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Patologicheskaia Fiziologiia I... 1991
Review
Topics: Animals; Blood Viscosity; Capillaries; Cerebral Cortex; Hematocrit; Humans; Microcirculation
PubMed: 1923611
DOI: No ID Found -
Cryobiology Nov 1998As the modern era of cryosurgery began in the mid 1960s, the basic features of cryosurgical technique were established as rapid freezing, slow thawing, and repetition of... (Review)
Review
As the modern era of cryosurgery began in the mid 1960s, the basic features of cryosurgical technique were established as rapid freezing, slow thawing, and repetition of the freeze-thaw cycle. Since then, new applications of cryosurgery have caused numerous investigations on the mechanism of injury in cryosurgery with the intent to better define appropriate or optimal temperature-time dosimetry of the freeze-thaw cycles. A diversity of opinion has become evident on some aspects of technique, but the basic tenets of cryosurgery remain unchanged. All the parts of the freeze-thaw cycle can cause tissue injury. The cooling rate should be as fast as possible, but it is not as critical as other factors. The coldest tissue temperature is the prime factor in cell death and this should be -50 degreesC in neoplastic tissue. The optimal duration of freezing is not known, but prolonged freezing increases tissue destruction. The thawing rate is a prime destructive factor and it should be as slow as possible. Repetition of the freeze-thaw cycle is well known to be an important factor in effective therapy. A prime need in cryosurgical research is related to the periphery of the cryosurgical lesion where some cells die and others live. Adjunctive therapy should influence the fate of cells in this region and increase the efficacy of cryosurgical techniques.
Topics: Animals; Cell Death; Cryosurgery; Freezing; Humans; Ischemia; Microcirculation; Necrosis; Neoplasms; Time Factors
PubMed: 9787063
DOI: 10.1006/cryo.1998.2115 -
Arthritis and Rheumatism Nov 2003
Review
Topics: Humans; Microcirculation; Microscopic Angioscopy; Nails; Raynaud Disease
PubMed: 14613262
DOI: 10.1002/art.11310 -
Iyo Denshi To Seitai Kogaku. Japanese... Jun 1980
Review
Topics: Animals; Blood Flow Velocity; Blood Pressure; Blood Volume; Computers, Analog; Erythrocytes; Hematocrit; Hemodynamics; Humans; Microcirculation; Rabbits; Rats; Rheology
PubMed: 6451735
DOI: No ID Found -
International Journal of Hyperthermia :... May 2006The most important physiological parameter influencing tissue response to heat is blood flow. At mild hyperthermia temperatures blood perfusion increases in many tumours... (Review)
Review
The most important physiological parameter influencing tissue response to heat is blood flow. At mild hyperthermia temperatures blood perfusion increases in many tumours and this effect is heating time-, temperature- and tumour-dependent. These flow increases can improve tumour oxygenation. When heating is terminated, perfusion and oxygenation commonly recover, although how quickly this occurs appears to be tumour-specific. While these effects are unlikely to have any anti-tumour activity they can be exploited to improve the combination of heat with other therapies. However, since similar physiological effects should occur in normal tissues, such combination therapies must be carefully applied. Heating tumours to higher temperatures typically causes a transient increase in perfusion during heating, followed by vascular collapse which if sufficient will increase tumour necrosis. The speed and degree of vascular collapse is dependent on heating time, temperature and tumour model used. Such vascular collapse generally occurs at temperatures that cause a substantial blood flow increase in certain normal tissues, thus preferential anti-tumour effects can be achieved. The tumour vascular supply can also be exploited to improve the response to heat. Decreasing blood flow, using transient physiological modifiers or longer acting vascular disrupting agents prior to the initiation of heating, can both increase the accumulation of physical heat in the tumour, as well as increase heat sensitivity by changing the tumour micro-environmental parameters, primarily an increase in tumour acidity. Such changes are generally not seen in normal tissues, thus resulting in a therapeutic benefit.
Topics: Blood Vessels; Combined Modality Therapy; Humans; Hyperthermia, Induced; Microcirculation; Neoplasms; Regional Blood Flow; Vasodilator Agents
PubMed: 16754339
DOI: 10.1080/02656730600689066 -
Medical Hypotheses Feb 1998Despite the great efforts to find new drugs or devices to suppress cancer cells, attempts to modify microcirculation and therefore the state of tumor cells and their...
Despite the great efforts to find new drugs or devices to suppress cancer cells, attempts to modify microcirculation and therefore the state of tumor cells and their surrounding normal tissues have not been given the attention they deserve. Solid tumors are composed of highly heterogeneous populations of malignant, stromal and inflammatory cells in a continuously adapting extracellular matrix. All of the above components interact and regulate each other to produce distinct microenvironments within the tumor mass. Abnormal microcirculation plays a particular role in the maintenance of this anomalous condition and favors the formation of metastasis, but on the other hand provides the therapist with an important site for intervention. In this brief overview we attempt to outline three aspects: (a) how the anomalous tumor blood flow provokes the nonuniform distribution of oxygen and nutrients within the tumor mass, thus determining different responses to the various cancer therapies; (b) how hemorheology is the clinical parameter most easily modified and (c) how omega-3 essential fatty acids are natural drugs that could be used in this sense beyond their antitumoral properties.
Topics: Animals; Antineoplastic Agents; Cell Hypoxia; Fatty Acids, Omega-3; Humans; Hyperthermia, Induced; Immunotherapy; Microcirculation; Models, Biological; Neoplasms; Photochemotherapy; Radiation Tolerance
PubMed: 9572573
DOI: 10.1016/s0306-9877(98)90204-3 -
Histopathology Jan 2003
Review
Topics: Humans; Hypertension, Portal; Liver Circulation; Liver Cirrhosis; Microcirculation; Practice Guidelines as Topic
PubMed: 12493019
DOI: 10.1046/j.1365-2559.2003.01464.x -
Annals of Biomedical Engineering 1998Presented is a discussion of steps towards the creation of a database of the microcirculation encompassing anatomical and functional experimental data, and conceptual...
Presented is a discussion of steps towards the creation of a database of the microcirculation encompassing anatomical and functional experimental data, and conceptual and computational models. The discussion includes issues of database utility, organization, data deposition, and linkage to other databases. The database will span levels from gene to tissue and will serve both research and educational purposes.
Topics: Animals; Biomedical Engineering; Databases, Factual; Humans; Microcirculation; Models, Cardiovascular; Research
PubMed: 9846930
DOI: 10.1114/1.112 -
Diabetes Care Aug 2001To review evidence for a relationship between dermal neurovascular dysfunction and other components of the metabolic syndrome of type 2 diabetes. (Review)
Review
OBJECTIVE
To review evidence for a relationship between dermal neurovascular dysfunction and other components of the metabolic syndrome of type 2 diabetes.
RESEARCH DESIGN AND METHODS
We review and present data supporting concepts relating dermal neurovascular function to prediabetes and the metabolic syndrome. Skin blood flow can be easily measured by laser Doppler techniques.
RESULTS
Heat and gravity have been shown to have specific neural, nitrergic, and independent mediators to regulate skin blood flow. We describe data showing that this new tool identifies dermal neurovascular dysfunction in the majority of type 2 diabetic patients. The defect in skin vasodilation is detectable before the development of diabetes and is partially correctable with insulin sensitizers. This defect is associated with C-fiber dysfunction (i.e., the dermal neurovascular unit) and coexists with variables of the insulin resistance syndrome. The defect most likely results from an imbalance among the endogenous vasodilator compound nitric oxide, the vasodilator neuropeptides substance P and calcitonin gene-related peptide, and the vasoconstrictors angiotensin II and endothelin. Hypertension per se increases skin vasodilation and does not impair the responses to gravity, which is opposite to that of diabetes, suggesting that the effects of diabetes override and counteract those of hypertension.
CONCLUSIONS
These observations suggest that dermal neurovascular function is largely regulated by peripheral C-fiber neurons and that dysregulation may be a component of the metabolic syndrome associated with type 2 diabetes.
Topics: Diabetes Mellitus, Type 2; Humans; Insulin Resistance; Laser-Doppler Flowmetry; Microcirculation; Regional Blood Flow; Skin
PubMed: 11473088
DOI: 10.2337/diacare.24.8.1468 -
Microcirculation (New York, N.Y. : 1994) Feb 2001Cell activation in the microcirculation leads to an inflammatory cascade and is accompanied by many cardiovascular complications. There is a need to identify the trigger... (Review)
Review
Cell activation in the microcirculation leads to an inflammatory cascade and is accompanied by many cardiovascular complications. There is a need to identify the trigger mechanisms that lead to the production of in vivo activating factors. We review here mechanisms for cell activation in the microcirculation and specifically the production of humoral cell activators in physiological shock. The elevated levels of activating factors in plasma could be traced to the action of pancreatic enzymes in the ischemic intestine. New interventions against the production of the activators are proposed. The evidence suggests that pancreatic enzymes in the ischemic intestine may attack several tissue components and generate cellular activators that are associated with multiorgan dysfunction in physiological shock.
Topics: Animals; Enzyme Inhibitors; Humans; Inflammation Mediators; Microcirculation; Multiple Organ Failure; Pancreas; Shock
PubMed: 11296853
DOI: No ID Found