Effects of midodrine on exercise-induced hypotension and blood pressure recovery in autonomic failure

2004 ◽  
Vol 97 (5) ◽  
pp. 1978-1984 ◽  
Author(s):  
William G. Schrage ◽  
John H. Eisenach ◽  
Frank A. Dinenno ◽  
Shelly K. Roberts ◽  
Christopher P. Johnson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Autonomic Failure ◽  
Peripheral Resistance ◽  
Venous Occlusion ◽  
Open Circuit ◽  
Induced Hypotension ◽  
Calf Exercise ◽  
Exercise Induced ◽  
Similar Peak

We tested the hypothesis that the oral α1-adrenergic agonist, midodrine, would limit the fall in arterial pressure observed during exercise in patients with pure autonomic failure (PAF). Fourteen subjects with PAF underwent a stand test, incremental supine cycling exercise (25, 50, and 75 W), and ischemic calf exercise, before (control) and 1 h after ingesting 10 mg midodrine. Heart rate (ECG), beat-to-beat blood pressure (MAP, arterial catheter), cardiac output (Q̇, open-circuit acetylene breathing), forearm blood flow (FBF, Doppler ultrasound), and calf blood flow (CBF, venous occlusion plethysmography) were measured. The fall in MAP after standing for 2 min was similar (∼60 mmHg; P = 0.62). Supine MAP immediately before cycling was greater after midodrine (124 ± 6 vs 117 ± 6 mmHg; P < 0.03), but cycling caused a workload-dependent hypotension ( P < 0.001), whereas increases in Q̇ were modest but similar. Midodrine increased MAP and total peripheral resistance (TPR) during exercise ( P < 0.04), but the exercise-induced fall in MAP and TPR were similar during control and midodrine ( P = 0.27 and 0.14). FBF during cycling was not significantly reduced by midodrine ( P > 0.2). By contrast, recovery of MAP after cycling was faster ( P < 0.04) after midodrine (∼25 mmHg higher after 5 min). Ischemic calf exercise evoked similar peak CBF in both trials, but midodrine reduced the hyperemic response over 5 min of recovery ( P < 0.02). We conclude midodrine improves blood pressure and TPR during exercise and dramatically improves the recovery of MAP after exercise.

Effect of the Somatostatin Analogue, Octreotide, on Exercise-Induced Hypotension in Human Subjects with Chronic Sympathetic Failure

1995 ◽  
Vol 89 (4) ◽  
pp. 367-373 ◽  
Author(s):  
G. D. P. Smith ◽  
M. Alam ◽  
L. P. Watson ◽  
C. J. Mathias
Keyword(s):  
Blood Pressure ◽  
Postural Hypotension ◽  
Autonomic Failure ◽  
Somatostatin Analogue ◽  
Induced Hypotension ◽  
Post Exercise ◽  
Blood Pressure Fall ◽  
Before And After ◽  
Exercise Induced ◽  
Pressure Fall

1. In autonomic failure, supine exercise lowers blood pressure and worsens postural hypotension. The somatostatin analogue, octreotide, reduces postprandial and postural hypotension, but its effects on exercise-induced hypotension and on postural hypotension post-exercise are unknown. 2. Eighteen subjects with chronic sympathetic denervation were studied; 12 had pure autonomic failure and six had additional neurological features of the Shy—Drager syndrome. Haemodynamic, hormonal and biochemical changes were measured before, during and after incremental supine leg exercise on two occasions: on no treatment and after subcutaneous octreotide. Exercise was performed 120 min after octreotide in eight subjects and 60 min after octreotide in ten subjects. 3. Octreotide did not improve exercise-induced hypotension; the blood pressure fall was greater during exercise, but the blood pressure level was no different than without treatment. Heart rate, stroke distance, cardiac index and systemic vascular resistance were similar at rest and changed to the same degree with exercise on and off octreotide. After octreotide, resting levels of serum growth hormone, plasma noradrenaline, adrenaline and renin were unchanged, but glucose was higher and insulin was lower. There was no change in biochemical and hormone levels during exercise either off or on octreotide. 4. After octreotide, although the rate of blood pressure recovery was similar post-exercise, the levels of blood pressure were higher than in the non-treatment phase and postural hypotension was improved before and after exercise. 5. In conclusion, in primary autonomic failure, octreotide did not improve exercise-induced hypotension in the supine position, suggesting that octreotide-sensitive vasodilatory peptides do not contribute to the blood pressure fall. With octreotide, supine blood pressure levels were higher post-exercise and postural hypotension was improved both before and after exercise.

Central and peripheral haemodynamic effects of hyperglycaemia, hyperinsulinaemia, hyperlipidaemia or a mixed meal

2003 ◽  
Vol 105 (6) ◽  
pp. 715-721 ◽  
Author(s):  
Andreas FUGMANN ◽  
Jonas MILLGÅRD ◽  
Mahziar SARABI ◽  
Christian BERNE ◽  
Lars LIND
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Venous Occlusion ◽  
Mixed Meal ◽  
Hyperglycaemic Clamp ◽  
Calf Blood Flow ◽  
Haemodynamic Changes

The aim of the present study was to evaluate the haemodynamic changes during hyperinsulinaemia, hyperglycaemia or hypertriglyceridaemia in relation to those following a mixed meal. Ten subjects were subjected to hypertriglyceridaemia (3.9 mmol/l) for 2 h by an infusion of Intralipid® and heparin. Nine subjects received a hyperglycaemic clamp (12.5 mmol/l) with octreotide and low-dose insulin infusion to maintain normoinsulinaemia (10 m-units/l). Ten subjects received saline for 2 h as a control and, thereafter, 2 h of normoglycaemic hyperinsulinaemic clamp (80 m-units/l). Finally, ten subjects were evaluated for 2 h following an ordinary mixed meal. Calf blood flow was measured by venous occlusion plethysmography and cardiac index by thoracic bioimpedance. Both the mixed meal and normoglycaemic hyperinsulinaemia lowered total peripheral resistance, and increased calf blood flow and cardiac index, whereas blood pressure decreased (P<0.05-0.001). Both hyperglycaemia and hypertriglyceridaemia increased calf blood flow, but blood pressure was unchanged. Total peripheral resistance was unchanged in hypertriglyceridaemia, whereas hyperglycaemia induced a significant increase. Normoglycaemic hyperinsulinaemia induced a haemodynamic pattern similar, but to a lesser extent, to the pattern seen following a mixed meal. Hyperinsulinaemia seems to be a major mediator of the haemodynamic response, but other factors are obviously also of great importance. Hypertriglyceridaemia and hyperglycaemia induced haemodynamic responses that are not similar to those seen following a mixed meal.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

Abstract P222: Venous Dilation Contributes to 5-HT-induced Hypotension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Imaging System ◽  
Isometric Force ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Mesenteric Arteries ◽  
Conscious Rat ◽  
Cross Sectional ◽  
Induced Hypotension ◽  
Vascular Bed

Serotonin (5-hydroxytryptamine, 5-HT) infusion in a normal conscious rat decreases mean arterial pressure (MAP), in part by reduction in total peripheral resistance. Microsphere experiments have shown 5-HT increases blood flow within the splanchnic vascular bed, with the greatest being in the intestine and spleen. Interestingly, 5-HT does not cause a direct relaxation of resistant (small or large) mesenteric arteries. The present study addresses the possibility of the venous circulation contributing to the 5-HT induced fall in blood pressure. Our working hypothesis is venous dilation, specifically dilation of veins measurable within the splanchnic vascular bed, contributes to 5-HT-induced hypotension. Using an ultrasound imaging system (Vevo 2100 imaging system; 21 MHz probe,Visual Sonics Inc.), telemetry-implanted, anesthetized male Sprague Dawley rats underwent cross-sectional imaging which was controlled for respiration and cardiac cycles. The following vessels were imaged: abdominal aorta (AA); portal vein (PV); abdominal inferior vena cava (IVC); and superior mesenteric vein (SMV). Following the collection of baseline MAP and vessel diameter measurements, Alzet osmotic mini-pumps containing vehicle (saline; n=9) or 5-HT (25 ug/kg/min; n=9) were implanted for 1 week. After, 24 hours of infusion, 5-HT increased the vein diameter (SMV 17.48±2%; PV 17.67±2%; IVC 46.87±8%) and maintained the AA diameter ( AA 0.93±1%) from baseline while reducing MAP (vehicle 101.93±3; 5-HT 84.68±2 mm Hg; p<0.05).One-week post removal of all osmotic mini-pumps, there was no difference in the MAP or diameter of all noted vessels between the two treatment groups. To correlate with in vivo findings, the PV and IVC, when isolated in a tissue bath for measurement of isometric force and contracted with endothelin 1, relaxed in a concentration dependent fashion to 5-HT and 5-carboxamidotryptamine (5-HT 1/7 receptor agonist;1 nM-10 uM). Collectively, these findings highlight the contribution of splanchnic venous dilation in 5-HT-induced hypotension and propose a possible mechanism for 5-HT reduction in blood pressure.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Circulatory effects of acute or chronic endotoxemia in rats

1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee
Keyword(s):  
Escherichia Coli ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gastrointestinal Tract ◽  
Peripheral Resistance ◽  
Circulatory Effects ◽  
Arterial Blood ◽  
Flow Changes ◽  
Fractional Distribution

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.

The selective closure of feline carotid arteriovenous anastomoses (AVAs) by GR43175

Cephalalgia ◽  
1989 ◽  
Vol 9 (9_suppl) ◽  
pp. 41-46
Author(s):  
Marion J Perren ◽  
Wasyl Feniuk ◽  
Patrick Pa Humphrey
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Arterial Blood Flow ◽  
Arteriovenous Anastomoses ◽  
Arterial Blood ◽  
Flow Through ◽  
Carotid Arterial ◽  
Dose Dependent

The haemodynamic effects of the selective 5-HT1-like agonist GR43175 have been compared with that of ergotamine in anaesthetized cats. Both GR43175 (30–1000 μg/kg intravenously) and ergotamine (0.3–30 μg/kg intravenously) caused a dose-dependent reduction in the proportion of cardiac output passing through arteriovenous anastomoses (AVAs). However, unlike GR43175, the effect of ergotamine (30 μg/kg intravenously) was associated with marked increases in diastolic blood pressure and total peripheral resistance. In further studies, the effect of GR43175 on the distribution of blood flow within the carotid bed has been examined. GR43175 caused a reduction in total carotid arterial blood flow which was entirely due to a reduction in flow through carotid AVAs. These results demonstrate that GR43175, unlike ergotamine, has a highly selective vasoconstrictor action on AVAs within the cranial circulation of anaesthetized cats. Such a mechanism may be important in its antimigraine activity.

Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Vascular Beds ◽  
Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

Failure of impedance plethysmography to follow exercise-induced changes in limb blood flow

1988 ◽  
Vol 75 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Richard L. Hughson
Keyword(s):  
Blood Flow ◽  
Supine Position ◽  
Venous Occlusion ◽  
Impedance Plethysmography ◽  
Electrode Position ◽  
Limb Blood Flow ◽  
Mean Values ◽  
Leg Exercise ◽  
Exercise Induced ◽  
Induced Changes

1. The blood flow in the forearm and the calf of six healthy volunteers was measured at rest and after exercise by impedance plethysmography using pulsatile (QZp) and venous occlusion (QZocc) methods, and by venous occlusion strain gauge plethysmography (Qsg). 2. At rest, the impedance QZp method gave values slightly higher than those of Qsg. In the forearm, the ratio QZp to Qsg was 1.26 in the supine position and 1.97 in the upright sitting position. For the calf muscle, the ratios were 1.08 in the supine position and 1.23 in the upright position. 3. Immediately after exercise, Qsg increased from resting values of approximately 2–4 ml min−1 100 ml−1 to mean values of 16–25 ml min−1 100 ml−1 in upright and supine arm or leg exercise. In contrast, the QZp values after exercise increased to only 3.1–4.6 ml min−1 100 ml−1. QZocc likewise failed to show increases in flow except in the supine leg exercise, where flow increased to 8.7 ml min−1 100 ml−1. 4. In an additional subject, it was shown that electrode position had no significant effect on the QZp blood flow measurement after exercise. 5. The failure of QZp to accurately follow the change in Qsg with exercise was probably due in part to pulsatile venous outflow. In addition, changes in microvessel packed cell volume and shear rate may influence the observed QZp. It is concluded that impedance plethysmography is not valid for estimation of limb blood flow during reactive hyperaemia after exercise.

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