Hemodynamics of obesity: influence of pattern of adipose tissue cellularity

1986 ◽  
Vol 251 (2) ◽  
pp. R314-R319
Author(s):  
D. L. Crandall ◽  
B. M. Goldstein ◽  
F. H. Lizzo ◽  
R. A. Gabel ◽  
P. Cervoni
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Tissue Expansion ◽  
Cellular Hypertrophy ◽  
Obese Rats ◽  
Hemodynamic Profile ◽  
Regional Vascular Resistance

Direct quantitation of blood flow with radioactive microspheres in conscious spontaneously obese rats indicated that the development of obesity was associated with an elevated cardiac output and stroke volume, a normotensive blood pressure, and a reduced total peripheral resistance when directly comparing obese rats with their lean counterparts. Obesity was also associated with increased blood flow and decreased regional vascular resistance in a variety of vascular beds, whereas cardiac index and total peripheral resistance per unit of body weight were similar between groups. When corrected for tissue weight, unique alterations in flow and resistance were observed in the adipose tissue. When expressed as resistance per organ, the greatest relative alterations in vascular resistance with the development of obesity also occurred in the adipose tissue. Furthermore, localized adipose tissue expansion through cellular hypertrophy was consistently associated with a different pattern of blood flow and vascular resistance than adipose tissue that expanded through both cellular hypertrophy and hyperplasia, implying an association between depot cellularity and its hemodynamic profile.

Microvascular rarefaction and tissue vascular resistance in hypertension

1989 ◽  
Vol 256 (1) ◽  
pp. H126-H131 ◽  
Author(s):  
A. S. Greene ◽  
P. J. Tonellato ◽  
J. Lui ◽  
J. H. Lombard ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Flow Distribution ◽  
Cheek Pouch ◽  
Tissue Blood Flow ◽  
Hamster Cheek Pouch ◽  
Relative Contribution ◽  
Microvascular Rarefaction

The purpose of this study was to quantitatively estimate the relative contribution of arteriolar rarefaction (disappearance of microvessels) and arteriolar constriction to the increases in total peripheral resistance and changes in the patterns of flow distribution observed in hypertension. A mathematical model of the hamster cheek pouch intraluminal microcirculation was constructed based on data from the literature and observations from our own laboratory. Separate rarefaction and constriction of third-order (3A) and fourth-order (4A) arterioles were performed on the model, and the results were quantified based on the changes of the computed vascular resistance. The degree of increase in resistance depended both on the number and the order of vessels rarefied or constricted and also on the position of those vessels in the network. The maximum increases in resistance obtained in the model runs were 21% for rarefaction and 75% for constriction. Rarefaction, but not constriction, produced large increases in the degree of heterogeneity of blood flow in the various vessel orders. These results demonstrate that vessel rarefaction significantly influences tissue blood flow resistance to a degree comparable with vessel constriction; however, unlike constriction, microvascular rarefaction markedly altered blood flow distribution in our model of the hamster cheek pouch vascular bed. These findings conform with the hypothesis that a significant component of the increase in total peripheral resistance in hypertension may be due to vessel rarefaction.

Short-Term Autoregulation of Systemic Blood Flow and Cardiac Output

Physiology ◽  
1989 ◽  
Vol 4 (6) ◽  
pp. 219-225 ◽  
Author(s):  
AWJ Cowley ◽  
C Hinojosa-Laborde ◽  
BJ Barber ◽  
DR Harder ◽  
JH Lombard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Circulation ◽  
Short Term ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Experimental Approaches ◽  
Regional Vascular Resistance

The contribution of local autoregulatory mechanisms to the overall control of the systemic circulation has been analyzed using theoretical and experimental approaches. Mechanisms that regulate regional vascular resistance and contribute importantly to the overall moment-to-moment regulation of cardiac output and total peripheral resistance are reviewed.

Angiotensin II: nitric oxide interaction and the distribution of blood flow

1993 ◽  
Vol 265 (6) ◽  
pp. R1276-R1283 ◽  
Author(s):  
D. H. Sigmon ◽  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Conscious Rats

Nitric oxide (NO) contributes to the regulation of regional blood flow. Inhibition of NO synthesis increases blood pressure and vascular resistance. Using radioactive microspheres and the substrate antagonist N omega-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) to block NO synthesis, we tested the hypothesis that there is a significant interaction between the vasodilator NO and the vasoconstrictor angiotensin II, which regulates regional hemodynamics. Further, we investigated the influence of anesthesia on this interaction. L-NAME increased blood pressure, decreased cardiac output, and increased total peripheral resistance in both anesthetized and conscious rats. In anesthetized rats, L-NAME decreased blood flow to visceral organs (i.e. kidney, intestine, and lung) but had little effect on blood flow to the brain, heart, or hindlimb. Treating anesthetized rats with the angiotensin II receptor antagonist losartan (10 mg/kg) attenuated the decrease in cardiac output and the increase in total peripheral resistance without affecting the pressor response to L-NAME. Losartan also attenuated the visceral hemodynamic responses to L-NAME. In conscious rats, L-NAME decreased blood flow to all organ beds. Treating these rats with losartan only marginally attenuated the increase in total peripheral resistance to L-NAME without significantly affecting the pressor response or the decrease in cardiac output. Losartan had no effect on the regional hemodynamic responses to L-NAME. These data suggest that NO-mediated vascular relaxation is an important regulator of total peripheral and organ vascular resistance. (ABSTRACT TRUNCATED AT 250 WORDS)

Atrial extract: hemodynamics in Wistar-Kyoto and spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. H265-H271 ◽  
Author(s):  
B. L. Pegram ◽  
M. B. Kardon ◽  
N. C. Trippodo ◽  
F. E. Cole ◽  
A. A. MacPhee
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Organ Blood Flow ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Atrial Natriuretic

Partially purified low (LMW) and high-(HMW) molecular-weight atrial natriuretic extracts were administered intravenously (540 micrograms protein/kg) to conscious Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Both LMW and HMW atrial natriuretic extracts produced an immediate decrease in mean arterial pressure that reached maximum within 5 min and returned to control levels within 30 min. In both strains, cardiac output decreased approximately 14% following administration of LMW. Total peripheral resistance increased only in SHR. Organ blood flow was significantly decreased to skin, brain, heart, kidneys, and splanchnic organs of WKY and to skin, muscle, heart, and splanchnic organs of SHR following administration of LMW. Corresponding increases in organ vascular resistance index were observed in brain, heart, and splanchnic organs of WKY and in skin, heart, and splanchnic organs of SHR. To some extent, the changes in organ blood flow may be a reflection of the decrease in cardiac output induced by LMW. After administration of HMW, no significant changes were observed in cardiac output or total peripheral resistance, although they tended to decrease. Organ vascular resistance was decreased to skin, muscle, brain, and splanchnic organs of SHR. Little difference was observed between WKY and SHR responses to atrial natriuretic extracts. These data indicate that atrial natriuretic extracts have an effect on systemic and regional hemodynamics in conscious rats that differs markedly from those of vasodilators such as nitroglycerin or hydralazine.

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

Reflex effects of thoracic aorta wall stretch on regional vascular resistance

1978 ◽  
Vol 56 (3) ◽  
pp. 390-394
Author(s):  
Peter M. Szeto ◽  
Franco Lioy
Keyword(s):  
Arterial Pressure ◽  
Thoracic Aorta ◽  
Vascular Resistance ◽  
Carotid Arteries ◽  
Peripheral Resistance ◽  
Adrenergic Blockade ◽  
Vascular Responses ◽  
Regional Vascular Resistance ◽  
Vascular Beds ◽  
Intact Limb

In anesthetized, vagotomized cats with both carotid arteries occluded, a stretch of the walls of the thoracic aorta, performed without obstructing aortic flow, induced a significant reflex increase in arterial pressure (35 ± 2−26 ± 1 mmHg; systolic–diastolic). This pressure increase was accompanied by significant increases in peripheral resistance in the superior mesenteric (+30%), renal (+23%), and external iliac (+23%) vascular beds. The increase in iliac resistance observed in the skinned leg was comparable with that observed in the contralateral intact limb. All these vascular responses were drastically reduced by the administration of phenoxybenzamine. After α-adrenergic blockade no signs of reflex vasodilatation could be detected during aortic stretch in any of the vascular beds examined.

Effect of K ATP + channel inhibition on total and regional vascular resistance in guinea pig pregnancy

1998 ◽  
Vol 275 (2) ◽  
pp. H680-H688 ◽  
Author(s):  
Linda Keyes ◽  
David M. Rodman ◽  
Douglas Curran-Everett ◽  
Kenneth Morris ◽  
Lorna G. Moore
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Guinea Pig ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Ang Ii ◽  
Channel Activity ◽  
Vasoconstrictor Response ◽  
Regional Vascular Resistance

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the [Formula: see text]channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) ( n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that [Formula: see text] channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments[Formula: see text] channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased[Formula: see text] channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

Oestrogen-induced changes in renal haemodynamics in the rat: Influence of plasma and intrarenal renin

1986 ◽  
Vol 71 (5) ◽  
pp. 613-619 ◽  
Author(s):  
Mr J. K. Evans ◽  
P. F. Naish ◽  
G. M. Aber
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renal Haemodynamics ◽  
Renin Activity ◽  
Female Rats

1. The effect of oestrone acetate (in total doses of 5 and 10 mg) on systemic and renal haemodynamics and the renin-angiotensin system has been studied in adult female rats. 2. The administration of 10 mg of oestrogen resulted in a significant fall in renal blood flow associated with significant rises in both renal vascular resistance and mean arterial pressure. No changes were noted in cardiac output or total peripheral resistance at either dose. 3. Whilst the higher dose of oestrogen induced a significant increase in plasma renin activity, no change was noted in animals receiving 5 mg of oestrogen. Both regimens caused significant reductions in plasma and intrarenal renin concentrations. 4. Although renal blood flow correlated with plasma renin activity in animals with a normal renal blood flow, no such correlation was noted in animals with oestrogen-induced reductions in renal blood flow. 5. The present study demonstrates that oestrogen-induced reductions in renal blood flow result from a rise in intrarenal vascular resistance which cannot be accounted for by simultaneous changes in either plasma renin activity or renal renin concentration.

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