Hepato‐splanchnic circulatory stress: An important effect of hemodialysis

2019 ◽  
Vol 32 (3) ◽  
pp. 237-242 ◽  
Author(s):  
Claire J. Grant ◽  
Shih‐Han S. Huang ◽  
Chris W. McIntyre
Keyword(s):  
Circulatory Stress

Reduced venous compliance in lower limbs of aging humans and its importance for capacitance function

1998 ◽  
Vol 275 (3) ◽  
pp. H878-H886 ◽  
Author(s):  
Henrik Olsen ◽  
Toste Länne
Keyword(s):  
Muscle Tissue ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Subcutaneous Tissue ◽  
Lower Limbs ◽  
Venous Compliance ◽  
Reduced Pressure ◽  
Pressure Transmission ◽  
Circulatory Stress ◽  
Capacitance Response

Venous compliance in the calf of humans and its importance for capacitance function in relation to age were studied with the aid of 22, 44, and 59 mmHg lower body negative pressure (LBNP). Negative pressure transmission to the calf as well as changes in calf volume were studied, and venous compliance was calculated [change in volume with pressure change (dV/dP)]. The change in capacitance response of the calf with age (20–70 yr) was evaluated during LBNP 44 mmHg. Transmission of negative pressure to the subcutaneous tissue was almost full without any changes with age (92%). However, it was reduced to 80% in the underlying muscle tissue, irrespective of depth. Venous compliance in the young was 0.051 ml ⋅ 100 ml−1 ⋅ mmHg−1and was reduced by 45% to 0.029 ml ⋅ 100 ml−1 ⋅ mmHg−1in the old ( P < 0.05). Accordingly, the capacitance response was reduced by 0.015 ml ⋅ 100 ml−1 ⋅ yr−1( P < 0.005). Furthermore, the hemodynamic response to hypovolemic circulatory stress was attenuated with age. The reduced pressure transmission in muscle tissue is probably due to restriction of the muscle fascia envelope. The reduced venous compliance with age and the concomitant reduction in capacitance response during LBNP have implications for both the sympathetic reflex responses as well as the capacitance response during acute hypovolemic circulatory stress, which might be defected in aging humans.

EFFECT OF AGE AND CORONARY HEART DISEASE ON AUTONOMIC RESPONSES TO CIRCULATORY STRESS

1981 ◽  
pp. 357-365
Author(s):  
James J. Smith ◽  
Thomas J. Ebert ◽  
Felix E. Tristani ◽  
Carol J. Porth ◽  
William J. Stekiel ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Autonomic Responses ◽  
Circulatory Stress ◽  
Effect Of Age

Cell specific response of cardiac poly ADP-R and DNA synthesis to circulatory stress

1982 ◽  
Vol 38 (9) ◽  
pp. 1068-1069 ◽  
Author(s):  
G. Jackowski ◽  
M. A. Heymann ◽  
A. M. Rudolph ◽  
E. Kun
Keyword(s):  
Dna Synthesis ◽  
Specific Response ◽  
Circulatory Stress

scholarly journals Renal Perfusion during Hemodialysis: Intradialytic Blood Flow Decline and Effects of Dialysate Cooling

2019 ◽  
Vol 30 (6) ◽  
pp. 1086-1095 ◽  
Author(s):  
Raanan Marants ◽  
Elena Qirjazi ◽  
Claire J. Grant ◽  
Ting-Yim Lee ◽  
Christopher W. McIntyre
Keyword(s):  
Myocardial Stunning ◽  
Statistical Significance ◽  
Ischemic Injury ◽  
Residual Renal Function ◽  
Renal Perfusion ◽  
Circulatory Stress ◽  
The Brain ◽  
Perfusion Maps ◽  
Renal Computed Tomography

BackgroundResidual renal function (RRF) confers survival in patients with ESRD but declines after initiating hemodialysis. Previous research shows that dialysate cooling reduces hemodialysis-induced circulatory stress and protects the brain and heart from ischemic injury. Whether hemodialysis-induced circulatory stress affects renal perfusion, and if it can be ameliorated with dialysate cooling to potentially reduce RRF loss, is unknown.MethodsWe used renal computed tomography perfusion imaging to scan 29 patients undergoing continuous dialysis under standard (36.5°C dialysate temperature) conditions; we also scanned another 15 patients under both standard and cooled (35.0°C) conditions. Imaging was performed immediately before, 3 hours into, and 15 minutes after hemodialysis sessions. We used perfusion maps to quantify renal perfusion. To provide a reference to another organ vulnerable to hemodialysis-induced ischemic injury, we also used echocardiography to assess intradialytic myocardial stunning.ResultsDuring standard hemodialysis, renal perfusion decreased 18.4% (P<0.005) and correlated with myocardial injury (r=−0.33; P<0.05). During sessions with dialysis cooling, patients experienced a 10.6% decrease in perfusion (not significantly different from the decline with standard hemodialysis), and ten of the 15 patients showed improved or no effect on myocardial stunning.ConclusionsThis study shows an acute decrease in renal perfusion during hemodialysis, a first step toward pathophysiologic characterization of hemodialysis-mediated RRF decline. Dialysate cooling ameliorated this decline but this effect did not reach statistical significance. Further study is needed to explore the potential of dialysate cooling as a therapeutic approach to slow RRF decline.

Recurrent Circulatory Stress: The Dark Side of Dialysis

2010 ◽  
Vol 23 (5) ◽  
pp. 449-451 ◽  
Author(s):  
Christopher W. McIntyre
Keyword(s):  
Dark Side ◽  
Circulatory Stress

scholarly journals Left Ventricular Systolic Time Intervals as Indices of Postural Circulatory Stress in Man

Circulation ◽  
1970 ◽  
Vol 41 (3) ◽  
pp. 485-492 ◽  
Author(s):  
R. W. STAFFORD ◽  
W. S. HARRIS ◽  
A. M. WEISSLER
Keyword(s):  
Systolic Time Intervals ◽  
Left Ventricular ◽  
Time Intervals ◽  
Systolic Time ◽  
Circulatory Stress

Renin response and angiotensinogen control during graded hemorrhage and shock in the dog

1976 ◽  
Vol 231 (4) ◽  
pp. 1300-1307 ◽  
Author(s):  
O Beaty ◽  
CH Sloop ◽  
Schmid HE ◽  
Buckalew VM
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin ◽  
Renin Activity ◽  
Elevated Plasma ◽  
Renin Substrate ◽  
Hemorrhagic Hypotension ◽  
Shock Phase ◽  
Circulatory Stress ◽  
The Relationship

Hemorrhage and hemorrhagic hypotension have been shown to be potent stimulators of renin release. However, the relationship between angiotensinogen consumption and angiotensinogen production has yet to be completely defined during this type of circulatory stress. Peripheral renin activity increased progressively as the blood pressure was decreased stepwise by hemorrhage to 50 mmHg and remained elevated throughout the shock phase of the experiment. Angiotensinogen did not change from control (809 ng/ml) throughout hemorrhabic hypotension and shock. During hemorrhagic hypotension, with the infusion of the angiotensin antagonist, [1-sarcosine, 8-alanine]angiotensin II, angiotensinogen concentration fell progressively from 693 to 208 ng/ml at 50 mmHg. Intravenous angiotensin II infused continuously after the mean blood pressure reached 50 mmHg significantly elevated plasma angiotensinogen concentration. In conclusion, during hemorrhagic hypotension and shock, the kidney and the liver appeared capable of maintaining elevated plasma renin activity and adequate plasma renin substrate, angiotensinogen, respectively. The mechanism responsible for the maintenance of plasma angiotensinogen is suggested to involve a positive-feedback effect of angiotensin II on the liver.

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