Collateral vessel formation: isolation of a transferable factor promoting a vascular response

Cuttino, John T.; Bartrum, Royal J.; Hollenberg, Norman K.; Abrams, Herbert L.

doi:10.1007/bf01906387

Cited by 23 publications

(12 citation statements)

References 12 publications

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“…It also confirmed a significant increase in endothelial cell labeling of renal veins and epithelium of the ureter draining the kidney, previously demonstrated in this laboratory (Cowan et al, 1978). This observation provides further support for the presence of a humoral substance participating in vascular neogenesis (Cuttino et al, 1975;Schaper et al, 1971). …”

supporting

confidence: 87%

“…Earlier attempts to demonstrate growth-promoting factors in the drainage from ischemia tissues generally were performed late following arterial stenosis, in the 2nd to 4th week (Cuttino et al, 1975), primarly because the experimental protocol demanded arteriographic documentation of collateral formation. This study has confirmed that these vessels are generally difficult to visualize by angiography or gross inspection early in the course, when the mitogenic activity is at its height.…”

Section: Discussionmentioning

confidence: 99%

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Time course of increased collateral arterial and venous endothelial cell turnover after renal artery stenosis in the rat.

Ilich¹,

Hollenberg²,

Williams³

et al. 1979

Circulation Research

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We induced left renal artery stenosis in rats and studied collateral arterial formation by angiography, histology, and radioautography with tritiated thymidine. Endothelial cell turnover was estimated by radioautography with tritiated thymidine in the periureteric blood supply of 10 normal and 38 collateral-forming kidneys 1 to 100 days after stenosis. Periureteric arterial endothelial cell labeling showed a highly significant (P less than 0.005) increase, apparent within 1 day and gradually falling as the vessels grew, until a baseline was reached in 35 days. A smaller but statistically significant increase in the labeling index also was found in endothelial cells of the renal vein during the first week (P less than 0.01), and had a similar time course. A marked increase in epithelial cell labeling in the ureters draining the stenotic kidneys also was evident (P less than 0.005). Thus, collateral vessel development is characterized by active DNA synthesis in the cellular elements which is maximal during the first week. A humoral factor is implicated in the vascular response by the parallel proliferation of venous and uretic cellular elements that are unlikely to experience the biophysical forces, such as increased blood flow or tangential wall force, which might stimulate proliferation in ther arterial vessels.

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supporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Time course of increased collateral arterial and venous endothelial cell turnover after renal artery stenosis in the rat.

Ilich¹,

Hollenberg²,

Williams³

et al. 1979

Circulation Research

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“…Quite recently, a humoral factor that promotes growth of capillaries has been isolated from tumors 33 and from ischemic kidneys. 34 Perhaps in pathological hypertrophy there is insufficient production, excessive destruction, or inability to respond to a similar humoral stimulus. If so, therapy designed to shorten diffusion distance may become possible.…”

Section: -1mentioning

confidence: 99%

Intercapillary distance and capillary reserve in hypertrophied rat hearts beating in situ.

Henquell¹,

Odoroff²,

Honig³

1977

Circulation Research

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SUMMARY Functional intercapillary distance (ICD) was measured in stop-motion photomicrographs of hypertrophied, normally compensated, well oxygenated rat hearts beating in situ. Left ventricular hypertrophy was produced by salt loading and unilateral nephrectomy. Minimum ICD (when all capillaries are open) also was measured. Ventricular weight increased by 30-40% within 8-9 weeks after nephrectomy. To compare the effect of normal and pathological growth, ICD was also measured in normal rats. In normal animals, minimum ICD and functional ICD increased linearly and proportionately with left ventricular weight. Consequently, the extent to which capillary recruitment could decrease ICD was the same in large and small normal hearts (about 2 fun). In the hypertrophied hearts, capillary recruitment could have maintained ICD within normal limits at rest for several weeks. After 8-9 weeks, however, the capillary reserve in hypertrophy was fully utilized at rest, and mean functional ICD was 1.5-2.0 fitn greater than normal for the age of the animal. An analysis of O 2 transport indicates that anoxic foci would exist throughout the hypertrophied heart and particularly in subendocardium when the capillary reserve is exhausted. The calculated amount of anoxic tissue appears sufficient to account for the focal necrosis and fibrosis observed in hypertrophy and for the development of circulatory failure. WEARN et al.1 -2 were the first to report that myocardial capillary circulation is compromised by the hypertrophy of disease. They concluded that neither the fibers nor the capillaries proliferate, and that the distance between capillaries increases because fiber diameter increases. This view has been challenged by recent studies based on different histological methods which purport to show that capillaries proliferate in pathological hypertrophy. However, it seems likely that capillary growth is not proportional to hypertrophy of the muscle fibers. 9 and V4 the capillaries in left ventricle 9 ' 10 are not perfused at rest. These unperfused capillaries constitute a functional reserve, available for adaptation to stress or disease. Consequently, diffusion distances could be maintained at or near the normal value at rest despite hypertrophy, as long as enough capillaries are available in the reserve. The study to be described was undertaken to: (1) evaluate the capillary reserve in hypertrophied hearts, (2) determine the effect of hypertrophy on the uniformity of diffusion distance, and (3) estimate the effect of altered capillary circulation on O 2 transport. Methods GENERALWe studied female Sprague-Dawley rats. Eight pairs of littermates were fed a standard laboratory diet until they Received June 14, 1976; accepted for publication January 26, 1977. reached 160 g at about 45 days. One member of each pair then was subjected to unilateral nephrectomy. In addition, a 60-mg pellet of deoxycorticosterone was implanted under the skin of the back. One week later, 1% NaCl solution was added to the drinking water. Control rats were n...

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“…An unanticipated observation suggested that under some conditions this underlying premise might not hold. We employed the hamster cheek pouch to assay a vasoproliferative factor that may contribute to collateral arterial development (6). While using this assay system to characterize several candidates as mediator of the vascular response we found that one of them, the platelet-derived growth factor (PDGF), induced a vascular response that displayed a highly alinear dose-response relationship.…”

Section: Introductionmentioning

confidence: 99%

The microvascular response to growth factors in the hamster cheek pouch

Orlandi

Paskins-Hurlburt

1986

Basic Res Cardiol

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Implicit in attempts to characterize and purify biologically active factors is the premise that the bioassay system employed will show a progressive increase in the response as the concentration of the responsible factor increases. We employed the hamster cheek pouch to assay the neovascularization potential of growth factors, including endothelial cell growth supplement (ECGS), epidermal growth factor (EGF), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF). Each growth factor was applied to the system in graded concentration and two approaches used to assess neovascularization: first, direct serial inspection of the cheek pouches at 40 power; second, tritiated thymidine incorporation into endothelial cells, assessed by radioautography. PDGF induced a dose-related increase in neovascularization, with a threshold dose of 17.5 micrograms/ml and a peak, 56% response, at a PDGF concentration of 175 micrograms/ml. Progressive increases in PDGF concentration, thereafter, induced progressive reductions in the neovascularization rate. Under some conditions optimal bioassay requires serial dilutions of the assay material over a wide range.

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Collateral vessel formation: isolation of a transferable factor promoting a vascular response

Cited by 23 publications

References 12 publications

Time course of increased collateral arterial and venous endothelial cell turnover after renal artery stenosis in the rat.

Time course of increased collateral arterial and venous endothelial cell turnover after renal artery stenosis in the rat.

Intercapillary distance and capillary reserve in hypertrophied rat hearts beating in situ.

The microvascular response to growth factors in the hamster cheek pouch

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