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Biomedical subjects

J L Patterson

Publications and source records attributed to J L Patterson.

At least 73 records · Page 4Linked to original sources
PubMed1979

Responses of pial arterioles after prolonged hypercapnia and hypoxia in the awake rabbit.

The changes in the responsiveness of pial arterioles to CO2 and in the composition of cortical cerebrospinal fluid bathing these vessels were studied in the awake rabbit before and after 6 days exposure to hypercapnia (7% CO2) or hypoxia (10% O2). The vasodilator response of pial arterioles to inhalation of 3--10% CO2 was diminished after prolonged hypercapnia and enhanced after prolonged hypoxia. After both hypoxia and hypercapnia, pial arteriolar responsiveness to CO2 was immediately returned toward control levels by washing the brain surface with normal artificial cerebrospinal fluid. The bicarbonate concentration of cerebrospinal fluid bathing the pial vasculature showed a significant decrease after hypoxia and a significant increase after hypercapnia, whereas CSF pH remained unaltered. We conclude that the alteration in responsiveness of pial arterioles to CO2 is due to a change in the chemical composition of the CSF bathing these vessels, involving an adjustment in the concentration of bicarbonate ions.

Animals↗
PubMed1978

Responses of cerebral arteries and arterioles to acute hypotension and hypertension.

The responses of cerebral precapillary vessels to changes in arterial blood pressure were studied in anesthetized cats equipped with cranial windows for the direct observation of the pial microcirculation of the parietal cortex. Vessel responses were found to be size dependent. Between mean arterial pressures of 110 and 160 mmHg autoregulatory adjustments in caliber, e.g., constriction when the pressure rose and dilation when the pressure decreased, occurred only in vessels larger than 200 micron in diameter. Small arterioles, less than 100 micron in diameter, dilated only at pressures equal to or less than 90 mmHg; below 70 mmHg their dilation exceeded that of the larger vessels. When pressure rose to 170- 200 mmHg, small vessels dilated while the larger vessels remained constricted. At very high pressures (greater than 200 mmHg) forced dilation was frequently irreversible and was accompanied by loss of responsiveness to hypocapnia. Measurement of the pressure differences across various segments of the cerebral vascular bed showed that the larger surface cerebral vessels, extending from the circle of Willis to pial arteries 200 micron in diameter, were primarily responsible for the adjustments in flow over most of the pressure range.

Animals↗
PubMed1978

Role of tissue hypoxia in local regulation of cerebral microcirculation.

The mechanism of action of hypoxia on cerebral blood vessels and its role in the regulation of the cerebral circulation were investigated in anesthetized cats. Arterial hypoxia produced marked cerebral arteriolar vasodilation, which was partially reversed by perfusing the space under the cranial window with artificial cerebrospinal fluid (CSF) containing 6-94% oxygen. More marked increase in the local supply of oxygen, via perfusion of the space under the cranial window with fluorocarbon FC-80 equilibrated with 100% oxygen, completely eliminated the vasodilation induced by arterial hypoxia. Fluorocarbon equilibrated with 100% N2 had no effect on the vasodilation. The vasodilation associated with hypotension was completely reversed by perfusion with fluorocarbon equilibrated with 100% oxygen and was unaffected by perfusion with fluorocarbon or CSF equilibrated with gas not containing oxygen. The vasodilation associated with Metrazole-induced seizures was partially reversed by perfusion with fluorocarbon containing oxygen. The results show that hypoxia dilated cerebral blood vessels entirely via a local mechanism, that hypoxia is the dominant mechanism involved in the vasodilation associated with hypotension, and that it is, at least partially, responsible for the vasodilation associated with seizures.

Animals↗
PubMed1978

Inhibition of rat bronchiolar oxygen consumption by plasma proteins.

The oxygen consumption of rat bronchioles suspended in a physiological salt solution containing plasma proteins was measured with the Cartesian diver microrespirometer. The oxygen consumption of the bronchiolar tissue 100-300 and 300-400 micrometer in diam was significantly (P greater than 0.01) reduced as the protein concentration of the suspending solution was increased from the low to the high extreme of the normal plasma physiological range and as the diffusion distance through the suspending medium was increased from 25 to 50 micrometer. The reduction in the bronchiolar oxygen consumption was significantly (P greater than 0.01) reversed by using 95% oxygen-5% nitrogen instead of air as the diffusing gas in the Cartesian diver. Measurements of the oxygen diffusivity in the protein solutions using a diaphragm diffusion cell showed a large decrease in the diffusivity as the plasma protein concentration was increased over the same concentration range used in the oxygen consumption studies. These results suggest that the reduction in oxygen consumption was secondary to a decrease in oxygen diffusion and may provide at least a partial explanation for the diffusion abnormalities which exist in noncardiogenic pulmonary edema in which there is an increase in microvascular membrane permeability to proteins.

Animals↗
PubMed1977

Mass transfer properties of gases in fluorocarbons.

The solubility and diffusion coefficient of oxygen and carbon dioxide were measured in both the pure and emulsified of two fluorocarbons, perfluorotributylamine and perfluorobutyl perfluorotetrahydrofuran. The solubility coefficient and the diffusivity of oxygen in the pure form of the fluorocarbons decreased with decreasing partial pressure of Oxygen (PO2), but the solubility coefficient and the diffusivity of carbon dioxide were independent of its partial pressure. The solubility and diffusion of oxygen in the emulsified form of the fluorocarbons followed the pattern expected from the behavior of oxygen in the pure fluorocarbon. The experimental results suggest that there exists a physical and/or chemical interaction between oxygen and the fluorocarbons, and this interaction is more pronounced at partial pressures below 150 mm Hg. Comparisons of the oxygen content in the fluorocarbon emulsions with that in whole blood show that at PO2 of 760 mm Hg, the oxygen content in the fluorocarbon emulsions is approximately one-half that in whole blood, but at PO2 of 50-150 mm Hg, the oxygen content in the emulsions decreases to values which are less than one-tenth that of whole blood.

Carbon Dioxide↗
PubMed1976

Effects of respiratory gases on cytochrome A in intact cerebral cortex: is there a critical Po2?

Changes in the redox level of cytochrome a and in the amount of oxygenated hemoglobin were measured by dual wavelength reflectance spectrophotometry in the intact cerebral cortex of cats (cerveau isolé preparation) and in unanesthetized rabbits with chronically implanted cranial windows. Increases in inspired oxygen were accompanied by an increase in the oxidation level of cytochrome a and an increase in the amount of oxygenated hemoglobin in the optical field. These changes were larger in the presence of 5% CO2. Reduction of the inspired oxygen concentration produced a decrease in the oxidation/reduction ratio of cytochrome a and a disoxygenation of hemoglobin. The presence of CO2 at these lower oxygen levels diminished the reduction of cytochrome a and the disoxygenation of hemoglobin. These data indicate that, in the resting subject, the reduction levels of cytochrome a are well above the low values seen in isolated mitochondria. They also indicate that the blood supply to the cerebral cortex is regulated at a level of slight hypoxia.

Animals↗
PubMed1976

Circulatory effects of prolonged hypoxia before and during antihistamine.

Five chronically instrumented healthy dogs were exposed to a 5-day period of breathing 10% oxygen in a chamber. The response to hypoxia was found to be time dependent. During the first 24 h of hypoxia the circulatory response was characterized by increases in cardiac output, heart rate, pulmonary and systemic arterial blood pressures, and pulmonary vascular resistance. Systemic vascular resistance increased; left atrial pressure decreased. During the early part of hypoxia the animals became hypocapnic; the arterial blood pH rose significantly. During the rest of the hypoxic period cardiac output, heart rate, and arterial blood pH returned to the control values; pulmonary and systemic arterial pressures and pulmonary vascular resistance remained significantly elevated. Systemic vascular resistance rose; left atrial pressure remained below control. This response to hypoxia was not substantially modified when the experiment was repeated during the administration of the antihistamine promethazine, an H1-receptor blocking agent, in a dose which blocked the pulmonary vasoconstrictor response to small doses of exogenous histamine. The circulatory response to acute hypoxia in five anesthetized dogs was not modified by intravenous administration of metiamide, an H2-receptor blocking agent.

Animals↗