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Biomedical subjects

F G Welt

Publications and source records attributed to F G Welt.

6 recordsLinked to original sources
PubMed1998

Severe haemorrhage partially reverses moderate haemorrhage-induced decrease in intestinal vascular capacitance.

The purpose of the present study was to compare the effect of severe haemorrhage with moderate haemorrhage on intestinal vascular capacitance. In 12 chloralose-anaesthetized pigs, moderate and subsequent severe haemorrhage was induced by removal of 15 and 25% of blood volume, respectively. Six of the animals were vagotomized prior to induction of haemorrhage. The portal vein pressure/intestinal blood volume (P-V) relationship was measured by using blood pool scintigraphy and varying portal vein pressure. Moderate haemorrhage resulted in a leftward shift of the P-V relationship towards the pressure axis with decreases in cardiac output, portal blood flow and arterial pressure, and an increase in heart rate. Severe haemorrhage shifted the P-V relationship back towards the volume axis compared with moderate haemorrhage, with further decreases in cardiac output, portal blood flow and arterial pressure. While moderate haemorrhage reduced intestinal blood volume at a portal vein pressure of 7 mmHg (Vp7) to 81 +/- 3% of the control value (P < 0.01), severe haemorrhage increased Vp7 to 88 +/- 1% of the control value (P < 0.05 compared with moderate haemorrhage). After vagotomy, moderate haemorrhage decreased Vp7 to 84 +/- 4% of the control value (P < 0.01), whereas Vp7 did not change significantly after severe haemorrhage (Vp7 increased to 86 +/- 1% of the control value). Thus, severe haemorrhage is associated with an increase in intestinal vascular capacity compared with moderate haemorrhage. This increase is mediated in part via the cardiac vagal reflex. The attenuation of intestinal venoconstriction during severe haemorrhage probably contributes to further decreases in cardiac output and arterial pressure by redistribution of blood to the peripheral circulation.

Animals↗
PubMed1996

Monocyte recruitment and neointimal hyperplasia in rabbits. Coupled inhibitory effects of heparin.

Among the many effects of heparin independent of its effects on coagulation are inhibition of vascular smooth muscle cell proliferation and regulation of leukocyte-blood vessel interactions. The potential link between these effects was examined in an animal model of vascular injury rich in inflammatory cells: the placement of endovascular metal stents in rabbit iliac arteries. Monocyte adhesion stimulated by early focal thrombus was maximal after 3 days, with infiltrating monocytes and intimal cell proliferation maximal after 7 days. Tissue monocyte number dictated cell proliferation at each time point (R2 = .92, P < .0001). Heparin reduced both early monocyte adhesion as well as monocyte infiltration within the neointima 7 and 14 days after stent placement. Reductions in adherent and tissue monocytes were commensurate with reductions in intimal cell proliferation and intimal thickening. At 14 days, heparin's inhibition of mononuclear cell adhesion was correlated with its suppression of intimal thickening (R2 = .82, P < .0001). Monocytes have been hypothesized to serve as markers, initiators, and promoters of arterial occlusive diseases. Heparin's ability to inhibit mononuclear cell adhesion and penetration and reduce neointimal size and cell proliferation after vascular injury may further implicate monocytes in the pathogenesis of neointimal hyperplasia after mechanical arterial injury.

Animals↗
PubMed1992

Passive effect of reduced cardiac function on splanchnic intravascular volume.

It has been hypothesized that lowered cardiac output due to heart failure results in passive redistribution of intravascular volume from the peripheral circulation to the central circulation and that this redistribution acts to support cardiac output. To test this hypothesis, acute heart failure was induced by rapid atrial pacing to raise heart rate from 148 +/- 6 to 232 +/- 1 beats/min for 5 min, while splanchnic intravascular volume was assessed with radionuclide imaging in eight anesthetized pigs that had undergone prior carotid denervation and vagotomy. Cardiac output decreased from 3,350 +/- 410 to 2,170 +/- 290 ml/min (P less than 0.001), mean arterial pressure decreased from 103 +/- 5 to 84 +/- 4 mmHg (P less than 0.001), left atrial pressure increased from 5.9 +/- 0.6 to 10.8 +/- 0.9 mmHg (P less than 0.001), right atrial pressure increased from 2.4 +/- 0.5 to 4.8 +/- 0.9 mmHg (P less than 0.001), total splanchnic intravascular volume did not change (0 +/- 2 ml), splenic intravascular volume decreased 11 +/- 3% (P less than 0.001), hepatic intravascular volume increased 12 +/- 2% (P less than 0.001), and mesenteric intravascular volume did not change (-3 +/- 2%). Thus, when cardiac output is lowered with pacing-induced acute heart failure, lowered perfusion pressure acts to lower splenic intravascular volume and increased central venous pressure acts to increase hepatic intravascular volume; however, total splanchnic intravascular volume does not decrease to support cardiac filling and cardiac output.

Animals↗
PubMed1991

Effect of vasopressin on systemic capacity.

To assess the effect of vasopressin (VP) on systemic capacity (SC), blood was drained from the venae cavae to an oxygenator and returned to the aorta at a constant rate so that changes in SC could be measured as the inverse of changes in oxygenator volume in 17 anesthetized pigs. After 10 min of VP administration (1.1 U/min ia), mean arterial pressure increased from 67 +/- 2 to 144 +/- 7 mmHg (P less than 0.001). SC decreased promptly and reached a nadir of 110 +/- 32 ml (P less than 0.02, 5.5 ml/kg) below control at 5 min but returned to 35 +/- 65 ml (P = not significant, 1.8 ml/kg) below control at 10 min. Portal venous pressure decreased from 19.3 +/- 2.6 to 16.6 +/- 2.7 mmHg (P less than 0.001), and portal flow decreased from 828 +/- 68 to 458 +/- 92 ml/min (P less than 0.001). Transhepatic venous resistance increased. After evisceration, VP caused only an increase in SC. Thus VP causes an initial SC decrement due entirely to a decrease in splanchnic capacity. The decrease in splanchnic capacity must be caused, at least in part, by the decrease in gastrointestinal arterial inflow and subsequent decrease in portal venous pressure. These initial effects of VP on SC would be expected to enhance ventricular filling and cardiac output in the intact animal and could be important in the acute compensatory response to hemorrhage.

Analysis of Variance↗
PubMed1989

Transforming growth factor-beta activity is potentiated by heparin via dissociation of the transforming growth factor-beta/alpha 2-macroglobulin inactive complex.

The control of smooth muscle cell (SMC) proliferation is determined by the combined actions of mitogens, such as platelet-derived growth factor, and the opposing action of growth inhibitory agents, such as heparin and transforming growth factor-beta (TGF-beta). The present studies identify an interaction between heparin and TGF-beta in which heparin potentiates the biological action of TGF-beta. Using a neutralizing antibody to TGF-beta, we observed that the short term antiproliferative effect of heparin depended upon the presence of biologically active TGF-beta. This effect was observed in rat and bovine aortic SMC and in CCL64 cells, but not in human saphenous vein SMC. Binding studies demonstrated that the addition of heparin (100 micrograms/ml) to medium containing 10% plasma-derived serum resulted in a 45% increase in the specific binding of 125I-TGF-beta to cells. Likewise, heparin induced a twofold increase in the growth inhibitory action of TGF-beta at concentrations of TGF-beta near its apparent dissociation constant. Using 125I-labeled TGF-beta, we demonstrated that TGF-beta complexes with the plasma component alpha 2-macroglobulin, but not with fibronectin. Heparin increases the electrophoretic mobility of TGF-beta apparently by freeing TGF-beta from its complex with alpha 2-macroglobulin. Dextran sulfate, another highly charged antiproliferative molecule, but not chondroitin sulfate or dermatan sulfate, similarly modified TGF-beta's mobility. Relatively high, antiproliferative concentrations of heparin (1-100 micrograms/ml) were required to dissociate the TGF-beta/alpha 2-macroglobulin complex. Thus, it appears that the antiproliferative effect of heparin may be partially attributed to its ability to potentiate the biological activity of TGF-beta by dissociating it from alpha 2-macroglobulin, which normally renders it inactive. We suggest that heparin-like agents may be important regulators of TGF-beta's biological activity.

Animals↗