scholarly journals CARDIOVASCULAR EFFECTS OF THYROXINE TREATMENT IN NORMAL RATS

1962 ◽  
Vol 40 (12) ◽  
pp. 1647-1654 ◽  
Author(s):  
Margaret Beznák ◽  
A. Marcsán ◽  
T. Fournier
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Hypertrophy ◽  
Metabolic Rate ◽  
Normal Values ◽  
Cardiovascular Effects ◽  
Aortic Constriction ◽  
Thyroxine Treatment ◽  
The Right

Metabolic rate, blood pressure, weight and rate of the heart, cardiac output, and work were determined at weekly intervals in groups of normal rats receiving thyroxine. The measurements were made before and during the infusion of polyvinylpyrrolidone into the right side of the heart. The maximum values of cardiac output and work obtained during infusion were considered to be an approximate measure of the strength of the heart. Cardiac output and work in thyroxine-treated rats far exceeded the normal values before as well as during infusion. The greater strength was not merely the consequence of the greater size of the heart which developed in the course of thyroxine treatment. Hearts of similar size — coming from larger normal rats or from smaller normal rats with cardiac hypertrophy due to aortic constriction — did significantly less work than the hearts of thyroxine-treated rats.

scholarly journals CARDIOVASCULAR EFFECTS OF THYROXINE TREATMENT IN NORMAL RATS

1962 ◽  
Vol 40 (1) ◽  
pp. 1647-1654 ◽  
Author(s):  
Margaret Beznák ◽  
A. Marcsán ◽  
T. Fournier
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Hypertrophy ◽  
Metabolic Rate ◽  
Normal Values ◽  
Cardiovascular Effects ◽  
Aortic Constriction ◽  
Thyroxine Treatment ◽  
The Right

Metabolic rate, blood pressure, weight and rate of the heart, cardiac output, and work were determined at weekly intervals in groups of normal rats receiving thyroxine. The measurements were made before and during the infusion of polyvinylpyrrolidone into the right side of the heart. The maximum values of cardiac output and work obtained during infusion were considered to be an approximate measure of the strength of the heart. Cardiac output and work in thyroxine-treated rats far exceeded the normal values before as well as during infusion. The greater strength was not merely the consequence of the greater size of the heart which developed in the course of thyroxine treatment. Hearts of similar size — coming from larger normal rats or from smaller normal rats with cardiac hypertrophy due to aortic constriction — did significantly less work than the hearts of thyroxine-treated rats.

CARDIAC PERFORMANCE IN HEART–LUNG PREPARATIONS OF RATS WITH EXPERIMENTAL CARDIAC HYPERTROPHY

1966 ◽  
Vol 44 (1) ◽  
pp. 21-27 ◽  
Author(s):  
B. Korecky ◽  
M. Beznak ◽  
M. Korecka
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Arterial Pressure ◽  
Cardiac Hypertrophy ◽  
Cardiac Performance ◽  
Aortic Constriction ◽  
Chronic Anemia ◽  
Stepwise Increase ◽  
Thyroxine Treatment ◽  
Made In

Heart-lung preparations (h.l.p.) were made in normal rats and in rats with cardiac hypertrophy produced by aortic constriction, thyroxine treatment, or chronic anemia. In the h.l.p., arterial pressure was kept constant at 100 mm Hg, and maximum cardiac output (m.c.o.) was measured by stepwise increase in the inflow of blood until no further rise in cardiac output occurred. The m.c.o. of enlarged hearts was above normal, but not if it was expressed per gram of left ventricle weight. This latter value was not above normal in any of the enlarged hearts, contrary to earlier findings in whole animals. In fact, in one group of severely anemic rats it was significantly below normal.

THE EFFECT OF DIFFERENT DEGREES OF SUBDIAPHRAGMATIC AORTIC CONSTRICTION ON HEART WEIGHT AND BLOOD PRESSURE OF NORMAL AND HYPOPHYSECTOMIZED RATS

1955 ◽  
Vol 33 (1) ◽  
pp. 985-994 ◽  
Author(s):  
Margaret Beznák
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Heart Weight ◽  
Aortic Constriction ◽  
Hypophysectomized Rats ◽  
Intact Rats

The aortae of groups of normal and hypophysectomized rats were constricted with rings of five different sizes (0.93, 0.83, 0. 74, 0.71, and 0.63 mm. diameter). In normal rats constriction caused an increase in heart weight and blood pressure which was the greater the narrower the constriction. If constriction exceeded 0.74 mm., cardiac hypertrophy reached extremely high values, while the blood pressure was lower than in groups with less constriction. The blood pressure response to Adrenalin or Infundin increased in proportion to the degree of constriction down to 0.74 mm.; greater constriction reduced the response. In hypophysectomized rats no degree of aortic constriction produced hypertension or cardiac hypertrophy, yet the increase in blood pressure after Adrenalin or Infundin was as great as in the normal intact rats.

Effect of Growth Hormone Preparations on Cardiac Hypertrophy and Blood Pressure of Hypophysectomized Rats

1956 ◽  
Vol 184 (3) ◽  
pp. 563-566 ◽  
Author(s):  
Margaret Beznák
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Cardiac Hypertrophy ◽  
Body Growth ◽  
Bovine Growth Hormone ◽  
Aortic Constriction ◽  
Hypophysectomized Rats ◽  
Crystalline Growth

Of three growth hormone preparations only one (PGH 163-208A, Armour) restored cardiac hypertrophy and hypertension on aortic constriction in hypophysectomized rats near to the level seen in normal rats. The same aortic constriction caused no increase in the weight of the heart and no hypertension in untreated hypophysectomized rats and in similar rats treated with a bovine growth hormone preparation (R 285-174, Armour) or crystalline growth hormone (Dr. Li, Berkeley). The different action of the three preparations was not connected with their effect on appetite and on body growth. ACTH, 5 mg/rat/day, caused adrenal hypertrophy in hypophysectomized rats without raising their blood pressure. The weight of the heart and particularly the blood pressure after aortic constriction were, however, greater in hypophysectomized rats treated with ACTH than in their nontreated controls.

Quercetin-Supplemented Diets Lower Blood Pressure and Attenuate Cardiac Hypertrophy in Rats With Aortic Constriction

2006 ◽  
Vol 47 (4) ◽  
pp. 531-541 ◽  
Author(s):  
Thunder Jalili ◽  
Justin Carlstrom ◽  
Sun Kim ◽  
David Freeman ◽  
Huifeng Jin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Lower Blood Pressure ◽  
Aortic Constriction ◽  
Lower Blood

Cardiovascular actions of centrally and peripherally administered trout urotensin-I in the trout

2000 ◽  
Vol 279 (2) ◽  
pp. R484-R491 ◽  
Author(s):  
Nagi Mimassi ◽  
Fatemeh Shahbazi ◽  
Jörgen Jensen ◽  
Dominique Mabin ◽  
J. Michael Conlon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Effects ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Arterial Blood ◽  
Intracerebroventricular Injections ◽  
Aortic Blood Pressure ◽  
Dose Dependent

The cardiovascular effects of centrally and peripherally administered synthetic trout urotensin (U)-I, a member of the corticotropin-releasing hormone family of neuroendocrine peptides, were investigated in unanesthetized rainbow trout Oncorhynchus mykiss. Intracerebroventricular injections of U-I (5.0 and 12.5 pmol) produced a sustained increase in mean dorsal aortic blood pressure (PDA) without significant change in heart rate (HR). This elevation in PDA was associated with an increase in cardiac output, but systemic vascular resistance did not change. Intra-arterial injection of U-I (12.5–500 pmol) evoked a dose-dependent increase in PDA, but in contrast to the hemodynamic effects of centrally administered U-I, the hypertensive effect was associated with an increase in systemic vascular resistance and an initial fall in cardiac output. HR did not change or underwent a delayed increase. Pretreatment of trout with prazosin, an α-adrenoreceptor antagonist, completely abolished the rise in arterial blood pressure after intra-arterial administration of U-I, which was replaced by a sustained hypotension and tachycardia. Trout U-I produced a dose-dependent (pD2 = 7.74 ± 0.08) relaxation of preconstricted rings of isolated trout arterial vascular smooth muscle, suggesting that the primary action of the peptide in the periphery is vasorelaxation that is rapidly reversed by release of catecholamines. Our results suggest that U-I may regulate blood pressure in trout by acting centrally as a neurotransmitter and/or neuromodulator and peripherally as a neurohormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.

scholarly journals Mechanical support of the pressure overloaded right ventricle: an acute feasibility study comparing low and high flow support

2015 ◽  
Vol 309 (4) ◽  
pp. H615-H624 ◽  
Author(s):  
Tom Verbelen ◽  
Jelle Verhoeven ◽  
Motohiko Goda ◽  
Daniel Burkhoff ◽  
Marion Delcroix ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
High Flow ◽  
Low Flow ◽  
Mechanical Support ◽  
Arterial Blood ◽  
The Right

The objectives of this study were to assess the feasibility of low flow right ventricular support and to describe the hemodynamic effects of low versus high flow support in an animal model of acute right ventricular pressure overload. A Synergy Pocket Micro-pump (HeartWare International, Framingham, MA) was implanted in seven sheep. Blood was withdrawn from the right atrium to the pulmonary artery. Hemodynamics and pressure-volume loops were recorded in baseline conditions, after banding the pulmonary artery, and after ligating the right coronary artery in these banded sheep. End-organ perfusion (reflected by total cardiac output and arterial blood pressure) improved in all conditions. Intrinsic right ventricular contractility was not significantly impacted by support. Diastolic unloading of the pressure overloaded right ventricle (reflected by decreases in central venous pressure, end-diastolic pressure and volume, and ventricular capacitance) was successful, but with a concomitant and flow-dependent increase of the systolic afterload. This unloading diminished with right ventricular ischemia. Right ventricular mechanical support improves arterial blood pressure and cardiac output. It provides diastolic unloading of the right ventricle, but with a concomitant and right ventricular assist device flow-dependent increase of systolic afterload. These effects are most distinct in the pressure overloaded right ventricle without profound ischemic damage. We advocate the low flow strategy, which is potentially beneficial for the afterload sensitive right ventricle and has the advantage of avoiding excessive increases in pulmonary artery pressure when pulmonary hypertension exists. This might protect against the development of pulmonary edema and hemorrhage.

THE ROLE OF GROWTH HORMONE AND THYROXINE IN NEPHROGENIC HYPERTENSION AND CARDIAC HYPERTROPHY IN HYPOPHYSECTOMIZED RATS

1967 ◽  
Vol 45 (6) ◽  
pp. 993-1000 ◽  
Author(s):  
Margaret Beznak
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Cardiac Hypertrophy ◽  
Male Rats ◽  
Unilateral Nephrectomy ◽  
Aortic Constriction ◽  
Salt Loading ◽  
Hypophysectomized Rats

There was no indication of slowly developing hypertension and cardiac hypertrophy in hypophysectomized rats upon treatment with desoxycorticosterone and salt loading following unilateral nephrectomy. This was the case in both younger (less than 100 g) and older (220–260 g) male rats. However, the weight of the heart and kidney, the blood pressure, and the rate and output of the heart of normal and hypophysectomized rats following unilateral nephrectomy and treatment with desoxycorticosterone and salt loading were not too different when the hypophysectomized rats were given growth hormone and thyroxine. This agrees with the earlier conclusion that thyroxine and growth hormone are required in hypophysectomized rats for the development of hypertension and any significant enlargement of the heart, whether from aortic constriction or from nephrogenic causes.

Effect of a local cold stress on peripheral temperatures of Inuit, Oriental, and Caucasian subjects

1978 ◽  
Vol 56 (5) ◽  
pp. 877-881 ◽  
Author(s):  
S. D. Livingstone ◽  
J. Grayson ◽  
L. D. Reed ◽  
D. Gordon
Keyword(s):  
Blood Pressure ◽  
Cold Stress ◽  
Normal Values ◽  
Index Finger ◽  
Finger Temperature ◽  
Cold Stimulus ◽  
Blood Pressures ◽  
The Right ◽  
Male Subjects ◽  
Skin Temperatures

Male subjects comprised of six Inuit from Igloolik, N.W.T., and five Orientals and six Caucasians from Toronto, Ont., volunteered for tests to determine the effect of localized cold stress on peripheral temperatures. In each subject, skin temperatures of the right index finger, the arm, and the cheek, as well as blood pressure and heart rate, were measured before, during, and after foot immersion in water of 10 °C temperature for 10 min. There was an immediate decrease in finger temperature on foot immersion in all three subject groups; however, the Inuit finger temperatures recovered very quickly to control values, the Caucasian finger temperatures began to increase after decreasing for 7.5 min, and the Oriental finger temperatures decreased continuously during the foot immersion and remained cool even 10 min after the removal of the cold stimulus. The cold stimulus did not affect the cheek or arm temperatures of any of the groups. In all subjects, systolic and diastolic blood pressures and heart rates increased on foot immersion, gradually returning towards normal values. No intergroup differences were seen in these parameters.

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