspid regurgitation.
The deterioration of right ventricular function in dogs with intact cardiac septa appears to be related to overdistention of the right ventricle and possibly also to a disproportionate reduction in coronary blood flow to the myocardium caused by a decrease in systemic arterial pressure and the concomitant increase in resistance to coronary venous drainage from the right side of the heart due to the increased right atrial and right ventricular pressures.
It is concluded that under the conditions of these studies, an atrial septal defect provides a considerable increase in resistance to the heinodynamic effects associated with right ventricular hypertension caused by acute partial obstruction of the main pulmonary artery. The possible duration of this beneficial effect beyond the 33 to 160 minutes of observation in these studies has not been explored.
Failure mode and effects analysis outputs: are they valid?
Authors: Shebl Nada Atef , Franklin Bryony Dean , Barber Nick 
Published: June 2012

Abstract

Background
Failure Mode and Effects Analysis (FMEA) is a prospective risk assessment tool that has been widely used within the aerospace and automotive industries and has been utilised within healthcare since the early 1990s. The aim of this study was to explore the validity of FMEA outputs within a hospital setting in the United Kingdom.

Methods
Two multidisciplinary teams each conducted an FMEA for the use of vancomycin and gentamicin. Four different validity tests were conducted:
· Face validity: by comparing the FMEA participants’ mapped processes with observational work.
· Content validity: by presenting the FMEA findings to other healthcare professionals.
· Criterion validity: by comparing the FMEA findings with data reported on the trust’s incident report database.
· Construct validity: by exploring the relevant mathematical theories involved in calculating the FMEA risk priority number.

Results
Face validity was positive as the researcher documented the same processes of care as mapped by the FMEA participants. However, other healthcare professionals identified potential failures missed by the FMEA teams. Furthermore, the FMEA groups failed to include failures related to omitted doses; yet these were the failures most commonly reported in the trust’s incident database. Calculating the RPN by multiplying severity, probability and detectability scores was deemed invalid because it is based on calculations that breach the mathematical properties of the scales used.

Conclusion
There are significant methodological challenges in validating FMEA. It is a useful tool to aid multidisciplinary groups in mapping and understanding a process of care; however, the results of our study cast doubt on its validity. FMEA teams are likely to need different sources of information, besides their personal experience and knowledge, to identify potential failures. As for FMEA’s methodology for scoring failures, there were discrepancies between the teams’ estimates and similar incidents reported on the trust’s incident database. Furthermore, the concept of multiplying ordinal scales to prioritise failures is mathematically flawed. Until FMEA’s validity is further explored, healthcare organisations should not solely depend on their FMEA results to prioritise patient safety issues.