Reduced capillary hydraulic conductivity in skeletal muscle and skin in Type I diabetes: a possible cause for reduced transcapillary fluid absorption during hypovolaemia

Abstract

Patients with Type I (insulin-dependent) diabetes mellitus have a reduced transcapillary fluid absorption from skeletal muscle and skin to blood during hypovolaemic circulatory stress [1]. This fluid shift has been shown to have a major effect on early plasma volume restitution during rapidly started hypovolaemic circulatory stress [2,3]. The fluid absorption is caused by a sympathetic a-mediated and b-mediated decrease in capillary pressure and is enhanced by a concomitant increase in capillary surface area available for fluid transfer [3±5]. The reduction of this beneficial fluid absorption in diabetic patients might lead to reduced tolerance to hypovolaemia with an increased risk for complications in situations such as bleeding, rapid gastrointestinal fluid losses or burn injuries. The possible explanations for the reduced fluid absorption in diabetic patients are a decreased Diabetologia (2000) Abstract Aims/hypothesis. Patients with Type I (insulin-dependent) diabetes mellitus have a reduced transcapillary fluid absorption from skeletal muscle and skin and thus defective plasma volume regulation during hypovolaemia. Our aim was to find whether a defective capillary filtration coefficient or impaired transcapillary driving force are aetiologic factors for this reduction. Methods. We investigated 11 diabetic patients (diabetes duration 6.9 1.1 years, age 26 1 years), without complications and 12 control subjects (26 1 years). Their capillary filtration coefficient was measured in the upper arm using a volumetric technique at rest and during lower body negative pressure (LBNP). We calculated the driving force for transcapillary fluid transfer. Results. The increase in heart rate and the decrease in systolic blood pressure during lower body negative pressure were similar in diabetic and control subjects. The resting capillary filtration coefficient was decreased in the diabetic subjects, 0.033 0.003 vs 0.051 0.007 ml´100 ml ±1´m in ±1´m mHg ±1 (p < 0.05). During lower body negative pressure, the capillary filtration coefficient increased 35 % in both groups compared with resting capillary filtration coefficient and was still decreased in diabetes; 0.046 0.004 compared with 0.069 0.006 ml1 00ml ±1´m in ±1´m mHg ±1 (p < 0.01). The established driving force during lower body negative pressure was 1.37 0.11 vs 1.30 0.15 mmHg (NS) in diabetic and control subjects, respectively. Conclusions/interpretation. Our study indicates that a reduced capillary filtration coefficient rather than defective regulation of transcapillary driving force, is the reason for the reduced transcapillary fluid absorption during hypovolaemic circulatory stress found in Type I diabetic patients. [Diabetologia (2000)

Swelling and pressure-volume relationships in the dermis measured by osmotic-stress technique

“…Cell-controlled pressures of this order of magnitude could mediate compensatory reabsorption during hypovolemic shock by rapidly redirecting interstitial volumes. They would also help to explain the fast rate at which dermal edema fluid accumulates with the cell injury secondary to burns (7,10,12,19). Together, with previous findings on macromolecular reaction kinetics (13,14,21), these results point to future work based on the hypothesis that water potentials in biological media integrate transfer mechanisms across temporal and spatial scales.…”

“…More quantitative data on the nature and relative magnitude of swelling forces (3,9,15,16,18,19) are needed to explain experimental and clinical observations, as well as to develop and evaluate new therapeutic approaches to decrease or to prevent edema (7,12,30,31).…”

Impaired compensatory response to hypovolaemic circulatory stress in type 1 diabetes mellitus

“…Capillary fluid absorption is dependent on both high hydrodynamic conductivity as well as a decline in capillary pressure caused by autonomic reflex adjustments of both α-and β-adrenergic receptors, affecting the pre-to post-capillary resistance ratio, creating a net driving force over the capillary wall. 31,32 Reduced net capillary fluid absorption during hypovolaemic circulatory stress has earlier been found in type 1 diabetes patients without microvascular complications, 16 and seemed linked to a reduction in capillary filtration coefficient (CFC) rather than differences in the regulation of capillary hydrostatic pressure or changed metabolic milieu caused by changes in insulin and glucose concentrations, as discussed in Olsen and Lanne 14 and Olsen et al 15 Furthermore, there are indications of reduced precapillary resistance in type 1 diabetes patients, possibly reducing transcapillary driving force. 33 The attenuated FVR response in DMR+ during hypovolaemia could thus further aggravate the reduction in fluid absorption ( Table 1).…”

Reduced Venous Compliance in Young Women with Type 1 Diabetes – Further Aggravated by Prolonged Elevated Levels of HbA1c

“…However, compensatory mobilization of venous capacitance blood during hypovolemic stress (dependent on high venous compliance) is clearly associated with autonomic dysfunction ( 14 ). This discrepancy could be explained by physiological differences, where venous compliance in the present study is measured within the transmural pressures range of 9–36 mmHg and the decrease in transmural pressures in the venous section triggering compensatory mobilization of blood is well below 5 mmHg ( 24 ). As such, it is likely that the autonomic dysfunction present in DW more prominently affects compliance in the low pressure area in early stages of the disease.…”

“…The upper limit was chosen to avoid presyncope, frequently known to occur in women at LBNP levels over 45–50 mmHg ( 16 , 17 ), and men with type 1 diabetes have shown signs of hemodynamic instability well below this level ( 8 ). After correcting for LBNP pressure transmission of roughly 80% ( 11 ), the studied venous transmural pressure interval was 9–36 mmHg, a range previously applied to both healthy subjects and men with type 1 diabetes ( 8 , 17 , 22 – 24 ).…”