Biomedical subjects

A B Ritter

Publications and source records attributed to A B Ritter.

11 recordsLinked to original sources

PubMed1990

Ascites: its effect upon static inflation of the respiratory system.

This report presents a simple clinical method to quantify the pressure generated within ascites fluid and thus to examine the effect of that fluid upon lung volume. The intra-abdominal hydrostatic pressure (Pih) given in cm H2O is the height of the meniscus of a column of water above the anterior abdominal wall measured with the patient supine. Pih thus may be thought of as a pressure in excess of the height of the anterior abdominal wall. In 23 study subjects, Pih measured 7.0 +/- 4.8 cm H2O; Pih correlated inversely with all static volumes. Furthermore, abdominal compliance (measured as the ratio of 100 ml ascites fluid removed divided by the difference between Pih before and after fluid removal) correlated directly with functional residual capacity. We conclude that the effect of ascites upon respiratory function varies among patients; the variation may be explained in part by Pih.

Abdominal Muscles↗

PubMed1989

Analysis of microvascular permeability to macromolecules by video-image digital processing.

The dynamics of macromolecular transport across microvascular walls were studied in the hamster cheek pouch by intravital fluorescence microscopy. A graded series of fluorescein isothiocyanate-labeled dextrans (FITC-Dx) of 20,000-70,000 MW was used as macromolecular tracers. The time-dependent extravasation of FITC-Dxs was videotaped for about 2.5 hr to allow for tracer equilibration in the interstitial space. Permeation of macromolecules from individual microvessels was quantified by digital video-image processing. Histograms of the light intensity distributions for selected fields at various times were measured and used to construct integral optical density-time profiles of the extravasated fluorochromes for particular leaky sites. A nonlinear regression algorithm was employed to determine the effective microvascular permeability (P) for the macromolecules studied using a one-dimensional two-compartmental diffusion model and a step change in macromolecular concentration at the boundary. The calculated P's (X 10(-8) cm/sec) were 47.8 +/- 8.7 for FITC-Dx 20; 31.7 +/- 5.9 for FITC-Dx 40, and 17.5 +/- 4.1 for FITC-Dx 70. Our values are comparable to those obtained by whole organ techniques. The observed differences can be explained by explicit consideration of interstitial resistance in the calculations.

Algorithms↗

PubMed1988

Effect of platelet-activating factor on leukocyte adhesion to microvascular endothelium. Time course and dose-response relationships.

The hamster cheek pouch microcirculation was used to investigate the effects of platelet-activating factor (PAF) on leukocyte adhesion to microvascular walls by means of intravital microscopy. PAF was applied topically at concentrations ranging from 10(-11) to 10(-5) M. An inverse relationship between PAF concentration and number of adhering white cells per 100-microns length was found in venules ranging in diameter from 10 to 60 microns (grouped into 10-microns intervals). Importantly, the PAF-induced adhesion of leukocytes lasted for the 3-h experimental period. We postulate that induction of leukocyte adhesion to venular endothelium is an important role of PAF in inflammatory processes.

Animals↗

PubMed1988

Vasoconstrictor effects of platelet-activating factor in the hamster cheek pouch microcirculation: dose-related relations and pathways of action.

Platelet-activating factor (PAF) has been implicated as a potential mediator of inflammatory processes. In this study, we quantified the effects of PAF on vessel diameter in a microvascular bed and investigated the biochemical pathways of this compound. The hamster cheek pouch microcirculation was observed with intravital microscopy. Experiments were video-recorded and analyzed with an image shearing device. Vasoconstriction was the predominant vasomotor response to PAF. PAF (10(-10) -10(-5) M) was applied topically to the pouch for 3 minutes. Arterioles ranging in size from 8 to 15 micron were the most sensitive, and they constricted completely in response to PAF 10(-7) and 10(-5) M. Arterioles 21-40 micron in diameter constricted to 12-17% of control after PAF at 10(-7) and 10(-5) M, respectively; they reopened to about 70% of their control value after a few minutes and remained near that size throughout the experiment. Arterioles 41-60 micron in diameter constricted to about 20% control size in response to 10(-7) and 10(-5) M PAF, and by the end of the experiment, these vessels had returned to about 90% control size. To determine the pathways of PAF actions, inhibitors of the arachidonic acid cascade and receptor blockers were used. Dexamethasone, indomethacin, OKY-046 (a thromboxane A2 synthetase inhibitor), and kadsurenone (a PAF-receptor blocker) blocked the vasoconstrictor response to PAF. Our experiments demonstrate that PAF-produced arteriolar constriction in a microvascular bed is 1) dose-related, 2) dependent upon vessel size, 3) largely due to thromboxane A2 activity, and 4) mediated by PAF-receptor interactions.

Animals↗

PubMed1988

Inspiratory muscle strength in asthma.

Augmentation of inspiratory muscle strength (Pimax) represents an adaptive response to airway obstruction. We explore the possibility that respiratory muscle weakness may herald hospital admission during acute bronchospasm. The Pimax measured 81 +/- 25 percent of a predicted value in 20 patients with acute bronchospasm (forced expiratory volume in one second, 36 +/- 17 percent predicted). Pimax was related to both hyperinflation (functional residual capacity, as percent predicted) and body weight (subjects were 122 +/- 29 percent ideal body weight), but not to the degree of airway obstruction per se. Furthermore, measurements of axial (craniocaudal) motion of the rib cage and asynchrony of rib cage and abdominal motions during tidal breathing did not correlate with either the degree of air flow obstruction or Pimax. We conclude that little if any respiratory muscle weakness occurs with bronchospasm. Furthermore, Pimax does not correlate with the degree of airway obstruction and does not explain abnormalities of rib cage and abdominal motion associated with asthma.

Abdominal Muscles↗

PubMed1988

Dose-response relationships between platelet activating factor and permeability--surface area product of FITC-dextran 150 in the hamster cheek pouch.

Changes in vascular permeability to FITC-dextran 150 associated with topical application of platelet activating factor (PAF) in the hamster cheek pouch preparation were calculated using a mathematical model (Baxter et al., Microvasc. Res. 34:336, 1987). Least square estimates of apparent permeability-surface area product (PS) and interstitial diffusion coefficient (D) were calculated from the data and the mathematical model using a Marquart optimization algorithm. Calculated PS products varied with applied PAF concentration while the best-fit estimate of apparent D remained constant at 10.5 X 10(-10) cm2/s. Average baseline PS was 16.5 X 10(-8) ml/s. PS increased to 45.2 X 10(-8) ml/s and 52.3 X 10(-8) ml/s with application of 10(-8)M and 10(-7)M PAF, respectively. A further increase in PAF concentration to 10(-6)M decreased the calculated PS product to 30.5 X 10(-8) ml/s. PAF is a potential modulator of macromolecular permeability in the microcirculation. This is the first study which quantitates the changes in PS of FITC-dextran 150 as a function of PAF concentration.

Animals↗

PubMed1987

Microvascular transport and endothelial cell alterations preceding skeletal muscle damage in ischemia and reperfusion injury.

We determined the leakage of macromolecules using FITC-dextran-150 as a tracer and measured the extent of no-reflow phenomenon by video field analysis. The cremaster muscle of anesthetized rats was fashioned as a single layer, splayed on a lucite chamber and suffused with bicarbonate solution at 35 degrees C. After a 1 hour period of baseline data collection, ischemia was produced by cross-clamping the cremasteric vascular pedicle for periods of 30 minutes and 2 hours in separate experiments. Macromolecular leakage was visualized after reinstitution of perfusion. Leakage occurred at postcapillary venules 15 to 50 micron in diameter and quickly spread to the interstitium. The magnitude of leakage decreased as a function of time with continuous buffer suffusion, but remained higher than in the control period. No reflow occurred in approximately 30 percent of the muscle microvasculature upon reperfusion. The no-reflow values at 30 minute and 2 hour periods of ischemia were significantly different from the control values but were not from each other. Electron micrographs demonstrated endothelial cell swelling and migration of leukocytes and normal myocytes after 1 hour of reperfusion following 2 hours of ischemia. Our results demonstrate that permeability changes, occurrence of no reflow, and leukocyte migration precede the onset of damage to skeletal muscle in ischemia and reperfusion injury.

Animals↗

PubMed1987

Assessment of ischemia reperfusion injury in skeletal muscle by macromolecular clearance.

Qualitative changes in skeletal muscle injury after ischemia are well known; however, quantitative assessments have not been well documented. We have determined microvascular permeability changes by measuring the clearance of fluorescein-labeled dextran of MW 150,000 (FITC-Dextran-150). The cremaster muscle of anesthetized rats was fashioned as a single layer, splayed on a lucite chamber and suffused with bicarbonate buffer solution at 35 degrees C. Clearance is the product of suffusion rate times the ratio of suffusate to plasma concentrations of FITC-Dx 150. After a 1-hr period of baseline data collection, ischemia was produced by cross-clamping the cremasteric vascular pedicle for periods of 30 min and 2 hr in separate experiments. Clearance of FITC-Dx 150 increased from a control value (mean +/- SE) of 8.3 +/- 2.7 to 29.9 +/- 8.1 microliters/min/g after reperfusion following a 30-min period of ischemia, and from a control value of 36.2 +/- 13.6 to 274 +/- 94.5 after 2 hr of ischemia. The differences were statistically significant (P less than 0.05). Our results show a significant increase in microvascular permeability occurring after only 30 min of ischemia. They also demonstrate a direct relationship between the extent of the permeability change and the duration of the ischemic period.

Animals↗

PubMed1985

Visualization of the coronary microcirculation using digital image processing.

A system was constructed to allow direct visualization of the coronary microcirculation of a beating rat heart under a microscope. An electrocardiogram (EKG) triggered strobe is used on the video recording and display system to "stop" the action of the beating heart so the surface microvessels can be directly observed. Experimental results are recorded on videotape and played back for frame-by-frame analysis of the data using digital image extraction, image enhancement and edge detection. The digital image processing techniques are designed for multi-purpose applications using recorded video images.

Animals↗

PubMed1985

Alveolar microvessels in isolated perfused dog lungs: structural and functional studies after production of moderate and severe hydrodynamic edema.

We have reported earlier that increased endothelial vesiculation follows the development of septal edema and alveolar flooding in isolated dog lung preparations. In this report, established ultrastructural morphometric analyses are coupled with data from physiologic and indicator-dilution studies to evaluate the stage of edema development at which de novo formation of alveolar microvessel plasmalemmal vesicles occurs. The interpretation that alveolar microvessel plasmalemmal vesicles increase prior to alveolar flooding, the final stage of edema formation, is consistent with the results reported here. Moderate pulmonary edema, characterized by substantial fluid cuffing around extra-alveolar arteries and veins and by fluid accumulation restricted to the thick sides of the alveolar septa, is associated with increased vesiculation in alveolar vessel endothelium. Further, a larger percentage of the vesicle population seen is directly attached to the endothelial luminal or abluminal surfaces. The functional significance of an increased population and an altered intracellular distribution of vesicles remains undetermined. The vesicles may provide a minor defense against excessive septal interstitial fluid accumulation, and subsequent alveolar flooding, by contributing to retrograde transport to the blood. Increased vesiculation, on the other hand, may represent an adaptive cellular response to interstitial fluid accumulation.

Animals↗

PubMedDate not supplied

Reduction of pressure in postcapillary venules induced by EPI-fluorescent illumination of FITC-dextrans.

Blue light (488nm) irradiation of intravenously injected fluorescein isothiocyanate (FITC)-Dextrans induces platelet aggregation in microvessels. The build-up of the aggregates in the microvessel lumen results in a change in microcirculatory hemodynamics. We found that lumenal pressure falls to approximately 75% of the control pressure within the first 10 seconds following the onset of irradiation. The damage, however, is not permanent and pressure returns to control level after the illumination of the microcirculatory field is discontinued. This effect can lead to erroneous conclusions in studies of microcirculatory hemodynamics and macromolecular permselectivity in preparations in which intravital fluorescence microscopy is employed. Short time irradiation (1 min. or less) of the microcirculatory field is recommended as a means of minimizing the deleterious effects of blue light irradiation.

Animals↗