Effect of systemic blood pressure change produced by noradrenaline on brain blood flow and oxygenation in Neuro-ICU patients

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.

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Directly measuring spinal cord blood flow and spinal cord perfusion pressure via the collateral network: Correlations with changes in systemic blood pressure

Journal of Thoracic and Cardiovascular Surgery ◽

10.1016/j.jtcvs.2014.09.121 ◽

2015 ◽

Vol 149 (1) ◽

pp. 360-366 ◽

Cited By ~ 14

Author(s):

Yuya Kise ◽

Yukio Kuniyoshi ◽

Hitoshi Inafuku ◽

Takaaki Nagano ◽

Tsuneo Hirayasu ◽

...

Keyword(s):

Blood Pressure ◽

Spinal Cord ◽

Blood Flow ◽

Cord Blood ◽

Perfusion Pressure ◽

Systemic Blood Pressure ◽

Spinal Cord Blood Flow ◽

Systemic Blood ◽

Collateral Network

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Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00516.2002 ◽

2003 ◽

Vol 284 (6) ◽

pp. R1580-R1585 ◽

Cited By ~ 16

Author(s):

Susan Kaufman ◽

Jody Levasseur

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Portal Hypertension ◽

Portal Vein ◽

Venous Pressure ◽

Splenic Vein ◽

Systemic Blood Pressure ◽

Portal Venous Pressure ◽

Systemic Blood ◽

Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

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Excessive Zinc Intake Increases Systemic Blood Pressure and Reduces Renal Blood Flow via Kidney Angiotensin II in Rats

Biological Trace Element Research ◽

10.1007/s12011-012-9472-z ◽

2012 ◽

Vol 150 (1-3) ◽

pp. 285-290 ◽

Cited By ~ 13

Author(s):

Miyoko Kasai ◽

Takashi Miyazaki ◽

Tsuneo Takenaka ◽

Hiroyuki Yanagisawa ◽

Hiromichi Suzuki

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Angiotensin Ii ◽

Renal Blood Flow ◽

Systemic Blood Pressure ◽

Systemic Blood ◽

Zinc Intake

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Skeletal muscle vasodilation at the onset of exercise

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.5.1649 ◽

1998 ◽

Vol 85 (5) ◽

pp. 1649-1654 ◽

Cited By ~ 32

Author(s):

John B. Buckwalter ◽

Stephen B. Ruble ◽

Patrick J. Mueller ◽

Philip S. Clifford

Keyword(s):

Blood Pressure ◽

Skeletal Muscle ◽

Blood Flow ◽

Muscarinic Receptors ◽

Treadmill Exercise ◽

Systemic Blood Pressure ◽

Systemic Blood ◽

Iliac Arteries ◽

Blood Flows ◽

Peak Blood

The purpose of this study was to determine whether β-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 μg), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of β-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

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Baroreceptor influence on postural changes in blood pressure and carotid blood flow

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.205.2.360 ◽

1963 ◽

Vol 205 (2) ◽

pp. 360-364 ◽

Cited By ~ 18

Author(s):

Francis L. Abel ◽

John H. Pierce ◽

Warren G. Guntheroth

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Carotid Sinus ◽

Systemic Blood Pressure ◽

Systemic Blood ◽

Carotid Blood Flow ◽

Postural Changes ◽

Nembutal Anesthesia

The effects of 30° head-down and head-up tilting on mean systemic blood pressure, carotid blood flow, and heart rate were studied in 16 dogs under morphine and Nembutal anesthesia. The tilting procedure was further repeated after denervation of the carotid sinus and aortic arch baroreceptors and after administration of a dihydrogenated ergot alkaloid mixture (Hydergine). The results indicate that the drop in pressure in the head-down position is primarily due to baroreceptor activity and that the baroreceptors are necessary for compensatory vasoconstriction on head-up tilting. Carotid blood flow decreased in both tilted positions in the control animals; the possible relationship to cerebral blood flow is discussed.

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