scholarly journals Effects of bradykinin on venous capacitance in health and treated chronic heart failure

2009 ◽  
Vol 116 (5) ◽  
pp. 443-450 ◽  
Author(s):  
Prasad Gunaruwan ◽  
Abdul Maher ◽  
Lynne Williams ◽  
James Sharman ◽  
Matthias Schmitt ◽  
...  

In the present study, we investigated the effects of basal and intra-arterial infusion of bradykinin on unstressed forearm vascular volume (a measure of venous tone) and blood flow in healthy volunteers (n=20) and in chronic heart failure patients treated with ACEIs [ACE (angiotensin-converting enzyme) inhibitors] (n=16) and ARBs (angiotensin receptor blockers) (n=14). We used radionuclide plethysmography to examine the effects of bradykinin and of the bradykinin antagonists B9340 [B1 (type 1)/B2 (type 2) receptor antagonist] and HOE140 (B2 antagonist). Bradykinin infusion increased unstressed forearm vascular volume in a similar dose-dependent manner in healthy volunteers and ARB-treated CHF patients (healthy volunteers maximum 12.3±2.1%, P<0.001 compared with baseline; ARB-treated CHF patients maximum 9.3±3.3%, P<0.05 compared with baseline; P=not significant for difference between groups), but the increase in unstressed volume in ACEI-treated CHF patients was higher (maximum 28.8±7.8%, P<0.001 compared with baseline; P<0.05 for the difference between groups). In contrast, while the increase in blood flow in healthy volunteers (maximum 362±9%, P<0.001) and in ACEI-treated CHF patients (maximum 376±12%, P<0.001) was similar (P=not significant for the difference between groups), the increase in ARB-treated CHF patients was less (maximum 335±7%, P<0.001; P<0.05 for the difference between groups). Infusion of each receptor antagonist alone similarly reduced basal unstressed volume and blood flow in ACEI-treated CHF patients, but not in healthy volunteers or ARB-treated CHF patients. In conclusion, bradykinin does not contribute to basal venous tone in health, but in ACEI-treated chronic heart failure it does. In ARB-treated heart failure, venous responses to bradykinin are preserved but arterial responses are reduced compared with healthy controls. Bradykinin-mediated vascular responses in both health and heart failure are mediated by the B2, rather than the B1, receptor.


2006 ◽  
Vol 38 (Supplement) ◽  
pp. S326
Author(s):  
Jeremy A. Patterson ◽  
Steve E. Selig ◽  
Michael Rogers


2021 ◽  
Vol 14 (3) ◽  
Author(s):  
K Gulyamova ◽  
D Alimov

The aim of the study. To study the features of hepatoportal hemodynamics in patients with acute decompensated heart failure.Material and methods. The study included 138 patients with chronic heart failure admitted to the RRCEM due to the development of acute decompensation of heart failure. The average age of the patients was 66.02 ± 10.41 years. As a control group, the study included 20 healthy volunteers of the corresponding age. During hospitalization, all patients were assessed for the structural and functional state of the left and right heart, as well as the characteristics of the hepatic and pulmonary blood flow.Results. In patients with acute decompensation of heart failure, the hepatic artery was characterized by an increase in its diameter (p <0.001), the resistance index significantly exceeded the indicator recorded in healthy volunteers (p <0.001), which reflects the presence of portal hypertension. The study of hemodynamics in the portal vein revealed an increase in the diameter of the vein (p <0.05) and an acceleration of the volumetric blood flow velocity (p <0.001). At the same time, the pulsation index was increased (p <0.001), which is typical for a change in the flow profile against the background of right ventricular chronic heart failure. Signs of portal hypertension were recorded in the study of blood flow in the splenic artery: its diameter, linear and volumetric blood flow velocity were increased (p <0.001 for artery diameter and volumetric blood flow velocity and p <0.01 for linear blood flow velocity).Conclusion. In patients with acute decompensated heart failure, in addition to impaired systolic function of the left ventricle, there is a significant violation of hepatoportal hemodynamics with the development of portal hypertension, a decrease in arterial hepatic blood flow and obstruction of hepatic venous outflow with signs of fibrotic changes in the hepatic parenchyma. The degree of change increases with a decrease in the left ventricular ejection fraction.



2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.



Heart ◽  
1997 ◽  
Vol 78 (5) ◽  
pp. 437-443 ◽  
Author(s):  
M. Ohtsubo ◽  
K. Yonezawa ◽  
H. Nishijima ◽  
K. Okita ◽  
A. Hanada ◽  
...  


1995 ◽  
Vol 88 (s32) ◽  
pp. 18P-18P
Author(s):  
TP Chua ◽  
S McKinlay ◽  
M Volterrani ◽  
J Toman ◽  
AJS Coats


2003 ◽  
Vol 95 (3) ◽  
pp. 1055-1062 ◽  
Author(s):  
Troy E. Richardson ◽  
Casey A. Kindig ◽  
Timothy I. Musch ◽  
David C. Poole

Chronic heart failure (CHF) reduces muscle blood flow at rest and during exercise and impairs muscle function. Using intravital microscopy techniques, we tested the hypothesis that the speed and amplitude of the capillary red blood cell (RBC) velocity ( VRBC) and flux (FRBC) response to contractions would be reduced in CHF compared with control (C) spinotrapezius muscle. The proportion of capillaries supporting continuous RBC flow was less ( P < 0.05) in CHF (0.66 ± 0.04) compared with C (0.84 ± 0.01) muscle at rest and was not significantly altered with contractions. At rest, VRBC (C, 270 ± 62; CHF, 179 ± 14 μm/s) and FRBC (C, 22.4 ± 5.5 vs. CHF, 15.2 ± 1.2 RBCs/s) were reduced (both P < 0.05) in CHF vs. C muscle. Contractions significantly (both P < 0.05) elevated VRBC (C, 428 ± 47 vs. CHF, 222 ± 15 μm/s) and FRBC (C, 44.3 ± 5.5 vs. CHF, 24.0 ± 1.2 RBCs/s) in C and CHF muscle; however, both remained significantly lower in CHF than C. The time to 50% of the final response was slowed (both P < 0.05) in CHF compared with C for both VRBC (C, 8 ± 4; CHF, 56 ± 11 s) and FRBC (C, 11 ± 3; CHF, 65 ± 11 s). Capillary hematocrit increased with contractions in C and CHF muscle but was not different ( P > 0.05) between CHF and C. Thus CHF impairs diffusive and conductive O2 delivery across the rest-to-contractions transition in rat skeletal muscle, which may help explain the slowed O2 uptake on-kinetics manifested in CHF patients at exercise onset.



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