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Biomedical subjects

A Ries

Publications and source records attributed to A Ries.

25 records · Page 2Linked to original sources
PubMed1986

Pulmonary gas exchange in humans during exercise at sea level.

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

Altitude↗
PubMed1986

Pulmonary gas exchange in humans during normobaric hypoxic exercise.

Previous studies (J. Appl. Physiol. 58: 978-988 and 989-995, 1985) have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during heavy exercise at sea level and during hypobaric hypoxia in a chamber [fractional inspired O2 concentration (FIO2) = 0.21, minimum barometric pressure (PB) = 429 Torr, inspired O2 partial pressure (PIO2) = 80 Torr]. We used the multiple inert gas elimination technique to compare gas exchange during exercise under normobaric hypoxia (FIO2 = 0.11, PB = 760 Torr, PIO2 = 80 Torr) with earlier hypobaric measurements. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate (HR), minute ventilation, respiratory rate (RR), and blood temperature were recorded at rest and during steady-state exercise in 10 normal subjects in the following order: rest, air; rest, 11% O2; light exercise (75 W), 11% O2; intermediate exercise (150 W), 11% O2; heavy exercise (greater than 200 W), 11% O2; heavy exercise, 100% O2 and then air; and rest 20 minutes postexercise, air. VA/Q inequality increased significantly during hypoxic exercise [mean log standard deviation of perfusion (logSDQ) = 0.42 +/- 0.03 (rest) and 0.67 +/- 0.09 (at 2.3 l/min O2 consumption), P less than 0.01]. VA/Q inequality was improved by relief of hypoxia (logSDQ = 0.51 +/- 0.04 and 0.48 +/- 0.02 for 100% O2 and air breathing, respectively). Diffusion limitation for O2 was evident at all exercise levels while breathing 11% O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Restrictive ventilatory pattern in precapillary pulmonary hypertension.

Patients with precapillary pulmonary hypertension (PPH) have classically been reported to have normal pulmonary mechanical function. We reviewed spirometric data from 8 patients with primary pulmonary hypertension and from 17 patients with chronic thromboembolic pulmonary hypertension. All patients had undergone right heart catheterization and pulmonary angiography. Five of the 8 patients with primary pulmonary hypertension demonstrated a severe restrictive ventilatory pattern with a mean vital capacity (VC) of 50.4% predicted and a mean total lung capacity (TLC) of 64.3% predicted. Five of the 17 patients with chronic thromboembolic pulmonary hypertension manifested a restrictive pattern with a mean VC of 68.0% predicted and a mean TLC of 75.3% predicted. We conclude that restrictive ventilatory defects occur more frequently than previously described in patients with PPH. The physiologic mechanism responsible for the restrictive ventilatory pattern is not clear.

Adult↗
PubMedDate not supplied

Cardiovascular effects of AR-L115 BS in conscious dogs with and without chronic congestive heart failure.

AR-L115 BS is a phenyl-imidazo-pyridine derivative that combines positive inotropic and vasodilator properties. To analyze the mechanisms of action of AR-L115 in the presence or absence of heart failure, we administered it intravenously to conscious dogs (seven normals and eight with a volume-overload heart failure). In normals, at a plasma level around 1,000 ng/ml, AR-L115 BS increased left ventricular (LV) peak (+) dP/dt (+48%; p less than 0.02) and heart rate (+29 beats/min; p less than 0.05) without altering significantly cardiac filling pressures or cardiac output. The mean aortic pressure and the systemic vascular resistances (-20%; p less than 0.02) were reduced, but plasma renin activity (PRA) was unchanged. In heart failure, the same plasma level increased peak (+) dP/dt by 36% (p less than 0.01), but heart rate stayed unchanged. Mean aortic pressure, systemic vascular resistances (-20%; p less than 0.01), and LV end-diastolic pressure (-9.1 mm Hg; p less than 0.01) all dropped significantly, while cardiac output increased slightly; PRA did not rise significantly. After beta-blockade, the increases in peak (+) dP/dt and the changes in systemic vascular resistances were markedly reduced. In conclusion, AR-L115 BS has strong positive inotropic and vasodilator effects, both of which are partially dependent on the level of the sympathetic tone in the intact animal. These combined properties improve hemodynamics in heart failure; this improvement is already significant at relatively low plasma levels, at which deleterious changes in heart rate or PRA are absent.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Effects of dobutamine and sulmazol (AR-L115 BS) on myocardial metabolism and coronary, femoral, and renal blood flows: a comparative study in normal dogs and in dogs with chronic volume overload.

We compared the hemodynamic and metabolic effects of dobutamine and sulmazol (AR-L115 BS) in normal dogs and in dogs with chronic volume overload. In both cases, the doses of dobutamine and sulmazol were adapted to produce comparable increases in two indices of inotropic state, peak (+) left ventricular dP/dt and dP/dt normalized by a developed pressure of 40 mm Hg. In normal dogs, both drugs had similar effects on myocardial oxygen consumption, myocardial high-energy phosphate stores, and renal or femoral blood flows; in addition, mean aortic pressure (129 +/- 8 to 114 +/- 10 mm Hg; p less than 0.002), the renal vascular resistance (--18%; p less than 0.005), and the coronary vascular resistance (--30%; p less than 0.05) were all decreased significantly during sulmazol administration. In chronic volume overload, the changes in renal and femoral blood flows and in myocardial high-energy phosphate stores induced by dobutamine or sulmazol were again similar. However, sulmazol still decreased mean aortic pressure (--20 +/- 5 mm Hg; p less than 0.002) and markedly reduced the left ventricular filling pressure (--40%; p less than 0.006), while these parameters were not significantly modified after dobutamine. Myocardial oxygen consumption was unchanged after sulmazol but increased slightly with dobutamine. Finally, the frequency of ventricular premature beat was unchanged by sulmazol but increased after dobutamine. In conclusion, sulmazol is likely to be superior to dobutamine to stimulate a failing left ventricle when clinical status is characterized by markedly elevated filling pressures. It might also be superior when the coronary vascular reserve is reduced or in the presence of ventricular arrhythmias.

Animals↗
PubMedDate not supplied

Characterizing "blue blobs". Immunohistochemical staining and ultrastructural study.

OBJECTIVE: To investigate the nature and origin of "blue blobs" (Bbs) in atrophic Pap smears in postmenopausal women and to study their clinical significance. STUDY DESIGN: A retrospective study of 412 atrophic Pap smears from postmenopausal women was done to detect the presence of Bbs. The smears from 24 cases showing Bbs were further studied to evaluate the nature of the Bbs with special stains, immunohistochemistry and electron microscopy. RESULTS: Bbs showed a heterogeneous morphology, with variable numbers and staining intensity. The diameter of Bbs was approximately equivalent to that of a parabasal/intermediate squamous cell. Special stains showed Bbs to be positive for periodic acid-Schiff and methyl green pyronin and negative for mucicarmine and calcium. Immunohistochemistry revealed Bbs to be positive for cytokeratin, epithelial membrane antigen and carcinoembryonic antigen and negative for vimentin and muscle-specific actin. Some Bbs had residual ghost nuclear shadows. Electron microscopy revealed cellular skeletons with residual tonofilaments enmeshed within a loose cytoskeleton matrix and nuclei with variable degrees of degeneration. CONCLUSION: Special stains, immunohistochemistry and electron microscopy indicated that Bbs represent parabasal/intermediate squamous cells exhibiting various degree of degeneration. In general, Bbs appear to be of no clinical significance except as a source of potential diagnostic error.

Aged↗