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Biomedical subjects

M Horimoto

Publications and source records attributed to M Horimoto.

At least 109 records · Page 6Linked to original sources
PubMed1988

Lymphatic microcirculation in frog lung.

Lymphatic microvessels were microscopically observed on the surface of frog lungs. Magnified images of lymphatic microvessels were recorded on video tapes. The lymphatic microcirculation was studied on a TV monitor at the magnification of 1500 times. 1) valves were observed in lymphatic microvessels, whose diameter was 15 micron, in frog lungs, 2) the valves were incompetent, 3) contained particles repeatedly flowed backwards and forwards in each lymphatic section, 4) after repetition of the movements, particles passed through the outlet valve, 5) particles seldom flowed back through the inlet valve into the preceding section of the lymphatic, 6) the peak flow velocity of particles attained 0.5 mm/sec, and 7) the mean flow velocity was 11 +/- 4 micron on an average and +/- SD, 8) the diameter of a localized portion of the lymphatic microvessels changed periodically.

Animals↗
PubMed1984

Cessation of capillary blood flow induced by localized application of carbon dioxide.

A small test area of the pulmonary capillary bed of frog's lung was exposed to carbon dioxide. The capillary bed was observed by means of a dark field episcopal microscope and recorded on video tapes via a TV-camera. Swollen capillaries forming a hexagonal network surrounded concave alveolar cells. The flow velocity of red blood cells through capillaries was reduced to 17.5% of the flow velocity during the control condition by the application of the moistened gas mixture containing 30% CO2. The blood flow in capillaries ceased when wet 100% CO2 was applied to the test area. Red blood cells were packed in capillaries. They disaggregated by the introduction of air in five seconds and were quickly flowing in an elongated leaflet shape in 30 seconds after the introduction of air.

Animals↗
PubMed1984

Hypoxic reduction in blood flow velocity in pulmonary arterioles and capillaries.

A small ring chamber (I.D. = 6 mm) was placed on the exposed lung of anaesthetized bullfrogs. A localized hypoxia was induced in the ring chamber by introducing nitrogen in it. Blood flow velocity in pulmonary microvessels was measured by means of a laser Doppler microscope. The mean blood flow velocity was 1.98 +/- 0.45 and 1.52 +/- 0.10 mm/sec during the control condition in arterioles and capillaries, respectively. It was then reduced by the localized hypoxia to 1.63 +/- 0.32 and 1.33 +/- 0.08 mm/sec in arterioles and capillaries, respectively. The reduction, when expressed in the percentage ratio to the control flow velocity in each blood vessel group, was significantly larger in arterioles than in capillaries. A phase delay in the pulsation of the flow velocity contour was detected only in arterioles. These differences between pulmonary arterioles and capillaries in response to the localized hypoxia may be attributed to the dense interconnection of capillary network extending beyond the localized hypoxic area to the normoxic area.

Animals↗
PubMed1984

Pulmonary veno-occlusive disease in an elderly man: case report and review of the literature.

A 75-year-old man complaining of dyspnea and having sings of postcapillary pulmonary hypertension was diagnosed as pulmonary veno-occlusive disease and confirmed at autopsy. This is the oldest case ever reported. Almost all the small veins 2 mm or less in external diameter were partially or nearly completely occluded by intimal fibrous tissue, and the obstructive changes in the pulmonary arteries were much more limited. Pulmonary veno-occlusive disease is a rare, almost inevitably fatal disease of unknown etiology which has only recently been separated clearly from primary pulmonary hypertension as a distinct entity. Chest roentgenogram finding suggesting postcapillary pulmonary hypertension is a clue to a diagnosis and differentiates this from two other causes of clinical primary pulmonary hypertension, that is, recurrent pulmonary embolism and plexogenic pulmonary arteriopathy.

Aged↗
PubMed1983

Blood flow reduction in local pulmonary microvessels during acute hypoxia imposed on a small fraction of the lung.

Hypoxia was induced in a small fraction (less than 0.2%) of the whole lung by introducing pure nitrogen into a small gas chamber placed on the exposed lung surface of bullfrogs. This method of gas application exposed only the several alveoli encircled by the chamber to hypoxia. Thus it produced changes in the microcirculation within a small localized test area. Blood flow velocity and vessel diameter were measured by means of a laser Doppler microscope with a scaled ocular lens on a lateral viewer. Mean blood flow velocity in arterioles and capillaries within the test area decreased by 21.7 +/- 8.0% and 12.1 +/- 4.5%, respectively, during hypoxia. Arteriolar vessel diameters decreased by 15.3 +/- 7.0%. Therefore, the computed blood flow through the observed arterioles leading into the capillary bed within the test area decreased to 59% of its control value. This large decrement in arteriolar flow rate should result in a large reduction of the flow velocity in the capillaries, in contrast to the actually observed small reduction in capillary flow velocity. The efficiency of the hypoxic regulation of blood flow distribution in pulmonary capillary bed is probably reduced when hypoxia is imposed on a very small fraction of the frog lung.

Acute Disease↗
PubMed1982

Pulmonary microcirculatory response to localized hypercapnia.

Anesthetized bullfrogs were examined to study the effects of localized hypercapnia on the red blood cell (RBC) velocity in pulmonary alveolar microvessels on the exposed lung surface. Before and after the exposure of a small area of the lung surface 6 mm in diameter to a hypercapnic gas mixture, the region was exposed to CO2-free control gas. The RBC velocity was measured by the use of a laser Doppler microscope. Both mean flow velocity (MV) and pulsatile amplitude (PA) were determined from the resulting flow velocity contour. Responses of pulmonary microvessels to hypercapnia were examined by measuring the vessel diameters with an ocular microscale of the microscope while gas mixtures were applied to a 1-mm-diameter region of the surface. During hypercapnia both MV (2.31 +/- 0.27 mm/s) and PA (0.54 +/- 0.15 mm/s) in the alveolar arterioles (luminal diameter = 64 +/- 14 microns) were reduced, each reaching a minimum (2.01 +/- 0.24 and 0.43 +/- 0.19 mm/s, respectively) prior to gradual returns to their initial values. After reintroduction of the control gas, the values of MV and PA approached initial values more rapidly. In capillaries MV (1.44 +/- 0.18 mm/s) and PA (0.28 +/- 0.06 mm/s) decreased to 1.25 +/- 0.10 and 0.15 +/- 0.05 mm/s, respectively. The maximum reduction of PA (-44.6%) therefore clearly exceeded that of MV (-12.4%) in capillary flow. An analog model calculation suggested that the reduction in diameter of the arteriolar system could reduce PA more than MV in the pulmonary capillary network. The time course of the velocity change closely resembled that of the diameter change in relatively large arterioles. Vasoconstriction of the arterioles therefore appeared to be the major cause of these decrements in MV and PA.

Animals↗
PubMed1982

Red blood cell deformability in renal failure.

Red blood cell deformability was measured in 74 cases of renal failure and diabetic nephropathy by means of a modified nuclepore membrane filter method. Low red blood cell deformability was observed in a certain proportion of the patients. In cases of renal failure only weak correlation was found between reduced red blood cell deformability and BUN as well as between reduced red blood cell deformability and creatinine level, while simultaneous changes in these variable were observed in several patients. The reduction in red blood cell deformability in cases of diabetic nephropathy slightly exceeded that in cases of renal failure and correlated with an increment in HbA1c content. The effects of uremic toxins were unclear in in vitro tests. The red blood cell deformability was impaired in nephrectomized rabbits.

Animals↗
PubMed1982

Acute microcirculatory response to nicotine in frog web.

Acute effects of nicotine (NC) on the microcirculation of frog webs were studied by measuring the blood flow velocity in arterioles, and by determining the diameter of both arterioles and venules. Simultaneous recordings of the ventricular pressure and heart rate were obtained in order to compute the vascular resistance and to interpret the changes in microcirculation. The web of right hindlimb was immersed in a solution of NC (2.6 to 3.4 mg/ml) for 4 min. Blood flow velocity in web arterioles of left hindlimb was measured by means of a laser Doppler microscope. Internal diameters of web microvessels were determined using a micrometer on the ocular lens of the microscope. Mean flow velocity (MV) and pulsatile amplitude (PA) were calculated from the pulsatile flow-velocity contour for each vessel. Both MV and PA were increased after the immersion of the web in NC solution. Although the magnitude of the increment in MV was proportional to that in ventricular pressure, the vasodilation of both arterioles and venules and the flow rate in arterioles higher than the initial state continued even after the ventricular pressure had returned to the initial control value. Calculation of the relative change in vascular resistance in web arterioles following NC administration suggested a vasodilator response to NC. Furthermore, our results indicate that sufficient NC can be absorbed across the web epithelium to produce a systemic vascular response when the concentration of NC in the bathing solution is 2.6 mg/ml.

Animals↗
PubMed1982

White blood cell adhesion to endothelium and rheological behavior in microvessels of overinflated frog's lung.

The flow behaviors of white blood cells (WBCs) in frog's pulmonary microvessels were recorded and analyzed by means of a microscope-TV camera system. When the flow velocity in arterioles was reduced to a level lower than 1 mm/sec by a moderate overinflation of the exposed lung, WBCs rolled on the endothelial surface, frequently came in contact with the capillary orifice and passed it quickly without deformation. The time length which was required for WBCs to pass through the capillary orifice was shorter than the time length for red blood cells. This observation suggested that WBCs were no hinderance to blood delivery from arterioles to the capillary network in the normal and moderate overinflation of the lung. However, when the lung was strongly overinflated and the center line flow velocity was reduced to 0.1 mm/sec, WBCs adhered to the endothelium in ten minutes. The adhering WBCs could not be detached by the recovery of the blood flow. It seemed probable that a large shear stress up to 100 to 200 dynes/cm2 was necessary to pull down the interaction between the adhering WBCs and the endothelium.

Animals↗