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Biomedical subjects

R Fried

Publications and source records attributed to R Fried.

At least 55 records · Page 3Linked to original sources
PubMed1988

Developmental changes in proton magnetic resonance relaxation times of cardiac and skeletal muscle.

Proton magnetic resonance relaxation time measurements were used to study developmental changes in rabbit cardiac and skeletal muscles during the last days of gestation and at several postnatal times. Tissue water content decreased steadily during late fetal and early postnatal stages of development. During this period T1 and T2 for cardiac and skeletal muscles also decreased. The relaxation times stabilized after the 20th postnatal day, and at this juncture the T1 and T2 values for myocardium remained consistently higher than for skeletal muscle. The developmental changes in proton relaxation time probably represent changes in water distribution and mobility as well as macromolecular structure during muscle maturation.

Animals↗
PubMed1987

Relaxation with biofeedback-assisted guided imagery: the importance of breathing rate as an index of hypoarousal.

Fifteen men and 35 women, suffering from a number of psychological and somatic disorders, were taught to relax by biofeedback-assisted deep-diaphragmatic breathing together with guided mental imagery. No instructions were given about rate. Breathing rate and pattern, PETCO2, and EEG were monitored before training and after the first three 2-minute training trials (session 1). In 27 subjects (54%), breathing patterns and rate were noted to resemble those reported by meditation practitioners (3 to 5 b/min). The PETCO2 and EEG changes support a hypothesis of metabolic hypoarousal. Four subjects spontaneously reported experiencing altered awareness. A centrally mediated hypoarousal response is tentatively implicated.

Adult↗
PubMed1987

[Does optokinetic stimulation modify directional hearing?].

The directional hearing of 20 healthy test persons, all with normal hearing abilities, was tested using a special self constructed equipment. Under the repeated influence of an optokinetic stimulation (rotating light beams on a semicircular screen in a completely darkened room) no statistically significant deviation of the directional hearing reactions could be detected.

Adolescent↗
PubMed1987

[Hearing loss caused by a walkman radio?].

Investigations on 50 high school students showed that this group had been using the "Walkman" only 1.5 h. per day during the last 14 months. A comparison of the audiometric results obtained with these 50 "Walkman" users, with those of 20 age-related non-"Walkman" users, showed no statistically significant differences. The investigation further revealed that to avoid hearing loss, an upper threshold level of 93 dB (A) should not be exceeded for a daily "Walkman" user time of two hours.

Adolescent↗
PubMed1987

Cardiovascular responses to exercise and stress in the borderline hypertensive rat.

This report demonstrates the effect of voluntary exercise in attenuating increases in heart rate (HR) caused by chronic stress in an animal model of stress-induced hypertension, the borderline hypertensive rat (BHR). Exercise training also protected against the hypertensive effects of stress in 16-wk-old, but not 10-wk-old animals. In the first experiment, adult borderline hypertensive rats were subjected to 1 wk of signaled shock followed by 6 wk of signaled, unsignaled, or no shock. Half of these animals also had free access to a running wheel. Blood pressure (BP) and HR were measured before and after treatments by the tail cuff method. Exercise was found to significantly attenuate the rise in BP by 56% and HR by over 100%, as compared to non-exercised animals. In a second study, borderline hypertensive rats were subjected daily to anticipation of shock or handling for 6 wk. Half of these animals could exercise voluntarily. BP and HR, measured weekly under light ether anesthesia, increased over time due to both stressors alone. Exercise attenuated stress-induced increases in HR by 50%, but did not attenuate BP. These studies demonstrate that voluntary exercise can reliably attenuate increases in HR regardless of age or concurrent stress, but the protective effects of exercise on stress-induced hypertension may interact with the age of the subject.

Animals↗
PubMed1986

Pulmonary arterial changes in patients with ventricular septal defects and severe pulmonary hypertension.

In 25 patients, aged eight months to 31 years, with ventricular septal defect (VSD; isolated in 15, the others with atrial septal defect, PDA, coarctation or patent ductus arteriosus + coarctation), each with severe pulmonary artery hypertension (pulmonary artery systolic pressure [Ppa] at least 75% of systemic and an elevated pulmonary vascular resistance), we related morphologic and morphometric data from open-lung biopsy to hemodynamic measurements obtained at cardiac catheterization during the same hospital admission. Of the hemodynamic features measured, only the ratios of pulmonary-to-systemic flow and pulmonary-to-systemic resistance correlated significantly with structure. Neither pulmonary artery pressure (Ppa) nor pulmonary vascular resistance correlated significantly with any structural feature studied. The increased external diameter of respiratory bronchiolar arteries in those with the more advanced Heath-Edwards grades reflects dilatation and suggests that it is in the small arteries of the distal arterial bed that the changes of pulmonary hypertension are most significant. Neither age nor body weight correlated significantly with the degree of structural or hemodynamic abnormality. In the ten patients who underwent VSD closure, Ppa was measured postoperatively. The Heath-Edwards grade (no more than one grade-III lesion) and arterial density (at least one-half that normal for age) were the best correlates of the difference between preoperative Ppa and Ppa immediately after corrective surgery. The presurgical catheterization data, including pulmonary resistance and the resistance ratio, did not correlate significantly with change in Ppa following VSD closure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1986

Nuclear magnetic resonance spectroscopy of rat ventricles following supravalvar aortic banding. A model of left ventricular hypertrophy.

Left ventricular hypertrophy produced by supravalvar aortic banding in infant rats was studied by proton magnetic resonance spectroscopy. Weight gain at 11 weeks of age in the 11 male Sprague-Dawley rats with aortic bands placed at three weeks was similar to that of the 14 controls. The left ventricle of banded rats hypertrophied, increasing the ratio of left ventricle plus septum to body weight (LV + S/BW) by more than 50% (P less than .00001). Right ventricular weight (RV/BW) increased slightly (P less than .03). T1 and T2 relaxation times of LV + S, RV, and thigh muscle (Th) from the banded and control rats were compared. The T2 value distinguished hypertrophied from control LV + S (P less than .003), but not between RV or Th from the two groups. For banded rats only, the T2 value distinguished each muscle type: LV + S from RV, LV + S from Th, and RV from Th (P less than .00001 for each). For control rats, cardiac muscle was distinguished from Th (P less than .00001), but LV + S and RV were similar. The T1 value did not distinguish either the banded from the control group or any of the muscle types. Percent water content was similar for all tissues. Any correlation between water content and T1 or T2 was inconsistent or weak.

Animals↗
PubMed1986

Automated morphologic evaluation of pulmonary arteries in primary pulmonary hypertension.

Pulmonary wedge angiograms have been shown to reflect the severity of pulmonary vascular disease in congenital heart disease. Thirteen pulmonary wedge angiograms with a balloon occlusion catheter were performed in 11 adult patients (five normals and six with primary pulmonary hypertension [PPH]) and their features related to the resting pulmonary artery pressure (PAP). Individual cine frames from each study were selected and digitized with a computer-assisted operator-interactive program. By fitting densitometric profiles from the vessel segments, serial arterial cross-sectional diameters were calculated from mathematically derived points. There was a strong correlation between arterial taper (T, change in vessel caliber per unit axial length) and a power function of mean PAP with T = 0.304 X PAP-0.59, R = .91, P less than .001. These results demonstrate a correlation between an angiographically derived morphologic characteristic of the pulmonary vasculature (taper) and a hemodynamic parameter (PAP) in PPH. This offers a method to follow the course of the disease and the effects of drug therapy by assessing anatomic changes in the vessels.

Humans↗
PubMed1986

Endogenous modulation of alpha-adrenergic contraction in canine tracheal muscle.

We studied the effect of passive stretch on the contraction of canine tracheal smooth muscle (TSM) to alpha-adrenergic agonists and acetylcholine (ACh) in 211 epithelium-free TSM strips from 42 dogs in vitro. Passive stretch at a resting tension of 100 g/cm2 caused a time-dependent decrease in the contractile response to alpha-adrenergic agonists after beta-adrenergic blockade with propranolol. Initial contraction elicited by 10(-3) M phenylephrine (PE) and clonidine (CLO) decreased at 2 h by 31 and 100%, respectively. Decrease in alpha-adrenergic contractility did not result from tachyphylaxis; no contraction was elicited by PE or CLO given for the first time after 4-h passive stretch at 100 g/cm2. The TSM response to ACh was unchanged over the same time in the same strips. When TSM strips were incubated at zero resting tension for 6 h, some attenuation of the alpha-adrenergic contractile still occurred but was not substantial. Similarly, when strips were incubated with 10(-6) M indomethacin (INDO) or 10(-5) M mefenamic acid (MEF) at 100 g/cm2 resting tension, time-dependent attenuation of the response to PE and CLO was reduced for at least 6 h, and initial contraction elicited by PE was augmented. Response of TSM to ACh was not affected by prostaglandin synthetase inhibition with INDO. We conclude that passive stretch of canine TSM in vitro leads to decreased responsiveness to alpha-adrenergic stimulation that can be prevented with INDO or MEF. These data are consistent with the synthesis of an inhibitory eicosanoid in epithelium-free canine TSM that may be activated by mechanical deformation of the muscle.

Adrenergic alpha-Agonists↗
PubMed1986

Someplace to go.

Explore the source record for details and available documents.

Career Choice↗
PubMed1985

Nuclear magnetic resonance spectroscopy of rat ventricles following chronic hypoxia: a model of right ventricular hypertrophy.

Nuclear magnetic resonance spectroscopy was used to study the effect of chronic hypoxia on both right (RV) and left ventricular and septal (LV + S) muscle. Rats in the hypoxic group, kept in a hypobaric chamber at 1/2 atm pressure for 2 weeks, developed right, but not left, ventricular hypertrophy (p less than 0.001). Tissues were studied within 2.5 h of return to air. T1 and T2 relaxation times of RV, LV + S and thigh muscle (Th) from hypoxic and control rats were compared. The T2 value distinguished hypoxic from control RV (p less than 0.002), but not hypoxic from control LV + S or Th, indicating that the change in relaxation time reflects cellular hypertrophy, and not hypoxemia. For hypoxic rats only the T2 value distinguished each muscle type: RV from LV + S (p less than 0.009), RV from Th (p less than 0.001) and LV + S from Th (p less than 0001). The T1 value did not identify either the hypoxic or control group or the type of muscle. Percent water content was similar for all tissues. For hypoxic RV, T2 correlated with the percent water content (r = 0.89; p less than 0.01). The sensitivity of T2 to the cellular changes associated with hypoxic RV hypertrophy could provide a means of detecting right ventricular hypertrophy.

Animals↗
PubMed1985

The effect of isoproterenol on the development and recovery of hypoxic pulmonary hypertension. A structural and hemodynamic study.

Isoproterenol, administered intravenously during acute hypoxic exposure, is here shown to prevent about two-thirds of the rise in pulmonary artery pressure in unanesthetized male Sprague-Dawley rats with normal pulmonary vascular beds. In rats receiving continuous intravenous infusion of isoproterenol during 2 weeks' exposure to chronic hypobaric hypoxia (FiO2 0.1) the drug does not prevent either the hemodynamic or pulmonary structural changes caused by hypoxia. Similar drug administration to rats in air causes a mild increase in pulmonary artery muscularity including extension and hypertrophy of both the left and right ventricles, without changing hemodynamic findings. Isoproterenol administered during 2 weeks' recovery in air after 2 weeks' hypoxia not only prevents the usual structural recovery, but several structural features actually progress. In contrast, it does not prevent hemodynamic recovery, perhaps because the hematocrit is lower in the isoproterenol-treated rats than in rats recovering without isoproterenol. Administered in air to rats with pulmonary vascular beds remodeled by chronic hypoxia, it does not reduce pulmonary artery pressure.

Animals↗
PubMed1984

Congenital pulmonary vein stenosis: structural changes in a patient with normal pulmonary artery wedge pressure.

A male infant is described who died at 13 months of age with stenosis of all extrapulmonary veins except the left upper vein. The pulmonary artery wedge pressure was normal, the first time this is reported in this condition. At autopsy, there were structural changes of the pulmonary arteries and veins in all lobes with or without pulmonary vein stenosis. Arterial changes-muscle extension, medial hypertrophy and decreased arterial size--analyzed quantitatively were found to be similar in all lobes. Venous medial hypertrophy was more marked in obstructed lobes. These anatomic changes are presumably due to fixed venous obstruction in the pulmonary lobes drained by stenotic veins and to high flow in the left upper lobe.

Cardiac Catheterization↗
PubMed1984

Early recovery from hypoxic pulmonary hypertension: a structural and functional study.

This study follows the recovery during 1 mo in ambient air from the hemodynamic and structural changes found in Sprague-Dawley rats after 2 wk of hypobaric hypoxia. In the time studied there is some degree of recovery for all features analyzed. The only features that completely return to normal are hematocrit level, new muscle in arteries at alveolar wall level, medial thickness of intra-acinar arteries, and density of filled arteries. For some features much of the recovery is early or rapid; for other features the recovery is late or slow. The rapid changes, occurring within two days of removal from hypoxia, include a fall in pulmonary arterial pressure (36.6 +/- 1.5 to 30.1 +/- 1.1 mmHg), a drop in hematocrit (61.1 +/- 1.3 to 53.0 +/- 1.0%), and the disappearance of new muscle, as judged by light microscopy from many arteries at alveolar wall (39.5 +/- 4.9 to 17.7 +/- 4.0%) and alveolar duct (85.9 +/- 2.5 to 68.2 +/- 3.4%) levels. The slow recovery includes the decrease in right ventricular and arterial medial hypertrophy, disappearance of muscle from respiratory bronchiolar arteries, reduction in lung volume, and increased density of filled arteries. These slow changes are probably the response to a fall in pulmonary arterial pressure.

Animals↗
PubMed1984

Central-nervous-system toxoplasmosis in homosexual men and parenteral drug abusers.

Central-nervous-system toxoplasmosis developed in 7 of 269 patients with the acquired immunodeficiency syndrome reported to the New York City Health Department through July 1982. Focal neurologic abnormalities, mass lesions on computed-tomographic brain scans, lymphocytic cerebrospinal fluid pleocytosis, and detectable IgG antibody to Toxoplasma gondii were common; but IgG titers of 1:1024 or more, IgM antibody to T. gondii, and positive open brain biopsies were uncommon. Serologic findings suggested that the disease resulted from recrudescent rather than primary infection. Four of five patients improved when treated with sulfonamides and pyrimethamine, but 2 had relapses. An aggressive diagnostic approach and sometimes even empiric therapy are warranted when central-nervous-system toxoplasmosis is suspected in a seropositive patient with the acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗