Biomedical subjects
Publications and source records attributed to R Fried.
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.
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.
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.
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)
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.
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.
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.
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.
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.
Comparison of superoxide dismutase activity in homogenates of wild and vestigial strains of D. melanogaster revealed a lower enzyme activity in the short-living vestigial strain.
Prolonged treatment with relatively low doses of ionizing radiation did not induce synthesis of superoxide dismutase, either in Drosophila melanogaster or in mice liver.
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Membrane (Na +K)ATPase isolated from rat brain was preincubated in a medium in which superoxide radicals were generated enzymatically. Exposure to superoxide radicals caused an irreversible inactivation, which could be prevented by further addition of superoxide dismutase. (Na + K)ATPase was also protected by addition of allopurinol, a xanthine oxidase inhibitor, during preincubation. The K-activated nitrophenylphosphatase associated with (Na + K)ATPase was also found to be inactivated by preincubation with superoxide radicals, which could be prevented by superoxide dismutase.
1. Conditions of preparation and purification of superoxide dismutase from hog liver and erythrocytes were established. 2. The enzymes from both tissues were compared in respect to electrophoretic mobility, pI value, amino acid composition and spectrophotometric profiles and some differences were observed. 3. Conditions of enzyme dissociation were elaborated and molecular weights of subunits obtained from both kinds of SOD were found to be approx. 16,000. 4. Effect of heat and pH on the enzyme activity were tested. Both enzymes exhibited a relative thermostability.
Surprisingly, little is known about host factors in cases of bladder carcinoma. We investigated 2 families prone to transitional cell carcinoma of the bladder. A high degree of pathology verification of cancer of all anatomic sites and a meticulous recording of genealogy, associated diseases and environmental exposures, when known, have allowed a more cogent appraisal of cancer etiology. It is reasonable to assume that members of the subject families may be more susceptible to variable carcinogenic exposures, a concept that is in accord with a genetic-environmental interaction hypothesis for cancer etiology. In addition to increased surveillance of high risk patients for earlier detection of bladder cancer, cancer control measures also should take into consideration preventive programs directed toward the avoidance of known carcinogenic exposures, such as cigarette smoking in high risk relatives of cancer-affected probands. We propose that the etiology of familial bladder cancer may be complex, involving possible other associated malignant neoplasms and/or certain non-neoplastic disorders, in addition to specific carcinogenic exposures. There is a serious need for the detailed reporting of families prone to bladder cancer wherein all of these potentially important associated factors are considered, so that a fuller appraisal of etiology might be achieved.
In order to determine the effect of milk products on serum cholesterol, triglycerides, and diet, 54 volunteers were studied for varying periods with dietary supplementation of nonpasteurized yogurt, pasteurized yogurt and 2% butterfat milk. Serum cholesterol was significantly reduced by 5 to 10% after 1 week of supplementation with either nonpasteurized or pasteurized yogurt; 2% butterfat milk reduced serum cholesterol to a smaller and less significant effect. Serum triglycerides were unaffected by the diet and dietary intake studies confirmed that intake of other nutrients remained relatively stable throughout the study. Supplementation of diet with yogurt may have a helpful hypocholesterolemic effect.
Superoxide dismutase activity was determined by the adrenalin method in bovine erythrocytes separated according to age. Progressive loss of the enzyme activity was found, down to ca 65% of that of the youngest cells.