Haemodynamic Changes Associatedc with Obesity and High Blood Pressure in Crats with Ventromedial Hypothalamic Lesions

1980 ◽  
Vol 59 (s6) ◽  
pp. 397s-399s ◽  
Author(s):  
E. Reisin ◽  
D. H. Suarez ◽  
E. D. Frohlich
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
High Blood Pressure ◽  
Plasma Volume ◽  
Mild Hypertension ◽  
Male Rats ◽  
Volume Changes ◽  
Hypothalamic Lesions ◽  
Haemodynamic Changes ◽  
Mild Obesity

1. The haemodynamic and plasma volume changes associated with obesity and high blood pressure were studied in nine male rats with electrolytic ventromedial hypothalamic lesions and their paired sham-operated controls. Body weight and arterial pressure were greater in the rats with ventromedial hypothalamic lesions (565 ± 16 vs 462 ± 14 g, P<0.001; 128 ± 3 vs 118 ± 3 mmHg, P<0.05, respectively). Cardiac output was slightly elevated, and that portion of cardiac output distributed to the kidneys was reduced (P<0.001). Plasma volume was contracted in the rats with ventromedial hypothalamic lesions (21.0 ± 0.1 vs 2.8 ± 0.1 ml/100 g, P<0.001). 2. The haemodynamic characteristics of rats in which obesity and mild hypertension have been induced by electrolytic ventromedial hypothalamic lesion are similar to mild obesity essential hypertension in men.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

HEMODYNAMICS DURING THE ACUTE PHASE OF MYOCARDIAL DAMAGE CAUSED BY ISOPROTERENOL

1962 ◽  
Vol 40 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Margaret Beznak
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Acute Phase ◽  
Functional Capacity ◽  
Myocardial Damage ◽  
Male Rats ◽  
Histological Changes ◽  
Subcutaneous Injections ◽  
Norepinephrine Infusion ◽  
The Difference

One to three days after two consecutive subcutaneous injections of 40 mg/kg isoproterenol were given to male rats, severe histological changes occurred in the myocardium. Blood pressure, cardiac output, and work of these rats did not differ from normal. During polyvinylpyrrolidone infusion, normal rats raised their cardiac output to about three times the preinfusion value, while only a slight increase took place in the isoproterenol-treated rats. The difference was less marked during pitressin and norepinephrine infusion. It is concluded that during the acute damage of the myocardium by isoproterenol, the functional capacity of the heart is greatly reduced.

82 LOW MATERNAL BIRTH WEIGHT IS ASSOCIATED WITH TRANSMISSION OF NEPHRON DEFICITS AND HIGH BLOOD PRESSURE IN MALE RATS

2012 ◽  
Vol 30 ◽  
pp. e26 ◽  
Author(s):  
Linda A Gallo ◽  
Melanie Tran ◽  
Luise A Cullen-McEwen ◽  
Karen M Moritz ◽  
Mary E Wlodek
Keyword(s):  
Blood Pressure ◽  
Birth Weight ◽  
High Blood Pressure ◽  
Male Rats

Abstract P212: Kidney Injury Caused By Preeclamptic Pregnancy Improves Postpartum In A Transgenic Rat Model

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Sarah M Kedziora ◽  
Kristin Kraeker ◽  
Lajos Markó ◽  
Dominik N Mueller ◽  
Ralf Dechend ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Rat Model ◽  
Cardiac Remodeling ◽  
Kidney Injury ◽  
Male Rats ◽  
Transgenic Rat ◽  
Arterial Blood ◽  
Pregnancy And Postpartum ◽  
Transgenic Rat Model

Preeclamptic pregnancies involve mild renal injuries. However, there has been evidence that women with a history of preeclampsia (PE) have an increased risk to develop kidney disease in association to high blood pressure later in life. This study aims to characterize renal injury during pregnancy and postpartum in an established transgenic rat model for PE. Female Sprague-Dawley rats transgenic for the human angiotensinogen gene develop a PE phenotype in pregnancy, including cardiac remodeling, when mated with male rats harboring the human renin gene. Postpartum, blood pressure restores but cardiac remodeling persists. We hypothesize that PE during pregnancy mediates kidney injuries but does not fully restore after ending of the high blood pressure (postpartum). The renal alterations were analyzed by histological staining, gene expression and urine analysis. PE rats have elevated mean arterial blood pressure during pregnancy (PE d19 148.4 ± 20.7 mmHg) compared to normotensive values in control animals (WT d19 105.3 ± 4.6 mmHg). During PE increased expression of kidney injury marker 1 ( Kim-1/18S : PE d21 4.14 ± 3.26; WT d21 0.08 ± 0.02), neutrophil gelatinase associated lipocalin 2 ( Ngal/18S : PE d21 1.64 ± 0.83; WT d21 0.59 ± 0.28) and connective-tissue growth factor ( Ctgf/18S: PE d21 1.51 ± 0.46; WT d21 0.92 ± 0.32) were detected. Kidneys of PE rats showed mild glomerular (PAS-positive glomerular area PE d21 86.2 ± 4.4%; WT d21 79.1 ± 3.2%) and tubular changes during PE pregnancy resulting in albuminuria (albumin/creatinine ratio PE d19 2193.8 ± 1878.2; WT d19 290.4 ± 252.0). However, 4 weeks after pregnancy (approx. 2 years in humans) most of the PE related renal damages were absent including albuminuria and elevated expression of biomarkers ( Kim-1/18S : PE d50 0.09 ± 0.05; WT d50 0.23 ± 0.13; Ctgf/18S : PE d50 0.78 ± 0.25; WT d50 0.8 ± 0.25; Ngal/18S : PE d50 0.37 ± 0.17; WT 50 0.47 ± 0.11). Only mild enlargement of glomerular tuft area (PE d50 7523.8 ± 418.7 μm 2 ; WT d50 7058.4 ± 198.8 μm 2 ) was detected. Overall, the glomerular and tubular injuries are present during pregnancy in this transgenic PE rat. Most restore postpartum, speculating long-term kidney failure observed in humans is associated to hypertension and additional cardiovascular events.

Effects of vasopressin on arterial blood pressure and cardiac output in male and female rats

1991 ◽  
Vol 261 (5) ◽  
pp. R1118-R1125 ◽  
Author(s):  
K. Toba ◽  
J. T. Crofton ◽  
M. Inoue ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Arterial Blood ◽  
Male And Female Rats ◽  
Cycle Dependent

This study was performed to investigate further the mechanisms underlying the sexual dimorphism of the pressor responses to vasopressin. We have confirmed our earlier findings that the pressor response to graded infusions of vasopressin in conscious unrestrained male rats is similar to that in estrous females and greater than in diestrus, proestrus, and metestrus. This difference was due primarily to greater increases in total peripheral resistance (TPR) in males and estrous females, since there were no sex- or cycle-related differences in the vasopressin-induced reductions in cardiac output. Gonadectomy was without effect in males but, in females, increased blood pressure responses to vasopressin to levels found in males. Chronic treatment of ovariectomized rats with estradiol reduced pressor responsiveness to vasopressin; treatment with progesterone was without effect. These differences were also due to differences in TPR. It is concluded that the sex- and cycle-dependent differences in vasopressin-induced increases in blood pressure are due largely to attenuation of increases in TPR by estrogen.

Plasma Volume Decrease and Elevated Evans Blue Disappearance Rate in Essential Hypertension

1973 ◽  
Vol 45 (2) ◽  
pp. 173-181 ◽  
Author(s):  
Milos Ulrych
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Volume ◽  
Evans Blue ◽  
Disappearance Rate ◽  
The Mean ◽  
Volume Decrease

1. The disappearance rate of intravenously injected Evans Blue, plasma volume, cardiac output, and blood pressure were measured in seven normotensive and eighteen hypertensive subjects. 2. Plasma volume was found to be negatively correlated with the mean arterial pressure, Evans Blue disappearance rate and packed cell volume. 3. Faster disappearance rate of Evans Blue in hypertensive subjects may be due to an abnormality of mixing of the label or of the capillaries.

HEMODYNAMICS DURING THE ACUTE PHASE OF MYOCARDIAL DAMAGE CAUSED BY ISOPROTERENOL

1962 ◽  
Vol 40 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Margaret Beznak
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Acute Phase ◽  
Functional Capacity ◽  
Myocardial Damage ◽  
Male Rats ◽  
Histological Changes ◽  
Subcutaneous Injections ◽  
Norepinephrine Infusion ◽  
The Difference

One to three days after two consecutive subcutaneous injections of 40 mg/kg isoproterenol were given to male rats, severe histological changes occurred in the myocardium. Blood pressure, cardiac output, and work of these rats did not differ from normal. During polyvinylpyrrolidone infusion, normal rats raised their cardiac output to about three times the preinfusion value, while only a slight increase took place in the isoproterenol-treated rats. The difference was less marked during pitressin and norepinephrine infusion. It is concluded that during the acute damage of the myocardium by isoproterenol, the functional capacity of the heart is greatly reduced.

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