Search PubMed⌕ Search

Biomedical subjects

R M Navari

Publications and source records attributed to R M Navari.

35 records · Page 2Linked to original sources
PubMed1981

Mechanism of cerebral arteriolar abnormalities after acute hypertension.

Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. Scanning and transmission electron microscopy of such pial arterioles showed discrete destructive endothelial lesions the density of which correlated with the degree of vasodilation. Abnormalities of the vascular smooth muscle were seen in all dilated arterioles but affected only a small number of smooth muscle cells. The oxygen consumption of pial arterioles from cats subjected to hypertension was significantly reduced in comparison to that of vessels from normal animals. The arteriolar abnormalities induced by hypertension were inhibited by pretreatment with inhibitors of cyclooxygenase (indomethacin or AHR-5850) or by topical application on the brain surface of scavengers of free oxygen radicals (mannitol or superoxide dismutase). The results suggest that the mechanism of the arteriolar abnormalities from acute hypertension involves a sudden increase in prostaglandin synthesis that leads to generation of free oxygen radicals.

Animals↗
PubMed1979

Oxygen consumption of pial arteries.

Pial arterioles and arteries, normally responsive to alterations in PaCO2, were obtained by microdissection from the parietal cortex of 53 anesthetized cats. The oxygen consumption of these vessels, determined with the Cartesian diver microrespirometer, was found to be size dependent. It increased progressively from vessels 60 mum in diameter to vessels 250 mum in diameter. In vessels 250--375 mum in diameter there was a progressive decrease in oxygen consumption with increasing vessel size. The oxygen consumption was not altered by increasing the oxygen concentration in the diver from 20% to 95%, or that of glucose from 1.1 to 2.0 mM. Planimetry of histological sections showed that the percentage of endothelium and smooth muscle increased as vessel diameter increased from 60 to 200 mum, and thereafter decreased with increasing vessel size. When these differences in the composition of the vessel wall were taken into account, there was still residual dependence of the oxygen consumption on vessel diameter. This may represent intrinsic differences in the metabolic rate of vascular smooth muscle in vessels of different size.

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↗
PubMedDate not supplied

Glucose metabolism in advanced lung cancer patients.

Although it is generally accepted that altered nutrient intake and metabolism are responsible for the progressive loss of body weight observed in most advanced cancer patients, there is still considerable controversy regarding the contributory role of changes in both resting energy expenditure (REE) and glucose metabolism. Several studies suggest increases in both REE and glucose appearance in advanced cancer patients compared with healthy control subjects, whereas others revealed no changes in either metabolic parameter. We measured REE with indirect calorimetry and glucose kinetics with a primed constant infusion of D-[U-14C]glucose and D-[6-3H]glucose over the last 4 h of a 24-h fast in 32 advanced lung cancer patients immediately after diagnosis and before any chemotherapy or radiotherapy and in 19 healthy volunteer subjects. REE for the lung cancer group was not significantly different from that in the control group (1535.8 +/- 78.0 vs. 1670.2 +/- 53.9 kcal/day, respectively, p = 0.151). When REE was expressed as a function of body weight, or lean body mass, no differences between the two groups were observed. The rate of glucose appearance was 9.88 +/- 0.36 mumol.kg-1.min-1 in the cancer patients and 10.15 +/- 0.53 mumol.kg-1.min-1 in control subjects (p = 0.667), of which 50.4 versus 58.2%, respectively, was oxidized. The amount of glucose recycled was 13.54 +/- 1.22% in cancer patients and 15.08 +/- 0.99% in control subjects (p = 0.394). The amount of VCO2 from direct oxidation of glucose was 23.39 +/- 0.74% in cancer patients and 27.45 +/- 1.36% in control subjects (p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗