CENTRALLY MEDIATED INFLUENCES OF HYPERTONIC NaCI AND ANGIOTENSIN II ON REGIONAL BLOOD FLOW AND HEMODYNAMIC RESPONSES TO HYPOTENSIVE HEMORRHAGE IN CONSCIOUS SHEEP

Shock ◽  
1994 ◽  
Vol 2 (1) ◽  
pp. 60-67 ◽  
Author(s):  
Ulf Gunnarsson ◽  
Hans Hjelmqvist ◽  
Mats Rundgren
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Regional Blood Flow ◽  
Hemodynamic Responses ◽  
Conscious Sheep

scholarly journals Role of Nitric Oxide in Regional Blood Flow in Angiotensin II-Induced Hypertensive Rats.

2001 ◽  
Vol 24 (4) ◽  
pp. 421-427 ◽  
Author(s):  
Akira NISHIYAMA ◽  
Yoshihide FUJISAWA ◽  
Toshiki FUKUI ◽  
Matlubur RAHMAN ◽  
Naoki KONDO ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Regional Blood Flow ◽  
Hypertensive Rats

Effects of Meclofenamate and Captopril on Renal and other Regional Vascular Beds after Mild Haemorrhage in Conscious Rabbits

1982 ◽  
Vol 62 (2) ◽  
pp. 169-176 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys ◽  
L. Davidson
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Regional Blood Flow ◽  
Plasma Renin ◽  
Plasma Adrenaline ◽  
Renal Vasoconstriction ◽  
Vascular Beds ◽  
Conscious Rabbits

1. The role of prostaglandins and angiotensin II in blood flow regulation was studied in conscious rabbits subjected to mild haemorrhage. 2. Haemorrhage caused a 13% fall in arterial pressure and a 21% fall in cardiac output, responses which were unchanged by sodium meclofenamate, an inhibitor of prostaglandin synthesis, or captopril, an inhibitor of the angiotensin converting enzyme. 3. Haemorrhage doubled plasma adrenaline and noradrenaline levels. Plasma renin activity trebled after haemorrhage and was further elevated by captopril. 4. Renal blood flow was maintained after haemorrhage alone. Meclofenamate given immediately after haemorrhage caused a 31% fall in renal blood flow. Captopril given immediately after haemorrhage caused renal vasodilation, but when given after meclofenamate augmented renal vasoconstriction. 5. Splenic vasoconstriction was seen after haemorrhage and meclofenamate, and subsequently was augmented by captopril. 6. Results suggest that prostaglandins variably modulate regional blood flow in conscious rabbits subjected to mild haemorrhage. Enhanced sympathc—adrenal activity increases reno-vascular and splenic dependence on vasodilator prostaglandins, but not that of coronary, cerebral, hepatic or adrenal circulations. Renal and splenic vasoconstriction seen with meclofenamate are not due to circulating angiotensin II.

Evaluation of a transit-time system for the chronic measurement of blood flow in conscious sheep

1995 ◽  
Vol 78 (2) ◽  
pp. 524-530 ◽  
Author(s):  
J. A. Bednarik ◽  
C. N. May
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Transit Time ◽  
Regional Blood Flow ◽  
Flow Probe ◽  
Time Flow ◽  
Bilateral Carotid ◽  
Conscious Sheep

The accuracy of transit-time ultrasonic flow probes for measurement of regional blood flow and cardiac output was evaluated after long-term implantation in sheep. Transit-time flow probes (3, 4, 6, and 20 mm) accurately measured flow in vitro. Recalibration in vivo demonstrated that this accuracy was maintained after 1–9 mo of implantation on the left circumflex coronary (3-mm probe), cranial mesenteric (6-mm probe), left renal (4-mm probe), and left external iliac (6-mm probe) arteries of sheep. The flow probes also showed good zero stability. However, a transit-time flow probe (20 mm) chronically implanted on the pulmonary trunk significantly underestimated cardiac output compared with thermodilution or timed collection of blood. Although this flow probe underestimated flow, the response was linear. Bilateral carotid occlusion caused mesenteric, renal, and iliac vasoconstrictions, confirming that innervation of these vascular beds was undamaged. For experimental purposes, regional blood flow was measured with transit-time flow probes and cardiac output was measured with electromagnetic flow probes calibrated against thermodilution. In summary, transit-time flow probes reliably and accurately measure regional blood flow over many months in adult sheep, but, to measure cardiac output in sheep, the probes must be calibrated in vivo against another reference technique.

Role of angiotensin II in hemodynamic responses to dynamic exercise in miniswine

1995 ◽  
Vol 78 (1) ◽  
pp. 185-190 ◽  
Author(s):  
C. L. Stebbins ◽  
J. D. Symons
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Myocardial Contractility ◽  
Regional Blood Flow ◽  
Dynamic Exercise ◽  
Treadmill Running ◽  
Ang Ii ◽  
Arterial Blood

Angiotensin II (ANG II) is a potent vasoconstrictor of splanchnic and renal resistance vessels. Because ANG II increases during exercise and blood flow in the splanchnic and renal circulations decreases, we tested the hypothesis that ANG II plays a role in arterial blood pressure and regional blood flow responses to treadmill running in the miniswine. Consequently, 11 pigs were instrumented with epicardial electrocardiogram leads and left atrial and aortic catheters to assess mean arterial blood pressure (MAP), heart rate (HR), myocardial contractility, cardiac output, and regional blood flow during treadmill running. Each animal exercised for 20 min at 80% of its maximal HR reserve. Exercise was performed in the absence and presence of the ANG II AT1 receptor antagonist losartan (15–20 mg/kg). ANG II AT1 receptor blockade attenuated the MAP and systemic vascular resistance responses to dynamic exercise but had no effect on cardiac output, HR, or myocardial contractility. In addition, blood flow increased and/or regional vascular resistance decreased in the heart, kidneys, stomach, small intestine, and colon, whereas the reverse occurred in the skin and spleen. These data suggest that ANG II contributes to the increase in MAP and redistribution of cardiac output associated with dynamic exercise.

Vasopressin and angiotensin in the control of arterial pressure and regional blood flow in anaesthetized, surgically stressed rats

1983 ◽  
Vol 61 (12) ◽  
pp. 1494-1500 ◽  
Author(s):  
Catherine Cheuk Ying Pang
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Regional Blood Flow ◽  
Reference Sample ◽  
Peripheral Resistance ◽  
Peripheral Vascular ◽  
Vasopressin Antagonist ◽  
Anaesthetized Rats

The effects of vasopressin and angiotensin II in the control of regional blood flow (BF) in halothane-anaesthetized rats were investigated by the administration of specific antagonists of vasopressin and angiotensin II, namely, [1-(β-mercapto-β,β-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine-vasopressin [d(CH2)5Tyr(Me)AVP] and saralasin, respectively. Cardiac output and the distribution of BF was examined by the reference sample microsphere technique. The injection of the vasopressin antagonist into the left ventricle of rats caused reductions of mean arterial pressure (MAP) and total peripheral resistance (TPR), an increase of BF to the stomach and skin and a decrease of BF to the intestine. Intravenous infusion of saralasin caused reductions of MAP and TPR and an increase of BF to the kidneys and skin. The results show that both the vasopressin and the renin–angiotensin systems participate in the control of arterial pressure and peripheral vascular resistance in anaesthetized, surgically stressed rats.

Halothane Impairs the Hemodynamic Influence of Endothelium-derived Nitric Oxide 

1995 ◽  
Vol 82 (1) ◽  
pp. 135-143 ◽  
Author(s):  
David H. Sigmon ◽  
Ivan Florentino-Pineda ◽  
Russell A. Van Dyke ◽  
William H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Regional Blood Flow ◽  
Peripheral Resistance ◽  
Halothane Anesthesia ◽  
Hemodynamic Responses ◽  
Synthesis Inhibition ◽  
Conscious Rats ◽  
Anesthetized Rats

Background The endogenous vasodilator endothelium-derived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. Methods Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by NW-nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. Results NW-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 +/- 2 (P < 0.001) and 20 +/- 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 +/- 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). NW-nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. Conclusions Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.

Evidence for bradykinin potentiation by angiotensin congeners in conscious rats

1981 ◽  
Vol 240 (2) ◽  
pp. H255-H261
Author(s):  
S. C. Textor ◽  
H. Brunner ◽  
H. Gavras
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Dose Response ◽  
Enzyme Inhibitor ◽  
Regional Blood Flow ◽  
Converting Enzyme ◽  
Response Curves ◽  
Kininase Ii ◽  
Conscious Rats

It has become increasingly clear that the potent vasoactive peptides bradykinin and angiotensin share a common point of metabolism, i.e., angiotensin-converting enzyme or kininase II, and may interact with prostaglandins to regulate regional blood flow. To establish whether the sensitivity to exogenous bradykinin was affected by the presence of angiotensin, vasodepressor dose-response curves to injected bradykinin were performed in conscious rats before and during a 1-h infusion of angiotensin I (30 ng/min), angiotensin II (30 and 300 mg/min), and [Sar2,Ala8]angiotensin II (5 micrograms/min). All of these induced a parallel leftward shift of the bradykinin dose-response curve of approximately threefold. No similar changes were observed during control infusions of dextrose, similar pressor doses of lysine vasopressin, or norepinephrine. Sensitivity to bradykinin was enhanced by saralasin in normal and nephrectomized rats, suggesting that the antagonist itself was responsible. Similar potentiation was present during both acute (1 h) and chronic infusions (9 days) of angiotensin II and attenuated the effect of a converting-enzyme inhibitor on bradykinin sensitivity. Accordingly, these results suggest a competitive interaction in vivo between angiotensin congeners and bradykinin at a point of bradykinin degradation, probably angiotensin-converting enzyme or kininase II. This is a potential additional mechanism by which these systems may interact to affect regional blood flow and must be considered in the interpretation of results obtained during saralasin infusion.

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