Impact of Systemic Blood Pressure on the Relationship between Intraocular Pressure and Blood Flow in the Optic Nerve Head of Nonhuman Primates

2009 ◽  
Vol 50 (5) ◽  
pp. 2154 ◽  
Author(s):  
Yi Liang ◽  
J. Crawford Downs ◽  
Brad Fortune ◽  
Grant Cull ◽  
George A. Cioffi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intraocular Pressure ◽  
Optic Nerve ◽  
Optic Nerve Head ◽  
Nonhuman Primates ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
The Relationship

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.

scholarly journals The Impact of Intraocular Pressure Elevation on Optic Nerve Head and Choroidal Blood Flow

2018 ◽  
Vol 59 (8) ◽  
pp. 3488 ◽  
Author(s):  
Naoki Kiyota ◽  
Yukihiro Shiga ◽  
Kohei Ichinohasama ◽  
Masayuki Yasuda ◽  
Naoko Aizawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intraocular Pressure ◽  
Optic Nerve ◽  
Optic Nerve Head ◽  
Choroidal Blood Flow ◽  
Pressure Elevation ◽  
Intraocular Pressure Elevation ◽  
The Impact

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

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
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.

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

2012 ◽  
Vol 150 (1-3) ◽  
pp. 285-290 ◽  
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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