Enhanced left ventricular shortening during chronic volume overload in conscious dogs

1980 ◽  
Vol 238 (2) ◽  
pp. H126-H133 ◽  
Author(s):  
M. M. LeWinter ◽  
R. L. Engler ◽  
J. S. Karliner
Keyword(s):  
Volume Overload ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Stimulation ◽  
Ventricular Performance ◽  
Blood Pressure Elevation ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ejection Phase

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Nonsympathetic increased inotropic state early after aortic insufficiency

1982 ◽  
Vol 242 (6) ◽  
pp. H973-H979
Author(s):  
B. Crozatier ◽  
D. Caillet ◽  
J. L. Chevrier ◽  
P. Y. Hatt
Keyword(s):  
Volume Overload ◽  
Wall Stress ◽  
Aortic Insufficiency ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Internal Diameter ◽  
Inotropic State ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ventricular Response

The very early left ventricular response to chronic volume overload induced by aortic insufficiency (AI) was examined in conscious dogs previously instrumented with a left ventricular micromanometer and ultrasonic crystals measuring internal diameter, segmental length, and parietal wall thickness. Acute volume loading with dextran (AVL) was compared with that 24 and 48 h after AI induced by a perforation of the aortic valve. beta-Blockade was also produced before and after AI. For a similar increase in preload in AVL and after AI, the percent change in systolic shortening of diameters and segments (% delta L) increased from 30.4 to 34.1% after AI (P less than 0.01). For matched calculated wall stress during AVL and AI, % delta L and peak velocity of shortening were significantly increased after AI, and the same results were reproduced after beta-blockade. We conclude that, at the early phase of chronic volume overload before hypertrophy appears, left ventricular hyperfunction is mainly due to a nonsympathetic increased contractility and that, in the conscious dog, the inotropic state appears to be modified by a sustained increased preload.

Increased alpha 1-adrenergic vascular sensitivity during development of hypertension in conscious dogs

1993 ◽  
Vol 264 (4) ◽  
pp. H1259-H1268 ◽  
Author(s):  
N. Uemura ◽  
D. E. Vatner ◽  
Y. T. Shen ◽  
J. Wang ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Conscious Dogs ◽  
Aortic Tissue ◽  
Ang Ii ◽  
Receptor Density ◽  
Adrenergic Stimulation ◽  
Before And After ◽  
Vascular Responsiveness

The goal of this study was to determine whether enhanced vascular responsiveness during the development of perinephritic hypertension is selective or nonspecific. The effects of graded infusions of norepinephrine (NE), phenylephrine (PE), angiotensin II (ANG II), and vasopressin (VP) were examined on mean arterial pressure, total peripheral resistance (TPR), and aortic pressure-diameter relationships in conscious dogs. NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension. Analysis of aortic pressure-diameter relationships also demonstrated significant (P < 0.05) shifts in response to NE and PE, but not ANG II and VP, during the development of hypertension. In normotensive dogs, low doses of ANG II infusion also enhanced the vasoconstrictor response not only to NE and PE but also to VP. In contrast to what was observed in hypertension, in the presence of ANG II infusion after ganglionic blockade, enhanced responses to PE and NE were no longer observed. The alpha 1-adrenergic receptor density in membrane preparations from aortic tissue, as determined by [3H]prazosin binding, was higher (P < 0.05) in hypertensive dogs than control dogs. Thus the vascular responsiveness in the aorta and resistance vessels is enhanced to alpha 1-adrenergic stimulation, but not to all vasoconstrictors, during developing perinephritic hypertension. The mechanism appears to involve increased alpha 1-adrenergic receptor density.

scholarly journals NT pro- B-type Natriuretic Peptide in the Small Ventricular Septal Defect in Children

2021 ◽  
Vol 9 (B) ◽  
pp. 1677-1680
Author(s):  
Rahmat Budi Kuswiyanto ◽  
Putria Apandi ◽  
Dany Hilmanto ◽  
Muhammad Hasan Bashari ◽  
Sri Endah Rahayuningsih
Keyword(s):  
Natriuretic Peptide ◽  
Transcatheter Closure ◽  
Volume Overload ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Natriuretic Peptide Level ◽  
Peptide Level ◽  
Before And After ◽  
Male Patients

Background: Brain natriuretic peptide is a cardiac hormone secreted from the left ventricular myocardium due to ventricular expansion and volume overload. A recent study shows that small VSD will have risk of ventricular dysfunction in adulthood. Another complications such as endocarditis, congestive heart failure, aortic regurgitation, arrhythmia also we should be aware. Evaluations of the plasma B-type natriuretic peptide level (NT pro BNP) are currently being considered as methods to identify the possible presence of ventricular dilation in small VSD. Objective: To evaluate the change in plasma B-type natriuretic peptide after transcatheter closure of VSD. Methods: A pretest-posttest design was conducted on VSD patients before and after transcatheter closure. Plasma B-type natriuretic peptide level were measured before and 30 days after the transcatheter closure of VSD. Result: A total of 32 peri membranous VSD patients were included in this study with 62.5 % female patients (n=20) and 37.5 % male patients (n=12). A significant decrease was observed in the median NT pro BNP level when the level before closure of 1.08 (0.74 – 3.47) ng/ml was compared to the level after closure of 0.91 (0.68 – 2.07) ng/ml (p<0.05). Conclusion: Significant decreases in NT pro BNP level are seen in small VSD patients 30 days after transcatheter closure. Patients with small peri membranous VSD are generally considered to need occlusion for their childhood defect.  

Intracavitary ultrasound impairs left ventricular performance: presumed role of endocardial endothelium

1992 ◽  
Vol 263 (6) ◽  
pp. 1-1
Author(s):  
T. C. Gillebert ◽  
S. G. De Hert ◽  
L. J. Andries ◽  
A. H. Jageneau ◽  
D. Brutsaert
Keyword(s):  
Left Ventricular ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
December Issue ◽  
Endocardial Endothelium

Pages H857–H865: T. C. Gillebert, S. G. De Hert, L. J. Andries, A. H. Jageneau, and D. Brutsaert. “Intracavitary ultrasound impairs left ventricular performance: presumed role of endocardial endothelium.” Because of typographical errors in the numbering of the references, some of the text citations were inconsistent. Therefore this entire article is reprinted at the end of this December issue.

Influence of CO2 on cardiovascular response to hypoxia in conscious dogs

1980 ◽  
Vol 239 (4) ◽  
pp. H545-H545 ◽  
Author(s):  
Raymond C. Koehler ◽  
Brian W. McDonald ◽  
John A. Krasney
Keyword(s):  
Cardiovascular Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Coronary Vasodilation ◽  
Circulatory Response ◽  
Wide Range ◽  
Before And After ◽  
Tension Time ◽  
Arterial Chemoreceptor

The modulating effect of CO2 on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O2 [PaO2 (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO2 levels: hypocapnia (from PaCO2 of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating PaCO2 attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/d tmax was not affected by varying PaCO2 either before or after SAD. Coronary flow increased an additional onefold during hypoxia when PaCO2 was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominates in the renal and splanchnic beds when PaCO2 is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when PaCO2 is increased; and d) the augmented coronary vasodilation produced by CO2 is probably mediated by local CO2-hypoxic interactions.

Role of the descending pressor pathway in the conscious and pentobarbital-anesthetized dog

1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Control ◽  
Conscious Dogs ◽  
Cardiovascular Parameters ◽  
Bilateral Carotid ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Conscious Animals

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.

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