title: Platelet cytosolic calcium, peripheral hemodynamics, and vasodilatory peptides in liver cirrhosis.
abstract: 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.
authors.affiliation: Section of Digestive Diseases, West Haven Veterans Affairs Medical Center, Yale University School of Medicine, Connecticut.
authors.forename: F
authors.initials: F
authors.lastname: Rodríguez-Pérez
authors.forename: C M
authors.initials: CM
authors.lastname: Isales
authors.forename: R J
authors.initials: RJ
authors.lastname: Groszmann
mesh_terms: D000328:Adult; D000368:Aged; D001792:Blood Platelets / Q000737:chemistry* / Q000166:cytology / Q000648:ultrastructure; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000097:blood* / Q000502:physiology; D003600:Cytosol / Q000737:chemistry* / Q000648:ultrastructure; D005934:Glucagon / Q000097:blood* / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008099:Liver / Q000473:pathology / Q000503:physiopathology*; D008103:Liver Cirrhosis / Q000097:blood* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000502:physiology; D013373:Substance P / Q000097:blood* / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D014660:Vasoactive Intestinal Peptide / Q000097:blood* / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D005934:Glucagon; D002118:Calcium