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Published on: August 1, 2018
Platelet cytosolic calcium, peripheral hemodynamics, and vasodilatory peptides in liver cirrhosis
F Rodríguez-Pérez1, C M Isales, R J Groszmann
1Section of Digestive Diseases, West Haven Veterans Affairs Medical Center, Yale University School of Medicine, Connecticut.
Insights
Cirrhotic patients exhibit significantly lower platelet calcium levels, which correlate with altered blood pressure and blood flow. This suggests platelets may help understand vasodilation in chronic liver disease.
Area of Science:
- Cardiovascular Physiology
- Hepatology
- Hematology
Background:
- Platelet cytosolic calcium concentration ([Ca2+]i) is a potential indicator of vascular smooth muscle cell changes.
- Investigating platelet [Ca2+]i in cirrhosis is crucial for understanding associated hemodynamic alterations.
Purpose of the Study:
- To determine if platelet [Ca2+]i is altered in patients with cirrhosis.
- To examine the relationship between platelet [Ca2+]i, peripheral hemodynamics, and specific peptide levels in cirrhosis.
Main Methods:
- Compared platelet [Ca2+]i, glucagon, substance P (SP), and vasoactive intestinal peptide (VIP) levels in 14 cirrhotic patients and 11 healthy controls.
- Measured mean arterial pressure (MAP), forearm blood flow (FBF), and calculated forearm vascular resistance (FVR).
Main Results:
- Cirrhotic patients showed significantly lower platelet [Ca2+]i (50.1 vs. 73.0 nmol/L) and higher glucagon levels.
- MAP and FVR were significantly reduced in cirrhotic patients compared to controls.
- Platelet [Ca2+]i strongly correlated with MAP (r=0.81), FVR (r=0.87), and diastolic blood pressure (r=0.78) in cirrhotic patients.
Conclusions:
- Cirrhosis is associated with a marked reduction in platelet [Ca2+]i.
- The decreased platelet [Ca2+]i in cirrhosis is linked to peripheral hemodynamic changes.
- Platelets may serve as a valuable biomarker for studying vasodilation mechanisms in chronic liver disease.
Background:
Platelet cytosolic calcium concentration ([Ca2+]i) has been proposed to reflect changes in vascular smooth muscle cells. This study investigated if the platelet [Ca2+]i is altered in cirrhotic patients and determined its relationship with peripheral hemodynamics and peptide levels.
Methods:
Fourteen patients with cirrhosis and 11 healthy, age- and sex-matched controls had blood samples taken for determining platelet [Ca2+]i and glucagon, substance P (SP), and vasoactive intestinal peptide (VIP) values. Mean arterial pressure (MAP) and forearm blood flow (FBF) were measured on the same day of blood sampling. Forearm vascular resistance (FVR) was calculated.
Results:
Patients with cirrhosis had lower platelet [Ca2+]i (50.1 +/- 2 vs. 73.0 +/- 5 nmol/L; P < 0.001) than normal controls. Glucagon levels were significantly higher in patients with cirrhosis, but there was no difference in SP or VIP levels in both groups. MAP (80.5 +/- 3 vs. 94.7 +/- 3; P < 0.005) and FVR (20.1 +/- 1 vs. 36.3 +/- 2; P < 0.001) were significantly lower in patients with cirrhosis. A significant correlation was observed between platelet [Ca2+]i and MAP in patients with cirrhosis (r = 0.81; P < 0.001), between platelet [Ca2+]i and FVR (r = 0.87; P < 0.001), and between platelet [Ca2+]i and diastolic blood pressure (r = 0.78; P < 0.001). No correlation was found between platelet [Ca2+]i and peptide levels.
Conclusions:
Patients with cirrhosis have a significant reduction in the platelet [Ca2+]i. This finding correlates well with peripheral hemodynamics. Platelets may be a useful tool to study the etiologic mechanisms leading to the vasodilation of chronic liver disease.
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