bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abnormal atrial natriuretic peptide and renal responses to saline infusion in nonmodulating essential hypertensive patients.
Authors: Ferri C , Bellini C , Coassin S , Baldoncini R , Luparini R L , Perrone A , Santucci A 
Published: June 2012

BACKGROUND
Nonmodulation seems to represent an inheritable trait characterized by abnormal angiotensin-mediated control of aldosterone release and renal blood supply and salt-sensitive hypertension. Recently, we demonstrated that atrial natriuretic peptide (ANP) response to angiotensin II also is altered in nonmodulators. Moreover, an abnormal ANP response to acute volume expansion has been shown by others in hypertensive patients displaying some features of nonmodulators. These data induced us to hypothesize that nonmodulators. These data induced us to hypothesize that nonmodulation could be characterized by an abnormal ANP response to saline load.

METHODS AND RESULTS
Forty-three essential hypertensive men were subdivided into low-renin patients (n = 12), nonmodulators (n = 15), and modulators (n = 16) according to their renin profile and ability to modulate aldosterone and p-aminohippurate clearance responses to a graded angiotensin II infusion (1.0 ng.kg-1.min-1 and 3.0 ng.kg-1.min-1 for 30 minutes each) on both a low- (10 mmol Na+ per day) and a high- (210 mmol Na+ per day) Na+ intake. The intravenous saline load (0.25 mL.kg-1.min-1 for 2 hours) performed on a low-Na+ diet increased plasma ANP levels in low-renin (from 14.30 +/- 4.68 to 23.30 +/- 7.52 fmol/mL at 120 minutes, P < .05) and modulating patients (from 10.95 +/- 3.55 to 18.21 +/- 5.42 fmol/mL at 120 minutes, P < .05), whereas it did not change the hormone levels in nonmodulators (from 10.77 +/- 3.25 to 13.83 +/- 5.70 fmol/mL at 120 minutes, P = NS). When patients switched from a low- to a high-NaCl diet, plasma ANP levels increased significantly in all groups. However, when the saline load was repeated on a high-NaCl intake, ANP levels increased in both low-renin and modulating patients (P < .05), whereas it failed to increase in nonmodulators.

CONCLUSIONS
Nonmodulating hypertensive patients showed a reduced ANP response to saline infusion in the presence of a normal increase of plasma ANP with dietary NaCl load. The impaired ANP response to saline infusion could be due to a different distribution of volume load and contribute to determining the reduced ability to excrete sodium that is commonly described in nonmodulators.
HDL cholesterol and mortality in Finnish men with special reference to alcohol intake.
Authors: Paunio M , Heinonen O P , Virtamo J , Klag M J , Manninen V , Albanes D , Comstock G W 
Published: June 2012

BACKGROUND
There is substantial evidence that a low serum level of HDL cholesterol (HDLC) is a risk factor for coronary deaths. However, data on older people are scarce, and previous studies have not examined this association in relation to alcohol intake.

METHODS AND RESULTS
Coronary mortality, all-cause mortality, and mortality due to alcohol and violence were related to HDLC levels among 7052 male smokers 50 to 69 years old in south and west Finland enrolled from 1984 to 1988 in the ATBC (AT, alpha-tocopherol; BC, beta-carotene) Study placebo group. During the average follow-up period of 4.7 years, 620 men died; 222 of these deaths were from coronary heart disease and 82 from causes related alcohol and violence. HDLC levels were inversely associated with coronary mortality, irrespective of age, whereas high total cholesterol was positively associated with coronary mortality among the younger men, 50 to 59 years of age, but not among the older men, 60 to 69 years old. Correction for temporal variation in HDLC measurement indicated a 43% stronger inverse association between HDLC and coronary mortality compared with that based only on a single value. The inverse association of HDLC and coronary mortality was less marked at higher levels of alcohol intake. All-cause and alcohol- and violence-related mortality were positively associated with HDLC among the younger men. All-cause mortality showed a U-shaped dose response among men > or = 60 years old.

CONCLUSIONS
Previous studies may have underestimated the beneficial effect of high HDLC because of regression-dilution bias and the confounding effect of heavy alcohol intake. This study supports the view that, particularly among older men, lipoprotein fractions may be more appropriate for screening than total cholesterol.
Adenosine receptor involvement in a delayed phase of myocardial protection 24 hours after ischemic preconditioning.
Authors: Baxter G F , Marber M S , Patel V C , Yellon D M 
Published: June 2012

BACKGROUND
We previously reported a delayed phase of protection against infarction 24 hours after ischemic preconditioning in the rabbit. In the present study, we investigated the possibility that this "second window of protection," like the well-described early phase of protection in the rabbit, might be associated with adenosine receptor activation.

METHODS AND RESULTS
In the first series of experiments, we examined whether adenosine receptor blockade with 8-(p-sulfophenyl)-theophylline (SPT) during preconditioning could abolish the delayed protection against infarction 24 hours later. Open-chest rabbits were subjected to myocardial preconditioning (PC) with the four 5-minute coronary occlusions or they were sham operated on (SHAM). During these procedures, animals received either SPT (PC + SPT, n = 6; and SHAM + SPT, n = 6) or vehicle (PC + VEH, n = 12; and SHAM + VEH, n = 11). Twenty-four hours later, infarct development after a 30-minute coronary occlusion/120-minute reperfusion insult was assessed with triphenyltetrazolium staining. In vehicle-treated rabbits, the infarct-to-risk ratio (I/R) was reduced from 53.6 +/- 5.7% (SHAM + VEH) to 32.9 +/- 4.6% (PC + VEH) (P < .05), clearly indicating a delayed phase of protection. Although I/R was not significantly different between SHAM + VEH (53.6 +/- 5.7%) and SHAM + SPT (61.7 +/- 5.4%), in PC + SPT the delayed protection was abolished (I/R = 56.8 +/- 3.8%). In the second series of experiments, we examined if pharmacological adenosine A1 receptor stimulation could evoke a delayed phase of protection. Conscious rabbits were pretreated with intravenous boluses of saline or the A1 receptor-selective agonist 2-chloro-N6-cyclopentyladenosine (CCPA), and infarct size in response to 30-minute ischemia/120-minute reperfusion was assessed 24 hours later. I/R was 54.5 +/- 2.7% in saline-pretreated controls (n = 12). Pretreatment with 25 micrograms/kg CCPA (n = 6), 50 micrograms/kg CCPA (n = 6), or 100 micrograms/kg CCPA (n = 6) resulted in I/R ratios of 37.1 +/- 4.2% (P < .01), 37.7 +/- 2.2% (P < .01), and 26.3 +/- 5.7% (P < .01), respectively. In both series of experiments, there were no differences in systemic hemodynamics during the infarct protocol, assessed as rate-pressure product, between the different experimental groups.

CONCLUSIONS
Twenty-four hours after repetitive brief coronary occlusions, susceptibility to infarction in rabbit myocardium is reduced, an effect that may have clinical relevance. Results of the present study suggest that this second window of protection following preconditioning may, like the early phase of protection, be initiated by an adenosine-related mechanism.
Effect of chronic dihydropyridine (isradipine) on the large arterial walls of spontaneously hypertensive rats.
Authors: Levy B I , Duriez M , Phillipe M , Poitevin P , Michel J B 
Published: June 2012

BACKGROUND
The effect of genetic hypertension and of chronic therapy by calcium entry blocker (CEB, isradipine) on the function and structure of large arteries has been studied in adult spontaneously hypertensive rats (SHR, n = 30) and in their normotensive control Wistar-Kyoto (WKY) rats (n = 30).

METHODS AND RESULTS
Fifteen-week-old rats were randomly allocated to treatment with isradipine (3 mg/kg subcutaneously once a day) or to placebo and followed for 12 weeks. Hemodynamic parameters, including instantaneous pressure and aortic velocity, were recorded under anesthesia at the end of the treatment period. Passive mechanical properties of carotid arteries were measured in situ in the presence or the absence of smooth muscle cell activity (potassium cyanide poisoning). Histomorphometric parameters of the carotid and aortic media, including cross-sectional area, medial thickness, nucleus density and size, and medial contents of proteins of interstitial matrix, were measured by an automated morphometric system. Untreated SHRs had greater peripheral resistance, stiffer and thicker arterial walls because of smooth muscle cell hyperplasia (thoracic aorta and carotid artery) and/or hypertrophy (thoracic aorta), and increased collagen content than did normotensive control rats. SHRs showed a significant left ventricular hypertrophy. For the whole duration of treatment, treatment with CEB normalized the arterial pressure in SHRs. We observed a significant decrease in peripheral resistance, increased cardiac output, and left ventricular contractility without significant reduction in left ventricular hypertrophy. Increases in diuresis and natriuresis were associated during the last week of treatment in both treated strains with marked increase in plasma renin activity; in contrast, urinary aldosterone was increased by treatment in WKY rats but not in SHRs. Arterial compliance was significantly increased by CEB under control and passive conditions. CEB induced a significant reduction in the medial hypertrophy of the aortic walls of SHRs and WKY rats associated with a reduction in medial hyperplasia. In the carotid artery, CEB reduced smooth muscle cell hypertrophy but did not affect the smooth muscle cell hyperplasia. Isradipine significantly reduced the arterial wall collagen contents in both strains, with marked increases in the elastin content in the carotid but not in the aortic wall.

CONCLUSIONS
These results suggest that (1) despite normalization of arterial pressure, chronic treatment with CEB in SHRs does not significantly reduce left ventricular hypertrophy, probably because of increase in myocardial contractility and/or increase in plasma renin activity; (2) mechanical properties of the arterial wall are normalized by treatment; and (3) remodeling of the arterial wall by CEB is not uniform according to the studied vessel.
Relative effects of alpha 1-adrenoceptor blockade, converting enzyme inhibitor therapy, and angiotensin II subtype 1 receptor blockade on ventricular remodeling in the dog.
Authors: McDonald K M , Garr M , Carlyle P F , Francis G S , Hauer K , Hunter D W , Parish T , Stillman A , Cohn J N 
Published: June 2012

BACKGROUND
Progressive ventricular remodeling after myocardial damage is associated with a poor prognosis. Optimal prevention of the histopathological processes involved in remodeling requires a more complete understanding of the mechanisms involved in initiating and maintaining these structural changes. Since the sympathetic nervous system and the renin-angiotensin system may be involved in the remodeling process, the structural effects of pharmacological inhibitors have been evaluated in a canine model of localized myocardial injury resulting from transmyocardial DC shock.

METHODS AND RESULTS
The study is comprised of two protocols run in series. In protocol 1, zofenopril (Z), a converting enzyme inhibitor (CEI), prevented the increase in left ventricular mass (LVM) and end-diastolic volume (LVV) observed in the control group (C) at 16 weeks (Z: LVM, 69.8 +/- 3.4 to 65.4 +/- 2.6 g, P = NS; LVV, 45.4 +/- 2.7 to 51.6 +/- 2.7 mL, P = NS; C: LVM, 68.4 +/- 3.2 to 91.4 +/- 2.9 g, P = .0001; LVV, 56.6 +/- 3.0 to 71.9 +/- 2.4 mL, P = .0003). Terazosin, an alpha 1-adrenoceptor antagonist, failed to prevent remodeling at 16 weeks despite continued receptor blockade. In protocol 2, the antiremodeling effect of full-dose CEI therapy with ramipril was confirmed. Low-dose ramipril that exerted no hemodynamic effect failed to prevent remodeling (LVM, 89.7 +/- 4.6 to 105.7 +/- 3.4 g, P = .01; LVV, 61.8 +/- 3.8 to 76.8 +/- 3.3 mL, P = .002). An angiotensin II subtype 1 receptor blocker also failed to prevent the increase in LVM or LVV (LVM, 89.0 +/- 4.6 to 109.7 +/- 5.3 g, P = .0001; LVV, 66.0 +/- 1.9 to 78.4 +/- 3.6 mL, P = .007).

CONCLUSIONS
High-dose CEI therapy can prevent progressive structural changes resulting from localized myocardial damage induced by DC shock. the failure of alpha 1-adrenoceptor blockade and angiotensin II subtype 1 blockade to attenuate remodeling argues against an important direct role for norepinephrine acting through alpha 1-receptors or angiotensin II acting through the type 1 receptor in the remodeling process in this model.
Survival and predictors of survival in patients with congestive heart failure due to Chagas' cardiomyopathy.
Authors: Mady C , Cardoso R H , Barretto A C , da Luz P L , Bellotti G , Pileggi F 
Published: June 2012

BACKGROUND
The fundamental determinant of the natural history of Chagas' disease is cardiac involvement.

METHODS AND RESULTS
We studied 104 male patients with congestive heart failure due to Chagas' disease to estimate the survival distribution function and to evaluate age, functional class (FC), maximal oxygen consumption (VO2max), and ejection fraction (EF) as predictors of survival. Statistical evaluation was performed through univariate (Student's t test and chi 2 test) and multivariate analyses (Cox's regression model). Overall survival was 66% at 1 year, 56% at 3 years, and 48% at 5 years. Ages were not statistically different (P = .9811) between survivor (40.3 +/- 8.7) and nonsurvivor (40.3 +/- 9.4) groups. The ejection fraction(s) were statistically different (P = .0001) between survival (43.6 +/- 9.9) and nonsurvival (30.6 +/- 8.1) groups, as was VO2max (P = .0001) (21.0 +/- 4.7 and 15.0 +/- 4.9, respectively). Most of the surviving patients were in FC II and most of the nonsurvivors were in FC IV (P = .0001). VO2max (P = .0001) and EF (P = .0008) are highly associated with survival time in the multivariate analysis, but FC (P = .0578) is less important. Age (P = .9811) did not influence survival.

CONCLUSIONS
We conclude that 50% of the patients with heart failure due to Chagas' disease die in 47 months and that VO2max and EF are important indices of survival in this group.
Electrophysiological Study of Human Heart Muscle
Authors: TRAUTWEIN WOLFGANG , KASSEBAUM DONALD G. , NELSON RUSSELL M. , HECHT HANS H. 
Published: June 2012

Membrane potential changes in human ventricular and atrial muscle, excised from patients undergoing open-heart surgery, were recorded by micro-electrodes in vitro.
Mean ventricular resting and action potentials were -87 mv. and 115 mv., respectively. The mean atrial resting potential was -70 mv., mean action potential 75 mv. Two forms of atrial action potential were found, one having conventional contour, the other with prominent spike and plateau. A disturbance in repolarization is believed to underlie the latter type of atrial potential cycle.
The relation between the upstroke velocity of the action potential and the extracellular sodium concentration and membrane potential was shown to be similar to that in other mammalian cardiac tissue. The mean conduction velocity determined in ventricular fibers (1.3 M./sec.) was somewhat greater than that of the dog, and the possible relationship to hypertrophy of the cardiac fibers in the preparations studied is described.
The effect of increased rate and anoxia in reducing the action potential duration is like that found in the hearts of other mammals.
The conductance type of inhibition was produced by acetylcholine in spontaneously beating atrial tissue. The excitatory effect of epinephrine was preceded by a transitory inhibition.
The basic mechanisms underlying the action potential, automaticity and transmitter effects, derived from investigation of other mammalian cardiac tissue are applicable to the human heart.
Use of External Counting Technics In Studies of the Circulation
Authors: Conn Hadley L. 
Published: June 2012

A variety of external counting technics has been used to study the circulation. Brief consideration has been given to some of those concerned with measurement of cardiac output, myocardial and other regional blood flows, and cardiopulmonary volumes, and to those related to the evaluation of vascular shunts.
These technics have much in common. They are simple to carry out, require little time to accomplish, and entail little risk for the subject. At the same time, they are to varying extents imprecise, and are not as accurate as methods currently available or methods of undetermined validity or both. They do not offer the means to measurement of intravascular pressures and so cannot replace cardiac catheterization. As yet, little new information about the circulation has been gained by application of these methods.
The ultimate place of external counting technics in the study of the circulation is still undetermined. The best prediction is that these methods will probably supplement but not replace diagnostic methods now in use. They should serve a valuable function as tests for screening of subjects being considered for more definitive and laborious procedures and as supplementary tools in the performance of these more definitive astudies.
Architecture of Small Arteries during Vasoconstriction
Authors: Van Citters Robert L. , Wagner Bernard M. , Rushmer Robert F. 
Published: June 2012

The cytoarchitectural changes which take place in the walls of small arteries (about 1 mm. O.D.) during vasoconstriction and vasodilation have been studied. Vessels were fixed while in their functional state by immersion in liquid isopentane at -170 C. and prepared for microscopic examination by freeze substitution.
The walls of control vessels were thin in relation to the diameter of lumina (WT:L 1:30), indicating that they are more distended than they appear in routinely fixed sections. Vessels dilated with ACH had even thinner walls (WT:L 1:40). Vasoconstriction, induced by local application of epinephrine, increased the wall thickness and reduced the size of the lumen (WT:L 1:2) but in no case was the lumen obliterated in arteries of this size.
Although an increase in the WT:L ratio is commonly employed as evidence of vascular hypertrophy, normal vessels which are fixed and sectioned while in a functional state of vasoconstriction may exhibit similar gross characteristics. Constricted vessels are characterized by progressive deformation of the internal elastic lamina, crowding of endothelial cells, and distortion of smooth muscle cells and their nuclei, particularly in the region immediately adjacent to the lumen. During intense vasoconstriction, the wall tension appears to be supported only by the outer layers of the vessel.
Hemodynamic Alterations of Acute Pulmonary Thromboembolism
Authors: Parmley Loren F. , North Robert L. , Ott Bruce S. 
Published: June 2012

A method is described of producing pulmonary embolism in the dog by the use of various-sized autologous clots made radiopaque. This method of experimental pulmonary embolism results in dilatation of the large- to small-sized pulmonary arteries and a consistent hemodynamic response in the pulmonary circulation, characterized by a marked rise in pulmonary arteriolar resistance with increased pulmonary arterial pressure but persistently normal pulmonary venous and "capillary" pressures.
Data are presented to support the concept that the pulmonary hemodynamic changes that result from an initial pulmonary thromboembolism are primarily the result of vasoconstriction of the small pulmonary arteries or arterioles, presumably by a reflex mechanism. Mechanical blockage of the pulmonary vascular bed is considered to be of importance in causing hemodynamic alterations only after massive or repeated pulmonary embolism. The increase in pulmonary arteriolar resistance that results from the vasomotor response to pulmonary embolism is transient, whereas that due to mechanical blockage results in sustained pulmonary hypertension.
Systemic arterial pressure does not show a consistent response to pulmonary embolism and could not be related to the hemodynamic alterations that occurred in the pulmonary circulation. Severe systemic hypotension resulted unpredictably but was more frequent after repeated or extensive pulmonary embolism. The systemic hypotensive reaction to pulmonary embolism is only in part due to a decreased cardiac output. The more severe responses are best explained on the basis of a vasomotor reflex producing a decrease in systemic arterial resistance.
The two mechanisms of death in this experimental series were severe systemic hypotension with development of fatal ventricular arrhythmias and, almost as frequent, pulmonary edema that was characterized by severe pulmonary hypertension in the presence of a normal pulmonary venous pressure.
There are many similarities between the experimental findings of this study and the clinical event of human pulmonary thromboembolism. Attention is drawn to the need for further investigation of the mechanism of the systemic arterial pressure response that often causes death and appears to be independent of the magnitude of the pulmonary hemodynamic changes.
Hemodynamic Effects of Guanethidine in Man
Authors: COHN JAY N. , LIPTAK THOMAS E. , FREIS EDWARD D. 
Published: June 2012

Guanethidine was administered in a single intravenous infusion to supine hypertensive and normotensive subjects. Hemodynamic changes during the transient pressor phase were consistent with catechol amine effect. The later hypotensive effect occurred only in the hypertensive subjects and was usually associated with a slight decrease in cardiac output in patients without cardiac decompensation and a slight increase in output in those with congestive heart failure. Total peripheral resistance decreased although there was an increase in splanchnic vascular resistance and a decrease in the percentage of the cardiac output perfusing the hepatic-portal bed.
Tests of sympathetic nervous system activity revealed that, although the Valsalva "overshoot" usually was blocked, complete inhibition of digital vasoconstrictor reflexes did not always occur and vascular responsiveness to tyramine and ephedrine was not diminished up to six hours following intravenous guanethidine. Tyramine responses were also demonstrated in a group of patients on effective long-term oral therapy with guanethidine.
These studies suggest that guanethidine has unique hemodynamic effects not necessarily shared by ganglionic blocking agents, bretylium tosylate, or reserpine. Catechol amine depletion probably is not important in the mechanism of the antihypertensive and sympathetic inhibitory actions in man, and the possibility of an additional non-adrenergic effect is considered.
Systems Behavior, Feed-back Loops, and High Blood Pressure Research
Authors: PETERSON LYSLE H. 
Published: June 2012

A major challenge to those investigating the etiology and progress of hypertension, as well as of other diseases, results from the fact that the control and regulation of most bodily functions are comprised of multiple feedback loops involving many bodily "systems." Thus, mechanisms which seem to offer clues as to the etiology of an abnormality, when investigated as an isolated function, fail to explain the etiology when sought in the intact experimental animal or patient.
Examples of simple closed-loop systems are described to illustrate the effects of feed-back. A simplified diagram of several factors known to play a role in the control and regulation of the characteristies of the blood vessel wall is described to illustrate the multiplicity of the feed-back pattern which probably occurs. Furthermore, it is evident that almost none of the factors which constitute the loops have been evaluated sufficiently to permit characterization of the system. It is not surprising that apparently promising clues turn out to be disappointing and to become lost in the system.
The medical investigator must learn to deal with methods of analyzing systems containing multiple factors and functions as well as to characterize the properties and behavior of the parts of the system.