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F Hammersen

Publications and source records attributed to F Hammersen.

At least 37 records · Page 2Linked to original sources
PubMed1989

Direct monitoring of nutritive blood flow in a failing skin flap: the hairless mouse ear skin-flap model.

A new experimental skin-flap model is presented in which direct observations of blood flow in individual capillaries can be made from the time of flap creation throughout the entire evolution of the establishment of necrosis. After flap creation, one observes through the microscope that at 1 hour a large area of tissue is nonperfused as a result of the surgical trauma. This is followed by vasodilatation at 6 hours, resulting in an increase in the area of perfused tissue. At 24 hours, the vasodilatation persists, and the red cells that have entered the tissue during the vasodilatation (6 hours) accumulate in the capillaries, this being reflected by an increased area of nonperfused tissue. This increase continues to 72 hours, at which time the perfusion-nonperfusion interface becomes well defined and remains so throughout the 5-day experiment. Analyses of the relationship between early postoperative capillary perfusion and eventual necrosis are presented. Advantages and disadvantages of this model are listed.

Animals↗
PubMed1989

Angiogenesis and hemodynamics of microvasculature of transplanted islets of Langerhans.

Transplantation of isolated islets of Langerhans is frequently followed by early loss of islet function. Because whether this is caused by insufficient vascularization or graft rejection is unknown, angiogenesis and microvascularization of islet grafts were studied in vivo by means of intravital microscopy. After transplantation of syngeneic islets in hamster dorsal skin-fold chambers, 97% (n = 66) of the islets exhibited the first signs of angiogenesis at days 2-4, characterized by sinusoidal sacculations and capillary sprouts. After 10 days, angiogenesis was completed, consisting of a microvascular network similar to those of islets in situ: arterial supply, afferent and efferent capillary loops, and venular drainage. Functional density of microvessels was 700.1 +/- 127.0 cm-1, and erythrocyte velocity was 0.58 +/- 0.35 mm/s. Intracellular insulin was demonstrated immunohistochemically. Electron-microscopic studies revealed normal fine structure of the capillary wall. The model allows in vivo analysis of microvascular phenomena occurring in host-vs.-graft reaction after allogeneic and xenogeneic islet transplantation. Furthermore, it may be used to quantitatively assess immunosuppressive regimens.

Animals↗
PubMed1988

Tissue PO2 and functional capillary density in chronically ischemic skeletal muscle.

In order to study changes in functional capillary density and tissue PO2 in chronically ischemic skeletal muscle, a new model, using the Syrian golden hamster was developed. In the hamster dorsal skin fold, which receives its vascular supply from two cranial and two caudal feeding arteries, a double frame chamber was implanted and ischemia was induced in the cranial part by heat coagulation of the cranial arteries outside of the chamber. This technique allows for analysis of microvascular hemodynamics and local tissue PO2 prior to and during a prolonged period of ischemia in skin muscle. As result of ischemia the diameters of the arterioles increased (p less than 0.001) over the whole 11 day observation period. Functional capillary density decreased significantly (p less than 0.01) during the first 7 days, while capillary RBC-velocity was reduced throughout the 11 days of observation. RBC-velocity in collecting venules was diminished significantly throughout the postischemic observation period. The diameters of the collecting venules first increased upon ischemia (p less than 0.001) but were found decreased at 4, 7 and 11 days. Measurements of tissue PO2 demonstrated a marked decrease from a mean PO2 of 20.5 mmHg prior, to 9.5 mmHg following induction of ischemia. The model allows for induction of chronic ischemia and is suitable to study the effect of therapeutic measures on the microcirculation in chronically ischemic skeletal muscle in vivo.

Animals↗
PubMed1988

[Microvascular perfusion of malignant tumors--a therapeutic measure for enhancing the hyperthermia effect?].

Hypoxic regions of malignant tumors are poorly vascularized; they appear to be more susceptible to hyperthermia in vivo than tumor cells in vitro after an exposure to heat. In an attempt to explain this discrepancy, changes of microcirculatory flow in the tumor have been proposed as key mechanism for destroying adjacent tumor cells in particular. This study was conducted to define the impact of the microcirculation on tumor destruction after local hyperthermia. A transparent chamber was implanted in the dorsal skin fold and two permanent indwelling catheters placed in carotid artery and jugular vein of 45 Syrian golden hamsters. 48 h later, 4 X 10(4) cells of the amelanotic melanoma A-Mel-3 were implanted into the s.c. tissue covered by the chamber. 5 days later, at a tumor diameter of 3 mm, the microcirculation of this tumor was studied using intravital microscopy, a platinum multiwire electrode, television as well as micropuncture techniques for the determination of local PO2, microcirculatory blood flow and microvascular pressure. Measurements were taken at 30 degrees C and 15 min after reaching a tumor temperature of 35 degrees and 42.5 degrees C. When heating up the melanoma to 35 degrees C, an increase in capillary perfusion by 35% was noted. With an apparent maximum of capillary perfusion, there was no change in arteriolar pressure but a significant drop in venular pressure from 11.0 +/- 1.1 to 7.4 +/- 0.6 mmHg resulting in an increase of the arteriolo-venular pressure gradient while the systemic pressures were unchanged. At a tumor temperature of 42.5 degrees C, prestasis and stasis became apparent in capillaries and collecting venules. This was accompanied by a rise in capillary and venular pressure by 5 mmHg. At the same time, pronounced tissue hypoxia was present in the tumor with more than 50% of the values within the hypoxic range between 0 and 5 mmHg. Despite tissue hypoxia, the constriction of all tumor arterioles became evident 15-30 min after reaching a tumor temperature of 42.5 degrees C. The deterioration of tumor oxygenation was associated with damage of tumor cells such as swelling and destruction of mitochondria which was seen under the electron microscope. After 40 min at 42.5 degrees C, the attenuation of the endothelial lining around the entire vascular perimeter was seen in tumor capillaries.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

[Histochemical and ultrastructural studies on the anti-edema and radiation-protective effects of 0-(beta-hydroxyethyl)-rutosides in the rat brain after single-dose irradiation. 1. Electron microscopy study of terminal blood circulation].

The changes in the terminal blood stream appeared with and without protection by 0-(beta-hydroxyethyl)-rutoside (HR) were studied in irradiated rat brains by means of the electron and light microscope. Thirty minutes before irradiating the animals with doses of 1, 5, 10, and 20 Gy, they were given simultaneous i.p. and s.c. doses of 250 mg each of HR per kg of body weight or, as a control, of physiologic NaCl solution. 2, 6, 9, and 14 days after the irradiation, small tissue specimens from the parasagittal parietal cortex were examined according to the following criteria: 1. number of widely open, i.e. well perfused capillaries and small vessels, 2. number and size of perivascular, optically unstructured "light haloes" which are signs of intracellular oedemas of the perivascular astrocyte processes, 3. incidence of hyperchromic, partly shrunken neurons. The control animals not pretreated with HR showed a collapse of most capillaries and an increase in number and size of "light haloes" around capillaries, arterioles and venules. In the electron microscope, these haloes corresponded to the strongly swollen parts of the perivascular neuropile consisting mainly of oedematous astrocyte processes. These severe perivascular cell alterations were prevented for all dose ranges by the pretreatment with HR. Thus our findings do not only demonstrate a clear antiedematous effect of HR on the radiogenic cell oedema of the perivascular neuropile, they support moreover the working hypotheses with regard to the mode of action of this substance as a "membrane protector".

Animals↗
PubMed1988

Fine structure of the human skeletal muscle capillary. A morphometric analysis.

Capillary dimensions in muscle biopsies from human musculus quadriceps femoris, sectioned at right angle to the muscle fibers, were analysed with a computerized planimetric technique giving distributions of dimensional parameters with statistics. Without corrections for estimated preparative shrinkage mean maximal diameter of lumen was 3.82 +/- 0.82 microns (5.31 +/- 1.14 micron shrinkage corrected), mean second maximal diameter, at right angle to maximal, 2.61 +/- 0.72 microns (3.62 +/- 1.00 microns corr.) and mean endothelial thickness in nuclear free sections 0.35 micron (0.49 micron corr.) micron. Using a capillarity of 360/mm2 for the human m. quadriceps femoris, the total surface area of skeletal muscle capillaries was calculated to be 5.50 X 10(3) cm2/100g and the total volume of the capillary network in the muscle to be 0.48 cm3/100g.

Adolescent↗
PubMed1988

The effect of prolonged total ischemia on the ultrastructure of human skeletal muscle capillaries. A morphometric analysis.

Human skeletal muscle shows reflow impairment after prolonged tourniquet ischemia of 1-3 hours, increasing with the duration of ischemia. A sample of 275 cross-sectioned capillary profiles from muscle biopsies of human m. quadriceps femoris made totally ischemic by tourniquet for 90-180 minutes (mean 110 min.) from 5 patients during surgery, show frequent evidence of ultrastructural damage to microvascular membranes and organelles. Frequency analyses demonstrate a significant increase in damage during ischemia (p = 0.03), but not increasing further following 5 min of reperfusion. One of the signs of ischemic damage was endothelial swelling, found in some endothelial cells, lying next to ultrastructurally intact ones. The swelling found cannot be explained by a general loss of volume control of the microvascular endothelium during ischemia, since a computerized morphometry on the entire sample shows a preserved capillary wall thickness during ischemia and following reperfusion. During reperfusion the capillaries dilate with an increase in median max. diameter from 3.4 micron (4.7 micron shrinkage-corrected) to 3.9 micron (5.4 corr.) (p less than 0.001), despite reported reperfusion impairment. However, since capillaries in skeletal muscle consist of 20-40 endothelial cells, a distribution of such localized endothelial swelling or luminal membrane changes in a few percent of the microvascular endothelial population after ischemia, trapping leucocytes, would affect microvascular hydraulic conductance to reperfusion.

Adult↗
PubMed1987

Permeability and vasomotor response of cerebral vessels during exposure to arachidonic acid.

Release of arachidonic acid (AA) in brain tissue is found in various cerebral insults. Blood-brain barrier function and vasomotor response were studied during cerebral administration of the fatty acid to obtain further evidence on its role as mediator of secondary brain damage under pathological conditions. Na+-fluorescein or fluorescein isothiocyanate (FITC)-dextran were i.v. administered as low- and high-molecular weight blood-brain barrier indicators. Cortical superfusion of arachidonic acid led to moderate constriction of ca. 90% of normal of pial arteries of 60-220 micron phi, whereas the venous diameters remained unaffected. On the other hand, AA caused opening of the blood-brain barrier not only for Na+-fluorescein but also for FITC-dextran (mol.wt. 62,000). Extravasation of Na+-fluorescein started at AA concentrations of 3 X 10(-5) M. Concentrations of 3 X 10(-4) to 3 X 10(-3) M always sufficed to induce barrier opening for fluorescein, whereas 3 X 10(-3) M was required for FITC-dextran. Leakage of the blood-brain barrier indicators started around venules. Pretreatment with indomethacin, or with BW 755 C, a dual inhibitor of both the cyclo- and lipoxygenase pathway did not prevent barrier opening by arachidonate for Na+-fluorescein. However, in the presence of indomethacin higher concentrations of AA were required to open the barrier for Na+-fluorescein, whereas BW 755 C did not influence the dose-effect relationship of AA and barrier opening observed in untreated animals. The latter findings imply that the pathophysiological effects induced by AA are likely to be attributed to the acid itself, rather than to its metabolites, a conclusion which might be in conflict with earlier observations reported in the literature. Electron microscopy revealed marked alterations of the venous endothelium, such as an attachment and eventual penetration of polymorphonuclear granulocytes through the endothelial barrier, while the small arteries and arterioles were unaffected. The findings may indicate that opening of the barrier by AA is mediated by granulocytes and/or their products. Taken together, our findings support the concept that release of AA in primarily damaged brain tissue enhances secondary processes, such as a failure of the blood-brain barrier function. The limited potency or even ineffectiveness, respectively, of indomethacin or BW 755 C provides evidence for a direct involvement of the fatty acid rather than of its metabolic degradation products. Therefore, therapeutic prevention of AA formation under these circumstances might be superior to mere inhibition of its metabolism.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1986

[Ultrastructure of the terminal vessels in squamous cell carcinoma of the human external ear. A transmission electron microscopy study].

Electron microscopic findings of vascular fine structure of the squamous cell carcinoma of the human auricle are reported. According to morphological criteria, the tissue was divided into three areas: non-infiltrated zone, transitional zone and centre of the tumor. In the non-infiltrated zone the vessels reveal the pattern of normal vessels of the skin. In the transitional zone endothelial cells bearing all signs of newly formed vessels can be detected as well as endothelial cells that show structural characteristics of severe cellular damage. In the tumour centre itself vessels are found with fenestrations and even true endothelial gaps. Interstitially located RBCs imitate the former outline of the vascular lumen. The observations are discussed and compared with the relevant literature.

Aged↗
PubMed1985

The fine structure of tumor blood vessels. I. Participation of non-endothelial cells in tumor angiogenesis.

This report provides fine structural evidence that, dependent upon the malignancy, tumor as well as mesenchymal cells may participate actively in the neovascularization of experimental tumors grown in transparent tissue chambers implanted into skinfolds of syrian hamsters. Such non-endothelial cells may help to promote angiogenesis in two different ways: (1) They are incorporated into capillary sprouts thereby accelerating the growth rate of the latter independent of endothelial cell proliferation. (2) Extravascular cells (tumor and mesenchymal elements) become integrated in varying numbers into the linings of comparatively large blood-perfused vessels. This facilitates the rapid establishment and functional remodelling of the microvascular bed to adapt the microcirculation to the varying local demands of the growing tumor. If these results can be confirmed for other tumors, and if they are independent of the tumor's environment and the experimental protocol, then we will have to reconsider the significance of tumor angiogenesis as a realistic biological model from which general conclusions with regard to neovascularization in non-tumorous tissues may be drawn.

Animals↗
PubMed1985

[Functional morphology of the endothelium with special reference to the coronary vessels].

Contrary to our former belief, endothelial cells can no longer be classified as a homogeneous cell population which, as a living border layer between the blood and the extravascular space, serves exclusively as a selective filter. The technique of routinely culturing endothelial cells from various sources has provided new insights into an unexpected multitude of synthetic and metabolic capacities of these cells, e. g. the degradation of arachidonic acid, the enzymatic activation of angiotensin I, and many others. However, many of these results are still contradictory, and therefore make any critical review of the data almost impossible. Some examples of this are briefly outlined in this contribution. Irrespective of this, these new results have to be taken into account, although the possibly high specificity of the endothelium will render the interpretation of future data, particularly those obtained from animal models, much more difficult. However, to simply neglect these complexities would be disastrous for all future endothelial research.

Angiotensin I↗
PubMed1984

Some structural aspects of precapillary vessels.

According to the present state of the art, the former Chambers-Zweifach conception is no longer tenable as the ubiquitous module of microvascular organization. Any attempt to define the consecutive segments of precapillary vessels in a random collection of sectioned tissues is impaired by the extreme scatter of variations and the lack of additional criteria necessary for a distinct classification. With these inadequacies in mind, arterioles, terminal arterioles, and their precapillary segments (sphincters?) are identified by applying the following parameters: luminal diameter, composition of the subendothelial space, and thickness as well as completeness of the media. Endothelial components of particular functional significance are different types of cytoplasmic filaments and myoendothelial junctions. The former serve as a cytoskeleton and may provide a mechanism to adapt endothelial tensile strength to variations of shearing forces. The latter appear to be sites of firm intercellular attachment and of electrotonic coupling of the endothelium to the underlying smooth-muscle cells. The former unanimously accepted helicoidal arrangement of vascular smooth muscle (VSM) must be modified according to most recent findings, and the tridimensional shape of VSM and its transition to pericyte-like elements remain to be further elucidated. Future effects, from which solutions to the many open problems may be expected, must therefore aim at combined vital-, light-, and electron-microscopic studies of the methodically accessible microvascular beds. This necessity has already been recognized, and first promising steps have been taken.

Animals↗