Improvement of collateral circulation in chronic vascular occlusive disease of the lower extremity.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B Endrich.
Explore the source record for details and available documents.
A transparent chamber was implanted in the dorsal skin flap of 32 Syrian gold hamsters, 48 h after microsurgery, 4x10(4) cells of the amelanotic melanoma A-Mel-3 were transplanted s.c. in the area exposed for daily in vivo microscopy (16 animals). A platinum multiwire electrode and quantitative video-techniques were utilized for measurements of local pO2, microvascular morphology and measurements of local PO2, microvascular morphology and capillary hemodynamics. When compared to controls (16 animals), mean local PO2 on the tumor's surface decreased with tumor development. The density of erythrocyte perfused capillaries in the melanoma was elevated 4 days after humor transplantation indicating excessive neovascularization. Probably due to increased intratumor tissue pressure and thrombosis, capillary density decreased significantly until day 12, whereas mean capillary blood cell velocity did not change. Of microhemodynamic significance were huge platelet conglomerates consistently noted in short, dilated capillaries as the melanoma edge. As a result, the capillary filling time (15.7 s for melanoma capillaries, 3.2 s for control preparations) was prolonged suggesting an increase in capillary resistance. These findings might indicate that the efficacy of melanoma treatment is diminished by an enhanced capillary resistance. Intratumor tissue pressure and thrombosis with concomitant widening of intercapillary distances might significantly affect the therapy of melanomas.
Blood cell velocity, capillary diameter, and capillary length were determined in the microcirculation of the amelanotic hamster melanoma A-Mel-3 as well as in s.c. tissue of tumor-free animals. Studies were carried out using a dorsal skin flap chamber, intravital microscopy, and television techniques after transplantation of a 0.5-cu mm piece of tumor tissue. The tumor revealed a special microvascular configuration of short, thin-walled, sometimes dilated capillaries running around the edge of the tumor. Large avascular areas appeared in the center part approximately 5 days after tumor transplantation. Although mean capillary blood cell velocity was not different in tumor-containing and tumor-free preparations, localized irregularities of blood flow were observed close to points of endothelial sacculations. Huge platelet conglomerates were consistently noted in capillaries of the tumor, blocking the blood stream temporarily. Due to discrepancies in microvascular morphology and lack of visible vascularization, large parts of this tumor seem to be inaccessible to tumor treatment. This implies that better vascularization of these regions might enhance the efficiency of cancer treatment. The chamber technique, intravital microscopy, and television methods combined with the subsequent, quantitative microvascular analysis may provide a unique means for direct evaluation of local therapy, particularly during early melanoma growth.
An experimental model was designed for direct, quantitative studies of hemodynamic and morphologic parameters in the microcirculation. It consists of implanting a modified Algire chamber in the dorsal skin flap of hamsters and the implementation of two permanent catheters in jugular vein and carotid artery. The microcirculation was studied using intravital microscopy and television techniques for in situ measurements of blood cell velocity and vascular diameters. Due to the poor contrast between blood cells, blood capillaries and surrounding s.c. tissue, microvascular beds were visualized using fluorescent microscopy after i.v. injection of 0.2 ml of 5% FITC-Dextran 150. The combination of optical elements and low amounts of FITC-Dextran improved the contrast of the televised image without changing macro- and micro-hemodynamic parameters, and blood plasma was delineated as bright structure against the substantially darker background of red blood cells and surrounding tissue. This permitted the quantitative study of practically all blood vessels within a given field of s.c. tissue in unanesthetized animals. Blood cell velocity in arterioles was 0.7-1.1 mm/s, 0.2-0.7 mm/s in midcapillaries and reached 0.6 mm/s in collecting venules. Since i.v. injection of drugs and systemic pressure measurements are possible in this model, it provides a unique means for studying the reactivity of the microcirculation over a prolonged period.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Histamine concentration in plasma was measured and the microvasculature studied after injections of radiographic contrast materials and hypertonic NaCl solutions. Only 8 ml/kg of contrast material caused a prolonged decrease in systemic and microvascular pressure and a drop in erythrocyte velocity. Concomitantly, a significant increase in plasma histamine concentration was observed after two minutes. Signs of cellular defects and constriction of arterioles were noted after several minutes. These findings suggest that the hyperosmolality of the radiopaque materials tested could initiate the microhemodynamic reactions but is not responsible for cellular and endothelial damage in the microcirculation of the rabbit omentum.
Solutions of conventional stoma-free hemoglobin (SFH) and of pyridoxylated stoma-free hemoglobin (SFH-PLP) were compared in a dog model of reanimation from severe arterial blood loss. SFH and SFH-PLP restored central hemodynamics after infusion without yielding significant differences between the experimental groups. To cope with the developing hypovolemia, Ringer's lactate load amounted to about 120 ml/kg, edema formation was not encountered. Skeletal muscle oxygenation was studied by means of a multiwire platin electrode. The infusion of SFH-PLP was associated with a shift to the right of the cumulative PO2-distribution curve, indicating better tissue oxygenation. Oxygen was not unloaded from SFH in plasma unless the oxygen extraction from red cell hemoglobin exceeded 40%. Oxygen unloading was, however, improved when SFH-PLP with low oxygen affinity was used. Thus, SFH-PLP merits further consideration as a short-term oxygen-carrying blood substitute.
Tissue perfusion in BA 1112 sarcomas of WAG inbred Rijswijk rats was determined from in vivo measurements of capillary density, length, and erythrocyte velocity in modified Algire chamber preparations. Studies were done with the use of television techniques in situ during a period of 26 days, both in control chambers and after implantation of a 0.1-mm3 piece of tumor tissue. Perfusion in control areas void of tumor tissue. Perfusion in control areas void of tumor was approximately 8-10 ml/minute/100 g of tissue. Flow in active tumor growth regions on the outward side of the tumor edge was through undifferentiated channels and had characteristics of flow through a porous medium. Despite enhanced arterial supply, the stabilized tumor microcirculation at the inward side of the growing tumor retained its perfusion rate constant (15-18 ml/min/100 g). Perfusion in central portions of the tumor was about 2-4 ml/minute/100 g during 12 days, whereas the tumor doubled in diameter. Our findings support the concept of temporal and functional blood flow inhomogeneity in the microcirculation of spreading tumors.
Explore the source record for details and available documents.
The intravenous injection of RCM into rabbits produced dose-dependent changes in SAP, MVP, and RBCV, as well as plasma histamine and complement concentrations. After infusion of 8 ml/kg Hypaque-50, SAP dropped from 86 +/- 3 mm Hg to 50 +/- 3, MVP from 42 +/- 2 cm H2O to 26 +/- 3, and RBCV from 0.98 +/- 0.11 mm/sec to 0.37 +/- 0.13. The microvascular changes appeared 10 sec after injection and persisted for 10 to 40 min. During the course of the reaction it was observed that leukocytes adhered to the endothelial walls and red blood cells shrank and finally aggregated in the microvessels. The microvascular changes were accompanied by an increase in plasma histamine concentration, with an average of 44 ng/ml after 2 min, and a drop in total plasma CH50 by an average of 46%. Infusion of 8 ml/kg hyperosmolar saline solution (4.1 gm/dl or 1324 mOsm/L) produced initial changes in microvascular parameters which returned to normal within a few seconds. At the same time plasma histamine concentration increases slightly without changes in complement. It is concluded that the hyperosmolar properties of RCM may contribute to the initial hemodynamic changes observed after RCM infusion. However, the prolonged microcirculatory disturbances produced by RCM in rabbits appear to be a direct effect of the chemotoxicity of these compounds. Part of this chemotoxicity might result form initial release of vasoactive mediators such as histamine and activation of the complement system.
The intravascular persistence of hb-W is significantly longer than of pyridoxylated hb (hb-PLP), however, no significant differences in BV were observed after isovolemic exchange of 20 ml/kg b.w. Even though the oxygen affinity of hb-PLP in vitro was reduced when compared to the affinity of hb-W significant differences in vivo were lacking. The development of hypovolemia and thus the lack of an adequate increase in cardiac output have been recognized as the most relevant causes to explain the changes observed. Neither of the solutions is yet to be recommended for clinical blood replacement therapy.
Resuscitation and volume replacement after acute blood loss is possible for a short duration by means of 6% stroma-free hemoglobin solution (SFH). Despite transcapillary loss of SFH, pulmonary edema is not provoked after massive infusion of cristalloid solution. The oxygen supply to the tissues is maintained by a compensatory rise in cardiac output and O2-extraction, mainly from the remaining red cell hemoglobin.
Explore the source record for details and available documents.
A great number of investigators have, independently, shown that tumour blood flow is affected by a hyperthermic treatment to a larger extent than normal tissue blood flow. While the majority of the studies on experimental tumours show a decrease and even a lapse in blood flow within the microcirculation during or after hyperthermia, the data on human tumours are less conclusive. Some of the investigators do not find a decrease in circulation, while others do. Obviously, this is an important field of investigation in the clinical application of hyperthermia because a shut down of the circulation would not only facilitate tumour heating (by reducing venous outflow, this reducing the 'heat clearance' from the tumour), but would also facilitate tumour cell destruction. The same holds for alterations that occur subsequently to the circulatory changes, like a heat-induced decrease of tissue pO2 and pH. If the frequently reported circulatory collapse of the tumour circulation could selectively be stimulated by, e.g. acidification or by vasoactive agents, hyperthermic treatment of patients would possibly be greatly facilitated and intensified. In hyperthermic tumour therapy a number of complex processes and interactions takes place, especially when the treatment is performed in combination with radiation therapy. One of them represents the group of processes related to the random probability of cell sterilization of individual tumour cells resulting in exponential survival curves which are typically evaluated with e.g. cell survival assays. This aspect has not been the issue of this paper. The other group of processes deals with the heat-induced changes in the micro-physiology of tumours and normal tissues which, as discussed before, may not only enhance the exponential cell kill, but which may also culminate in vascular collapse with the ensuing necrosis of the tumour tissue in the areas affected. If this takes place, a process of bulk killing of tumour cells results, rather than the random type of cell sterilization. At present it is not clear to what extent the various separate mechanisms contribute to the total effect of tumour control. With all these considerations in mind, one should be aware of the fact that effects, secondary to heat-induced vascular stasis alone will never be efficient enough to eliminate all tumour cells, even though a heat reservoir is created. This is so because some malignant cells will inevitably have already infiltrated normal, surrounding structures and will therefore not be affected by changes in the tumour vascular bed.(ABSTRACT TRUNCATED AT 400 WORDS)