Comprehensive Analysis of Automatic Identification System (AIS) Data in Regard to Vessel Movement Prediction

AIS was primarily developed to exchange vessel-related data among vessels or AIS stations by using very-high frequency (VHF) technology to increase safety at sea. This study evaluates the formal integrity, availability, and the reporting intervals of AIS data with a focus on vessel movement prediction. In contrast to former studies, this study is based on a large data collection of over 85 million AIS messages, which were continuously received within a time period of two months. Thus, the evaluated data represent a comprehensive and up-to-date view of the current usage of AIS systems installed on vessels. Results of previous studies concerning the availability of AIS data are confirmed and extended. New aspects such as reporting intervals are additionally evaluated. Received messages are stored in a database, which allows for performing database queries to evaluate the obtained data in an automatic way. This study shows that almost ten years after becoming mandatory for professional operating vessels, AIS still lacks availability for both static and dynamic data and that the reporting intervals are not as reliable as specified within the technical AIS standard.

Capillary permeability: atrial peptide action is independent of "protein effect"

Perfusion of exchange microvessels with the vasoactive hormone, atrial natriuretic peptide (AP), acutely and reversibly elevates hydraulic conductivity (Lp) by mechanisms that are, as yet, unknown. This, the first of two studies to characterize AP responses when perfusate composition was altered, specifically focuses on the action of AP when perfusate albumin was lowered to change the transcapillary barrier properties for water by passive mechanisms (protein effect). Perfusion of frog (Rana pipiens) mesenteric microvessels with 1 nM AP in 10 mg/ml bovine serum albumin (BSA) elevated Lp by a median 2.1-fold (range 1.2-2.7, n = 13) from control levels (10 mg/ml BSA). Reduction of perfusate albumin from 10 to 1 mg/ml elicited a small rise in Lp (1.8-fold, n = 10); Lp rose a further 2.1-fold (n = 6) when 1 nM AP was added to 1 mg/ml BSA. Likewise, protein-free perfusion elevated Lp from a median 2.2 to 5.1 X 10(-7) cm.s-1.cmH2O-1 (n = 11); 1 nM AP in protein-free perfusate elevated Lp a further 2.1-fold (n = 8). Thus, regardless of protein content, the response to the peptide was a consistent, twofold increase in exchange vessel Lp (n = 27). These data are consistent with the suggestion that the AP-activated rise in Lp (twofold) occurs via an increase in the effective area of the transcapillary pathway for water without influencing the selectivity properties of the paracellular, albumin-sensitive portion of the barrier.

Capillary permeability: an albumin component attenuates active changes in Lp

The mechanisms whereby atrial natriuretic peptide (AP) acutely and reversibly elevates hydraulic conductivity (Lp) are not known. This is the second of two studies of the influence of perfusate albumin composition on AP alterations in capillary Lp. In this study, we investigated the effect of dialysis of the perfusate albumin. A 2.2-fold increase in frog (Rana pipiens) mesenteric microvessel Lp occurred when 100 nM AP was added to the control perfusate containing dialyzed, crystallized bovine serum albumin (DXL-BSA 10 mg/ml; n = 20). By contrast, Lp was unchanged by 100 nM AP in 10 mg/ml untreated, crystallized BSA (XL-BSA; n = 8). The response to AP was unaltered at DXL-BSA contents of 10, 20, or 30 mg/ml (2.4-, 2.2-, and 3.1-fold, respectively; n = 8). Dialysis of the albumin, per se, did not influence control Lp (LpXL-BSA/LpDXL-BSA = 1.0; n = 5). The receptor-independent nitrovasodilator, sodium nitroprusside (SNP; 1 microM) elevated Lp by 1.7-fold in DXL-BSA (n = 30). The response was abolished in XL-BSA (n = 8). We conclude that small hydrophilic albumin-associated substances antagonize AP- and SNP-induced elevations of exchange microvessel hydraulic conductance without interfering with albumin's role in the maintenance of normal exchange vessel permeability.

Differential sensitivity of exchange vessel hydraulic conductivity to atrial natriuretic peptide

Acute plasma volume reduction by atrial natriuretic peptide (ANP) may be mediated, at least in part, by increased exchange vessel water conductivity (Lp). The present study tests the hypothesis that physiological levels of ANP acutely and reversibly elevate single capillary Lp. Paired, in situ measurements of Lp were obtained using the modified Landis technique in individually perfused mesenteric capillaries of the frog, Rana pipiens. Control Lp measurements ranged from 0.1 to 40 x 10(-7) cm.s-1.cmH2O-1 (with a median value of 2.5 x 10(-7] in 81 microvessels perfused with frog Ringer solution containing dialyzed bovine serum albumin. Vessels were recannulated and perfused with one or more concentrations of human ANP (hANP) spanning the physiopathological range: 0.01, 0.1, 1, 10, and 100 nM. When possible, a final recannulation and Lp determination was performed in the absence of hANP. A median 2.2-fold rapid Lp increase was observed compared with control at each peptide concentration. Lp changes persisted for the duration of exposure to hANP, returning to control levels on withdrawal of the peptide. True and venular capillaries exhibited similar Lp responses: median 2.2- and 2.4-fold elevations, respectively. Sixty percent of true and venular capillaries exhibited twofold or greater hANP-induced increases in Lp, whereas only 25% of arteriolar capillaries exhibited such a response. Thus a differential sensitivity to the peptide exists across the exchange vessel network. The observations of this study demonstrate that physiological levels of ANP are capable of modulating exchange vessel Lp, one means by which the peptide may acutely alter plasma volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Humoral factors may mediate increased rat hindquarter blood flow in portal hypertension

Chronic portal hypertension is associated with systemic hypotension and reduced peripheral vascular resistance. Although it is well established that splanchnic and renal vascular resistances are reduced, the contribution of possible alterations in skeletal muscle hemodynamics in portal hypertension is unknown. The present study was designed to determine if skeletal muscle vascular resistance was reduced and blood flow increased in portal hypertensive rats. In portal hypertensive animals, hind-quarter blood flow was significantly increased while vascular resistance was significantly reduced. The fall in resistance in the portal hypertensive animals was associated with an increase in the capillary filtration coefficient, suggesting that an increase in functional exchange vessel surface area occurred. Cross perfusion of control hindquarters with portal hypertensive blood resulted in a 38% reduction in hindquarter vascular resistance. Raising the plasma glucagon concentration to levels reported in portal hypertensive animals resulted in no change in blood flow or vascular resistance in control hindquarters. Skeletal muscle vascular sensitivity to norepinephrine was assessed by constructing dose-response curves in control and portal hypertensive animals. Mean ED50 values were not different. The results of these studies indicate that skeletal muscle vascular resistance is reduced in portal hypertension and humoral factors, but not glucagon, are primarily responsible for the skeletal muscle hyperemia associated with portal hypertension.

Effects of bradykinin on intestinal transcapillary fluid exchange

Bradykinin (50 μg∙L−1) increases intestinal lymph flow sixfold when infused intraarterially into the cat ileum. The capillary filtration coefficient and capillary pressure increase and interstitial fluid pressure rises from negative to positive values. A slight increase in lymph:plasma protein concentration occurs with a resulting fall in the transcapillary oncotic pressure gradient. These results indicate that the effect of bradykinin on intestinal lymph flow is attributable, at least in part, to increased capillary pressure, exchange vessel surface area, and a reduction in the effective transcapillary oncotic pressure gradient.