Effect of the Type IV Phosphodiesterase Inhibitor Ro 20-1724 on Catecholamine-Induced Alterations in Regional Vascular Resistance and Regional Blood Flow

1998 ◽  
Vol 31 (6) ◽  
pp. 840-853
Author(s):  
Neal J. Thomas ◽  
William A. Herzer ◽  
Joseph A. Carcillo ◽  
Edwin K. Jackson
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Phosphodiesterase Inhibitor ◽  
Type Iv ◽  
Regional Vascular Resistance ◽  
Type Iv Phosphodiesterase

Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR

1985 ◽  
Vol 249 (6) ◽  
pp. R781-R786 ◽  
Author(s):  
R. W. Lappe ◽  
J. A. Todt ◽  
R. L. Wendt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sympathetic Nerves ◽  
Spontaneously Hypertensive ◽  
Regional Vascular Resistance ◽  
6 Hydroxydopamine ◽  
Renal Vascular ◽  
Renal Sympathetic

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

Regional blood flow and vascular resistance in response to oxytocin in the pregnant sheep and dog

1961 ◽  
Vol 16 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
N. S. Assali ◽  
L. Holm ◽  
H. Parker
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Uterine Blood Flow ◽  
Pregnant Uterus ◽  
Blood Flows ◽  
Uterine Contractions ◽  
Intravenous Drip ◽  
Pregnant Sheep ◽  
Regional Vascular Resistance

The effects of oxytocin on regional blood flow and regional vascular resistance were investigated in a group of pregnant ewes and bitches not in labor and in another group in early labor. Single injections or intravenous drip infusion did not change significantly arterial pressure, cardiac output, electrocardiogram, and renal, iliac, femoral, and carotid blood flows in any of the animals studied. The effects on the pregnant uterus were negligible before the onset of spontaneous labor. Only when the animal was in labor did oxytocin produce an increase in uterine contractions accompanied by a significant decrease in uterine blood flow. The data indicate that in the pregnant sheep and dog the circulatory action of oxytocin is limited to the pregnant uterus in labor and that the decrease in blood flow is probably due to an increase in intramural vascular resistance caused by the contracting myometrium around the uterine arterioles. Submitted on May 5, 1961

Regional blood flow and vascular resistance during hypothermia in dog

1961 ◽  
Vol 201 (3) ◽  
pp. 485-491 ◽  
Author(s):  
Bjorn Westin ◽  
N. Sehgal ◽  
N. S. Assali
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sine Wave ◽  
Blood Flows ◽  
Femoral Blood Flow ◽  
Regional Vascular Resistance ◽  
Femoral Blood ◽  
Carotid Flow

Changes in regional blood flow and regional vascular resistance during hypothermia in dogs with intact or abolished shivering mechanisms were measured with sine-wave electromagnetic flowmeters. In animals with shivering intact, cooling produced a fall in renal and carotid blood flows, despite a rise or no change in cardiac output. The fall was caused by an increase in renal and carotid vascular resistances. Femoral blood flow increased because of a decrease in vascular resistance. In animals with shivering abolished, cooling evoked a fall in the cardiac output and in renal and femoral blood flows, due to an increase in the vascular resistance. Upon rewarming, femoral flow immediately rose to values far above control. Carotid flow increased during cooling because of a decline in carotid resistance. Such a decline might have been related to the elevated blood Pco2 observed in the nonshivering animals.

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.

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.

Effects of oxygen on regional hemodynamics in hemorrhagic shock

1996 ◽  
Vol 271 (1) ◽  
pp. H203-H211 ◽  
Author(s):  
H. Bitterman ◽  
V. Brod ◽  
G. Weisz ◽  
D. Kushnir ◽  
N. Bitterman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Biceps Femoris ◽  
Total Blood ◽  
Biceps Femoris Muscle ◽  
Arterial Blood ◽  
Femoris Muscle

This study investigated mechanisms of the hemodynamic effects of oxygen in hemorrhagic shock induced by bleeding 30% of the total blood volume in anesthetized rats. An ultrasonic flowmeter was used to monitor regional blood flow. Changes in tissue perfusion were assessed by the laser-Doppler technique. The inhalation of 100% oxygen induced a significant increase in mean arterial blood pressure (MABP) and vascular resistance in the hindquarters, with a concomitant decrease in blood flow in the distal aorta and biceps femoris muscle. In contrast, oxygen did not change vascular resistance in the superior mesenteric artery (SMA) and renal beds and induced a significant increase in blood flow to the renal artery, SMA, and small bowel in hemorrhaged rats. L-Arginine (100 mg/kg iv) but not D-arginine or the vehicle (0.9% NaCl) completely abolished the effects of oxygen on blood pressure and reversed its effects on blood flow and resistance in the hindquarters and biceps femoris muscle. Administration of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (50 mg/kg iv) significantly increased MABP and the resistance in the three vascular beds. Pretreatment of hemorrhaged rats with a superoxide dismutase mimic, the NO-stable radical 2,2,6,6-tetramethylpiperidine-N-oxyl (5 mg/kg iv), resulted in significantly diminished effects of oxygen on hindquarter hemodynamics. These results demonstrate a differential effect of oxygen, which increases vascular resistance in the hindquarters without a significant effect in the splanchnic and renal beds, thus favoring an increase in splanchnic and renal perfusion. It is suggested that inactivation of NO by reactive oxygen species may underlie the effects of oxygen on hindquarter vascular tone during shock.

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