title: Microvascular filtration is increased in the forearms of patients with breast cancer-related lymphedema.
abstract: Breast cancer-related lymphedema (BCRL) is a frequent and debilitating complication of breast cancer treatment. The pathophysiology is complex and remains poorly understood; however, data suggest that changes in the peripheral circulation may contribute to edema formation. In 13 volunteers with unilateral BCRL, the following aspects of upper extremity peripheral circulation were examined: muscle relative microvascular volume; capillary filtration coefficient; central and local sympathetic vascular reflexes; skin blood flow; and forearm blood flow. These were studied via real-time, contrast-enhanced ultrasound; venous occlusion strain-gauge plethysmography; lower-body negative pressure; noninvasive blood pressure measurements; and skin (99m)Tc-pertechnetate clearance technique. Measurements were performed bilaterally and simultaneously in the forearms, enabling use of the nonedematous forearm as a control. Capillary filtration coefficients were additionally measured in healthy, age-matched controls. The capillary filtration coefficient was 7.98 ± 2.52 μl·100 ml(-1)·mmHg(-1)·min(-1) (mean ± SD) in edematous forearms and 6.09 ± 1.83 μl·100ml·(-1)·mmHg(-1)·min(-1) in nonedematous forearms in the patient group (P < 0.001). The capillary filtration coefficient was 3.32 ± 1.17 μl·100ml(-1)·mmHg(-1)·min(-1) in the forearms of healthy controls; significantly less than the both the edematous and nonedematous forearms of the patient group (P < 0.001). No significant differences were found in muscle relative microvascular volume, forearm blood flow, skin blood flow, or central or local sympathetic vascular reflexes. Forearm microvascular filtration is increased in patients with BCRL, and more so in the edematous arm. The vascular sympathetic control mechanisms seem to be preserved. We propose that the increased capillary permeability may be due to low-grade inflammation promoted by reduced clearance of inflammatory mediators.
authors.affiliation: Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital, University Hospital of Copenhagen, Copenhagen, Denmark. mjen0221@bbh.regionh.dk
authors.forename: Mads Radmer
authors.initials: MR
authors.lastname: Jensen
authors.forename: Lene
authors.initials: L
authors.lastname: Simonsen
authors.forename: Tonny
authors.initials: T
authors.lastname: Karlsmark
authors.forename: Jens
authors.initials: J
authors.lastname: Bülow
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D001943:Breast Neoplasms / Q000737:chemistry / Q000503:physiopathology*; D002196:Capillaries / Q000503:physiopathology; D002199:Capillary Permeability / Q000502:physiology; D005260:Female; D005542:Forearm / Q000098:blood supply* / Q000503:physiopathology; D006801:Humans; D008209:Lymphedema / Q000139:chemically induced / Q000503:physiopathology*; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D009132:Muscles / Q000098:blood supply / Q000503:physiopathology; D012018:Reflex / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012867:Skin / Q000503:physiopathology