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Biomedical subjects

L Reid

Publications and source records attributed to L Reid.

At least 55 records · Page 3Linked to original sources
PubMed1985

Effects of chronic hypoxia on structure and reactivity of rat lung microvessels.

The reactivity of lung microvessels is determined by a method based on planimetry of elastic laminae (EL) in vessel cross sections. Because wall structure is assessed, arteries that undergo remodeling during chronic hypertension can be identified. To study the structure and reactivity of such vessels, slices obtained from lungs of six rats exposed to hypobaric hypoxia for 14 days and from normoxic controls were incubated in culture with 10(-4) M l-epinephrine (EPI), then fixed and processed for microscopy. For muscular arteries (less than 200 microns diam), the circumferential length of internal EL (IEL) is positively correlated with length of external EL (EEL). In larger arteries, EEL is shorter than IEL and may restrict distension, but in smaller arteries the converse is true. After chronic hypoxia, the regression line shifts, indicating structural remodeling. For newly muscularized arteries found only after hypoxia the new IEL is always shorter than EEL, and a complex network of elastin connects the two. Muscular arteries constrict with EPI to the same degree after hypoxia as after normoxia. Nonmuscular vessels (arteries and veins) also constrict similarly after either exposure regimen. For newly muscularized arteries of the same size and location as the nonmuscular vessels, the response is significantly less.

Animals↗
PubMed1985

Oxygen toxicity and restructuring of pulmonary arteries--a morphometric study. The response to 4 weeks' exposure to hyperoxia and return to breathing air.

This study describes the pulmonary vascular lesions in rat pulmonary arteries and altered right ventricular weight after 1) prolonged exposure to hyperoxia (87% O2 for 4 weeks) at ambient pressure, 2) weaning from hyperoxia to air over 7 days, and 3) return to breathing air for 2, 4, or 8 weeks. Hyperoxia for 28 days narrows the lumen of intraacinar and preacinar arteries, increasing the percent medial thickness (%MT) by reducing the external diameter and thickening medial muscle. The ratio of patent intraacinar arteries to alveoli is significantly reduced, and pulmonary vascular obstruction and obliteration is evident by electron microscopy. A higher proportion of intraacinar and preacinar arteries have muscle in their wall than in the normal lung: in alveolar wall and duct regions, the proportion of partially muscular and muscular intraacinar arteries increases at the expense of nonmuscular ones (for both regions P chi 2 less than or equal to 0.001); and in arteries associated with terminal bronchioli and bronchioli the proportion of muscular arteries increases at the expense of partially muscular ones (for both regions P chi 2 less than or equal to 0.001). Both after weaning and after return to breathing air lumen size increases; but, even after 8 weeks, the %MT remains significantly increased, and the ratio of intraacinar arteries to alveoli is less than normal. After weaning, the proportion of muscularized intraacinar and preacinar arteries is similar to that after hyperoxia. Two weeks after return to breathing air, the proportion of muscularized alveolar wall and duct arteries is greater (for both regions P chi 2 less than or equal to 0.001). Even 8 weeks after return to breathing air more arteries are muscularized than normal (for both alveolar wall and duct regions P chi 2 less than or equal to 0.001), and within the alveolar wall still more are muscularized than after hyperoxia (P chi 2 less than or equal to 0.001). Hyperoxia causes right ventricular hypertrophy, reducing the ratio of the weight of the left ventricle and septum to that of the right ventricle (P chi 2 less than or equal to 0.001). Weaning further increases the hypertrophy, the ratio being further reduced (P chi 2 less than or equal to 0.001, compared with both hyperoxia and control values). On return to breathing air the degree of hypertrophy is less, but it persists, and even after 8 weeks the ratio is still less than normal (P chi 2 less than or equal to 0.01).

Animals↗
PubMed1984

The pulmonary hemodynamic response to perioperative anesthesia in the treatment of high-risk infants with congenital diaphragmatic hernia.

The continuing high mortality in congenital diaphragmatic hernia led us to study the cardiopulmonary disturbances associated with this lesion. Since these infants infrequently have right-to-left shunting in the operating room, we adopted a treatment protocol of: continuing general anesthesia in the postoperative period using fentanyl and pancuronium; cardiac catheterization postoperatively, including placement of a pulmonary artery line and a pulmonary angiogram; rapid frequency ventilation; moderate fluid restriction; and avoidance of vasodilators until other means of management had clearly failed. Fourteen high-risk infants, presenting within 6 hours of birth, were studied and compared to 17 high-risk infants, who served as historical controls. As revealed by the physiologic data acquired in the catheterization laboratory, high-risk infants divided into "Responder" and "Nonresponder" groups. Seven of 10 "Responders" actually shunted left to right during the catheterization, demonstrating a low pulmonary vascular resistance. Seven of 10 subsequently demonstrated significant right-to-left shunting at the level of the ductus and the foramen ovale, indicating the hyperreactivity of the pulmonary vascular bed. All but one was managed successfully by ventilatory adjustments and deepening of the level of anesthesia. "Nonresponders" had a fixed right-to-left shunt unresponsive to any medical or ventilatory manipulation. All "Nonresponders" died. Pulmonary angiography suggested a smaller diameter of the affected pulmonary artery compared to the main pulmonary artery in the "Nonresponders." This implies true hypoplasia resulting in a vasculature too small to accept a full cardiac output. Survival in the treatment group "Responders" was eight of 10 (80%) v seven of 14 (50%) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1984

Vascular structure in lung tissue obtained at biopsy correlated with pulmonary hemodynamic findings after repair of congenital heart defects.

At the time of surgical repair, a lung biopsy was performed on patients with congenital heart defects who either had pulmonary hypertension or in whom it would be likely to develop if the lesion were not corrected. Pulmonary vascular changes, assessed morphometrically and also according to the classification of Heath and Edwards (Circulation 18: 533, 1958), were correlated with the postoperative pulmonary hemodynamic findings: mean pulmonary arterial pressure the day after correction and mean pulmonary arterial pressure and pulmonary vascular resistance measured 1 year later. On the first postoperative day, increased mean pulmonary arterial pressure was uncommon in patients with morphometric grade A or B (mild) biopsy findings and Heath-Edwards grade N (normal), and if it was present it was of a mild degree. Mean pulmonary arterial pressure was commonly elevated in those with grade B (severe) or C (mild or severe) and Heath-Edwards grade I biopsy results and was more frequently elevated in those with grade II findings. Moderate-to-severe elevation of mean pulmonary arterial pressure was invariable in patients with Heath-Edwards grade III changes regardless of the morphometric grade. One year after repair, mean pulmonary arterial pressure and/or pulmonary vascular resistance were normal in all patients whose conditions were corrected surgically before 9 months of age regardless of the severity of the pulmonary vascular changes. Values were normal in patients whose conditions were repaired surgically at 9 months of age or later who had grade A or B (mild) morphometric findings with any Heath-Edwards grade or grade B (severe) morphometric findings with Heath-Edwards grade I but were increased in half of the patients with grade B (severe) morphometric findings and Heath-Edwards grade II or with grade C (mild or severe) and Heath-Edwards grade I or II changes. Pulmonary arterial pressure and pulmonary vascular resistance were increased in all patients whose conditions were repaired after 2 years of age with grade C morphometric findings and to a severe degree if associated with Heath-Edwards grade III. Thus, although the Heath-Edwards grade can usually be used to identify patients at risk for pulmonary hypertension in the early postoperative period, both the morphometric and the Heath-Edwards grades as well as the age of the patient at the time of repair can be used to determine whether pulmonary arterial pressure and resistance eventually return to normal or remain elevated.

Autopsy↗
PubMed1984

Morphologic correlation of physiologic changes caused by SO2-induced bronchitis in dogs. The role of inflammation.

Chronic bronchitis was induced in 6 mongrel dogs by exposure to SO2 gas for 6 to 18 months. All of the dogs developed cough and mucus hypersecretion. Chronic airway obstruction and decreased airway responsiveness to inhaled histamine developed in 5 of the dogs. Histologic changes in dogs evaluated after SO2 exposure included significant mucous gland hypertrophy and hyperplasia, epithelial thickening, and a decrease in the number of luminal cells containing undischarged secretory granules. Acute and chronic inflammation were found in the dogs with airway obstruction and decreased responsiveness to histamine, but such inflammation was absent in the one dog that failed to develop physiologic changes. After a period of recovery from SO2 exposure of 9 to 21 months, inflammation regressed dramatically and the other histologic changes returned toward normal. Physiologic changes regressed somewhat in those dogs that had had changes. These findings suggest that inflammation may be an important factor influencing the development of airway obstruction and altered airway responsiveness in the setting of chronic bronchitis.

Airway Resistance↗
PubMed1984

The response of microvessels in rat lung explants to incubation with norepinephrine.

Because of the difficulty in isolating precapillary or postcapillary segments of the pulmonary microcirculation, there is little information on their reactivity even though they are important in normal lung function and play a crucial role in the pathogenesis of pulmonary hypertension. In order to study the reactivity of microvessels in lung we have developed a method in which thin slices of tissue are incubated in vitro with a vasoactive drug and are then fixed, embedded, and sectioned at a thickness of 1 micron. Vessel profiles are analyzed on a computer graphics tablet, and their degree of constriction is determined morphometrically. In this system, muscular arteries less than 200 microns in diameter in adult rat lung explants are moderately constricted, but they constrict further when incubated with 1-norepinephrine (10(-4), 10(-5) M), an effect maintained for 30 min. Nonmuscular vessels (arteries and veins) less than 100 microns in diameter also constrict in response to similar doses of norepinephrine. Although the effector cells remain to be identified, it is likely that pericytes and precursor muscle cells in the walls of these vessels are at least partly responsible.

Animals↗
PubMed1984

Pulmonary artery remodeling and pulmonary hypertension after exposure to hyperoxia for 7 days. A morphometric and hemodynamic study.

This study shows by morphometric and hemodynamic techniques that exposure to hyperoxia at normobaric pressure causes rapid structural remodeling of rat pulmonary arteries and pulmonary hypertension. After 7 days of 90% O2, pulmonary artery cross-sectional area is reduced by a striking loss of intraacinar arteries (control, 13 +/- 1 sq mm; exposed, 8 +/- 1 sq mm; P less than 0.001), the ratio of arteries to alveoli being 4:100 in control rats and 2.5:100 after hyperoxia. The lumen of preacinar and intraacinar arteries is narrowed by a reduction of vessel external diameter (ED) and an increased medial wall thickness (MT). There is a significant reduction in the percent medial thickness [( 2 X 100 X MT]/ED) in both regions. The proportion of muscular and partially muscular intraacinar arteries increases at the expense of nonmuscular ones (P [chi 2] less than 0.01), and fully muscular arteries appear in the alveolar wall where they are not normally found. Intimal thickening occurs in 19% of alveolar duct and 34% of alveolar wall nonmuscular arteries. Right ventricular hypertrophy occurs, the ratio of the left ventricle plus the septum to the right ventricle being significantly reduced (control, 4.07 +/- 0.26; exposed, 3.23 +/- 0.10; P less than 0.02). After 3 days of 87% O2, pulmonary artery pressure is still normal (17.0 +/- 0.9 mmHg) but after 7 days it is significantly increased (26.2 +/- 0.9 mmHg; P less than 0.01), as is pulmonary vascular resistance (control, 0.033 +/- 0.003; exposed, 0.065 +/- 0.015 U/kg; P less than 0.05). Return to air breathing (after 7 days at 87% O2) causes pulmonary vasoconstriction and a further rise of the pulmonary artery pressure (to 38.3 +/- 3.3 mmHg after 60 minutes).

Animals↗
PubMed1984

The development of a model of subacute lung injury after intra-abdominal infection.

Acute respiratory failure in humans often follows extrathoracic sepsis. The purpose of this study was to determine the effect of repeated episodes of intra-abdominal sepsis over several weeks on the structure and function of rat lung. Intermittent peritonitis and a bacteremia of Escherichia coli and Bacteroides fragilis were produced by weekly intra-abdominal implants of gelatin capsules containing these organisms (3.0 +/- 1.0 X 10(7) and 5.0 +/- 1.0 X 10(7) colony-forming units/ml, respectively; mean +/- SEM). After 4 weeks alveolar walls were thickened and cellular with focal areas of alveolar space consolidation: circulating polymorphonuclear leukocytes were increased (12.2 +/- 1.2 to 19.9 +/- 2.0 X 10(3)/mm3; p less than 0.05), as were plasma levels of 6-keto-PGF1 alpha (0.56 +/- 0.08 to 1.02 +/- 0.18 ng/ml; p less than 0.01). After 8 weeks the capillary bed was dilated and the alveolar walls and ducts appeared less cellular but showed fibrosis: The WBC count had increased to 25.5 +/- 1.0 X 10(3) (p less than 0.01). After 4 or 8 weeks of intermittent sepsis there was no increase in the pulmonary artery pressure or vascular resistance or any change in arterial oxygen tension, plasma thromboxane beta 2 level, or platelet count. We conclude that repeated bouts of sepsis and bacteremia in the rat cause progressive injury to lung alveoli without evidence of altered blood gas tensions or pulmonary hemodynamics.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Polycythemia and the acute hypoxic response in awake rats following chronic hypoxia.

The acute hypoxic pressor response was studied in 22 chronically catheterized awake rats, 13 in whom the pulmonary arterial circulation had been remodeled by 10 days of exposure to hypobaric hypoxia. Five of these had their hematocrit lowered to normocytic levels after the chronic hypoxic exposure. Nine were controls. After 24 h in room air the pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (Rp) of hypoxic-polycythemic rats was at least twice the control value; in the hypoxic-normocytic rats Ppa and Rp were less than that of hypoxic-polycythemic animals and greater than that of controls. Cardiac index, heart rate, and O2 saturation were similar in all groups. In 10% O2 a rise in Ppa and Rp occurred in all groups; in absolute terms the rise was greater in hypoxic rats than in controls and greater in polycythemic than in normocytic animals. In the intact animal the acute hypoxic pressor response can still be elicited in a pulmonary vascular bed structurally altered by chronic hypoxia. When calculated as a percent increase over base line, its intensity was greater than in room air controls and for Ppa was independent of hematocrit.

Acute Disease↗
PubMed1983

Changes in pulmonary blood flow affect vascular response to chronic hypoxia in rats.

We banded the left pulmonary artery in rats to investigate, in the same animal, the effect of both increased and decreased flow on the lung vasculature and to determine how these hemodynamic states modify the structural changes produced by a 2-week exposure to hypobaric hypoxia. In unanesthetized rats, pressures were recorded from the main pulmonary artery and aorta via indwelling catheters, cardiac output was calculated by the Fick principle, and pulmonary and systemic vascular resistance estimated. Technetium-99m macroaggregated albumin was injected and radionuclide activity counted separately over the right and left lungs as a measure of flow. At postmortem, right and left ventricles of the heart were weighed and the lungs injected to permit analysis of arteriograms and morphometric assessment of structural changes in the pulmonary vascular bed. Flow in the left lung was reduced to one-fifth normal in rats with left pulmonary artery bands. In "room air" rats, pressure proximal to the left pulmonary artery band and in the right lung was slightly higher than in nonbanded controls, but not as high as in nonbanded or banded hypoxic rats. Changes in flow and pressure in both lungs of "room air" rats with left pulmonary artery bands were associated with a mild degree of extension of muscle into peripheral pulmonary arteries normally nonmuscular, medial hypertrophy of normally muscular arteries, and reduced arterial density. These three structural changes were present in both lungs of "hypoxic" rats but were much more severe. High flow in the right lungs of "hypoxic rats" with left pulmonary artery bands worsened only the degree of extension. Decreased flow and pressure in the left lungs of these animals prevented both the extension and the medial hypertrophy of hypoxia, but not the severe reduction in arterial density. It seems that the latter may occur as a direct response to low oxygen tension, whereas extension and medial hypertrophy are influenced by altered flow and pressure, respectively.

Animals↗
PubMed1983

Control and modulation of airway epithelial cells and their secretions.

Information on the control and modulation of airway epithelial cells and their secretion is obtained by three techniques: 1) in vivo studies of animal models of disease, 2) in vitro studies by organ culture of human and animal model airways, and 3) chemical analysis of human and animal bronchial secretion. The contribution of each of these techniques is described in this paper, including recent or new information. In vivo models of mucous hypersecretion can be produced by irritants, infection, and drugs more quickly than previously expected. In the rat, beta 1 and beta 2 receptors are present with evidence of different activity in various airway regions. Organ culture studies combine autoradiographic analysis of cell activity with chemical analysis of secretory product, and describe inhibitory effect of new agents such as VIP. The application of density-gradient ultracentrifugation gives total recovery of undegraded macromolecules from bronchial mucus; it is now possible to recover mucous glycoprotein of molecular weight larger than that previously isolated. The organ culture studies and density-gradient ultracentrifugation studies indicate that a proteoglycan is a significant constituent of total bronchial secretion. Differences between diseases are emerging in the macromolecular partitioning between sol and gel obtained at 160,000 X g, a higher speed than that previously applied systematically in such studies.

Animals↗
PubMed1983

The effects of hypophysectomy, thyroidectomy, and postoperative infusion of cortisol or adrenocorticotrophin on the structure of the ovine fetal lung.

We studied the effect of in utero hypophysectomy and replacement therapy with cortisol and adrenocorticotropin on maturation of lung structure in ovine fetuses. Twenty-two festuses underwent hypophysectomy in utero at 99-122 days of fetal gestation. At term (148-150 days), ten fetuses received an infusion of ACTH and six fetuses received an infusion of cortisol. The remaining fetuses were untreated. Morphometric analysis of the caudal lobe of the right fetal lung was performed and included measurement of minimum interalveolar wall thickness, numerical density of Type I and Type II pneumocytes in septal tissue, and volume density of septal tissue and air spaces in respiratory lung. The lung of the hypophysectomized animals differed from term controls in that alveolar walls were thicker, numerical density of Type I pneumocytes was less and that of Type II cells greater. Treatment with ACTH or cortisol caused lung structure to appear similar to the lungs of term control animals. We conclude that hypophysectomy impairs structural maturation and that structural maturation can be achieved by a relatively brief infusion of cortisol or ACTH at term.

Adrenocorticotropic Hormone↗
PubMed1983

Pulmonary hypertension. Anatomic and physiologic correlates.

The types of pulmonary arterial hypertension described here all focus attention on the changes produced in the lung's microcirculation, particularly the precapillary unit. Although one senses intuitively that obliteration of resistance arteries is an effective cause of hypertension, we emphasize that cell metaplasia and adaptation by structural remodeling of the precapillary arterial wall is also effective in reducing the vascular bed. A question often asked is whether "pruning" is the cause of the hypertension . . . perhaps an inappropriate question. While the reduced cross-sectional area of the vascular bed is the basis for the rise in pulmonary vascular resistance and for its severity, the real question is what is the cause of the "pruning." Hypoxia, monocrotaline, and high flow each causes pulmonary artery hypertension--and pruning--but with differences in cell adaptation, timing, and severity that indicate different pathogenetic mechanisms and pathways. It is paradoxical that hypoxia, whose lesions are more reversible, produces a more severe hypertension and faster than the others. While the pathophysiologic aspects are important to clinical diagnosis and management, it is analysis of cause and pathways of pathogenesis that will give the keys to prevention and cure of the disease.

Animals↗
PubMed1983

Pulmonary vasculature of piglets after correction of aorta-pulmonary shunts.

In a previous article we described the functional and structural changes produced in the pulmonary arterial circulation of the growing pig by an aorta-pulmonary shunt. The present work describes the hemodynamic and morphologic adaptation that follows correction of the shunt. In four piglets, aged 5 weeks, an anastomosis was made between the thoracic descending aorta and the pulmonary trunk and left patent for 5 weeks. At the end of that time the mean pulmonary artery pressure (PAP) was 20 +/- 3.8 mm Hg (mean +/- SD), compared with 9 +/- 2.1 mm Hg in a group of four age-matched sham-operated control piglets. The shunt was then surgically closed. After 10 weeks' recovery, the PAP was similar and normal in the two groups. We have already shown that pulmonary hypertension of similar degree and duration to that at the end of the patent shunt period produces the following structural changes, assessed by quantitative techniques: (1) preacinar arteries of normal external diameter but with a thicker medial coat than normal and (2) intra-acinar arteries in normal concentration, of smaller external diameter than normal, but with a medial coat appropriate to the external diameter: Smooth muscle is found in more peripheral arteries than is normal. In the present study, at the end of the recovery period, the shunt animals were compared with the sham-operated animals and had thicker medial coats in preacinar and intra-acinar arteries, muscle in more peripheral arteries than is normal, and an increased arterial and alveolar concentration for unit lung area. These results indicate that, in the growing porcine lung, "recovery" from an aorta-pulmonary shunt that was associated with moderate pulmonary hypertension restores external arterial diameter to normal but leaves a thicker medial coat at the preacinar and intra-acinar levels and muscle more peripheral in the arterial bed. In addition, after shunt correction, multiplication of alveoli and arteries proceeds at a faster rate than normal, at least during the first 10 weeks of recovery.

Animals↗
PubMed1982

Recurrent genital herpes simplex virus infection in pregnancy: infant outcome and frequency of asymptomatic recurrences.

Eighty pregnant patients with a history of recurrent genital herpes simplex virus (HSV) infection were followed up with frequent genital examinations and cultures for HSV during their pregnancies. Recurrences of genital HSV during pregnancy were documented in 67 patients. Ninety-six percent of these had external genital lesions noted at some time during their pregnancy. One hundred eighty-six (93%) of the 199 recurrences of the disease were associated with external genital lesions. Of 13 episodes of asymptomatic viral shedding documented in this patient population, six were from the vulva alone, five were from the cervix alone, and two were from both the vulva and the cervix. Of 11 episodes of cervical HSV shedding, seven were asymptomatic and four were associated with external symptomatic lesions. Despite frequent recurrences of genital HSV infection during pregnancy, all study patients were delivered at term, and although they had a high rate of delivery by cesarean section (32.5%), the outcome of their infants was good.

Adolescent↗