scholarly journals Effect of Acute Mitral Insufficiency of Various Degrees on Mean Arterial Blood Pressure, Coronary Blood Flow Cardiac Output and Oxygen Consumption

1958 ◽  
Vol 6 (3) ◽  
pp. 301-306 ◽  
Author(s):  
RENÉ WÉGRIA ◽  
GERHARD MUELHEIMS ◽  
ROBERT JREISSATY ◽  
JIRO NAKANO
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Arterial Blood Pressure ◽  
Coronary Blood Flow ◽  
Mean Arterial Blood Pressure ◽  
Mitral Insufficiency ◽  
Arterial Blood

Effect of Arteriovenous Fistula on Mean Arterial Blood Pressure, Coronary Blood Flow, Cardiac Output, Oxygen Consumption, Work and Efficiency

1958 ◽  
Vol 193 (1) ◽  
pp. 147-150 ◽  
Author(s):  
René Wégria ◽  
J. Nakano ◽  
J. C. McGiff ◽  
D. F. Rochester ◽  
M. R. Blumenthal ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Arterial Blood Pressure ◽  
Coronary Blood Flow ◽  
Mean Arterial Blood Pressure ◽  
Arteriovenous Fistulae ◽  
Arterial Blood ◽  
The Mean

In the anesthetized dog, acute arteriovenous fistulae sufficient to increase the cardiac output by from 16 to 130% resulted in an increase in the coronary blood flow even in the presence of a definite and even marked drop in the mean arterial blood pressure. The arteriovenous fistulae also resulted in an increase of the cardiac work and oxygen consumption as well as the cardiac efficiency.

EFFECT OF AURICULAR FIBRILLATION ON CARDIAC OUTPUT, CORONARY BLOOD FLOW AND MEAN ARTERIAL BLOOD PRESSURE

1950 ◽  
Vol 163 (1) ◽  
pp. 135-140 ◽  
Author(s):  
René Wégria ◽  
Charles W. Frank ◽  
George A. Misrahy ◽  
Robert S. Sioussat ◽  
Leonard S. Sommer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Coronary Blood Flow ◽  
Mean Arterial Blood Pressure ◽  
Arterial Blood

Cardiovascular Hemodynamics Consequence to Crossed Circulation in the Dog

1958 ◽  
Vol 192 (2) ◽  
pp. 345-352 ◽  
Author(s):  
W. J. Roberson ◽  
Steven M. Horvath
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Carotid Artery ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Arterial Blood ◽  
The Mean

Twelve experiments were conducted on anesthetized and paired dogs of similar weights subjected to unimpeded, unregulated crossed circulation. Shunts were made between the carotid arteries and external jugular veins and free flow allowed for 60 minutes or longer. Statistically significant changes occurred in the mean femoral arterial blood pressures, carotid shunt blood flow, heart rate, cardiac output, cardiac work, percentage of cardiac output flowing through the shunt and pulmonary systolic and diastolic pressures of one or both animals from their control values. The mean arterial blood pressure remained at control levels for several minutes and then dropped precipitously to hypotensive levels. The lowest mean pressures between 42 and 49 mm Hg occurred within the first 16.5 minutes of the open shunt phase with a gradual return toward control levels. The volume of blood flowing through the shunt was increased initially 250% above the control carotid blood flow, followed by a reduction in flow after 15 minutes; the volume flow at this moment was still double precross circulation levels. A secondary increase in the shunt blood flow occurred throughout the remainder of the open shunt phase. In general, the heart rates and peripheral vascular resistance were slightly elevated during the open shunt phase while cardiac output and work decreased below their control values. A marked and similar increase in the percentage of the cardiac output flowing through the carotid artery was observed in both animals. During the 60 minutes of the recovery period mean arterial blood pressure, cardiac output and work tended to return to control levels while the carotid artery blood flow and pulmonary systolic and diastolic pressure remained slightly below their control values.

Cyclooxygenase inhibition potentiates the renal vascular response to endothelin-1 in humans

1998 ◽  
Vol 85 (5) ◽  
pp. 1661-1666 ◽  
Author(s):  
Gunvor Ahlborg ◽  
Jan M. Lundberg
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Splanchnic Blood Flow ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Glucose Output ◽  
Renal Vascular

Vascular endothelin-receptor stimulation results in vasoconstriction and concomitant production of the vasodilators prostaglandin I2 and nitric oxide. The vascular effects of cyclooxygenase (COx) blockade (diclofenac intravenously) and the subsequent vasoconstrictor response to endothelin-1 (ET-1) infusion 30 min after diclofenac were studied in healthy men. With COx blockade, cardiac output (7%) and splanchnic (14%) and renal (12%) blood flows fell (all P < 0.001). Splanchnic blood flow returned to basal value within 30 min. Mean arterial blood pressure increased (4%, P < 0.001). Splanchnic glucose output fell (22%, P < 0.01). Subsequent ET-1 infusion caused, compared with previous ET-1 infusion without COx blockade (G. Ahlborg, E. Weitzberg, and J. M. Lundberg. J. Appl. Physiol. 77: 121–126, 1994; E. Weitzberg, G. Ahlborg, and J. M. Lundberg. Biochem. Biophys. Res. Commun. 180: 1298–1303, 1991; E. Weitzberg, G. Ahlborg, and J. M. Lundberg. Clin. Physiol. ( Colch.) 13: 653–662, 1993), the same increase in mean arterial blood pressure (4%), decreases in cardiac output (13%) and splanchnic blood flow (38%), but no significant change in splanchnic glucose output. Renal blood flow reduction was potentiated (33 ± 3 vs. 23 ± 2%, P < 0.02), with a total reduction corresponding to 43 ± 3% ( P < 0.01 vs. 23 ± 3%). We conclude that COx inhibition induces renal and splanchnic vasoconstriction. The selectively increased renal vascular responsiveness to ET-1 emphasizes the importance of endogenous arachidonic acid metabolites (i.e., prostaglandin I2) to counteract ET-1-mediated renal vasoconstriction.

Effect of the Ace Inhibitor Ceronapril on Cerebral Blood flow in Hypertensive Patients

1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diastolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Combined Therapy ◽  
Arterial Blood

Objective To assess the effect of the angiotensin-converting enzyme inhibitor ceronapril on cerebral blood flow (CBF) in patients with moderate hypertension. Design Patients received chlorthalidone 25 mg for 4 weeks, and if diastolic blood pressure remained in the range of 100–115 mm Hg, they were given titrated doses of ceronapril (10–40 mg/d based on blood pressure response) in addition to chlorthalidone for 9 weeks. Setting Outpatient research clinic. Subjects Eligible patients had moderate essential hypertension (diastolic blood pressure 100–115 mm Hg) assessed when the patients were receiving no medications. Thirteen patients were entered into the study; 1 withdrew for reasons unrelated to the study drug. Twelve patients (11 men, 1 woman; mean age 52 y) completed the study. Intervention Ceronapril, given with chlorthalidone. Main Outcome Measures CBF measurements were taken at the start and end of ceronapril therapy using intravenous 133Xe; blood pressures were determined weekly. Results Mean arterial blood pressure decreased from 130 ± 4 to 120 ±7 mm Hg after 4 weeks of chlorthalidone administration, and fell further to 108 ± 8 mm Hg after an additional 9 weeks of combined chlorthalidone-ceronapril therapy (p < 0.05). CBF fell from 44 ± 15 to 34 ± 5 mL/min/100 g during the 9 weeks of combined therapy (p = 0.05). No adverse effects consistent with decreased CBF were observed. The decrease in CBF was not linearly correlated with the change in systemic blood pressure, but was strongly correlated (r = –0.937; p < 0.001) with the initial CBF. Conclusions The decrease in mean arterial blood pressure was not associated with a decrease in CBF. Patients with high CBF may be predisposed to a decrease in CBF when treated with ceronapril and chlorthalidone.

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

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