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At least 19 recordsLinked to original sources
PubMed1978

[The influence of changes in body position on intraocular pressure, episcleral venous pressure, and blood pressure (author's transl)].

The intraocular pressure, the ophthalmic artery pressure, and the episcleral venous pressure increased after changes from sitting to recumbent body position, whereas the subclavian artery pressure remained unchanged or decreased slightly. Changing from recumbent to sitting position was followed by a decrease in IOP, ophthalmic pressure, and subclavian artery pressure. Comparing the last measurement in the first position to the first value after change, it was found that the IOP alters by about 20%, the ophthalmic artery pressure by 15%, and the episcleral venous pressure by 50%. In all series a decrease in subclavian artery pressure was observed during the first 15 min. The mean pressure in the ophthalmic artery diminished in the series that changed from sitting to recumbent position, whereas it increased in the other series during the first 15 min. The episcleral venous pressure increased more than the corresponding IOP after changing to the recumbent position.

Blood Pressure↗
PubMed1976

[Pulmonary artery pressure and left ventricular late diastolic pressure in rest and during dynamic load. Comparative studies on pressure transmission in the pulmonary circulation during simultaneous determination].

Left ventricular enddiastolic pressure (LVEDP), mean pulmonary artery pressure (PAPM) and enddiastolic pulmonary artery pressure (PADP) were simultaneously recorded in 19 subjects with normal left ventricular (LV) function, and in 109 patients with LV-dysfunction, 83 of whom were also studied during exercise. Patients with valvular heart disease or atrial fibrillation were excluded from this study. LVEDP and mean pulmonary capillary wedge (PCW) pressure were simultaneously recorded in 81 patients at rest, andin 16 patients also during exercise; the LV diastolic pressure prior to atrial contraction (LVPpreA) could accurately be identified in 45 patients at rest and in 23 patients with exercise. In contrast to the widely accepted opinion of others, the PADP (mean 8.2 +/- 2.2 mm Hg at rest and 12.3 +/- 3.4 mm Hg with exercise) showed a close approximation of LVEDP (10.0 +/- mm Hg at rest and 16.2 +/- 3.5 mm Hg with exercise) only in normal subjects at rest (p less than 0.05 and p less than 0.01 respectively). In patients with LV dysfunction there was no significant difference between PADP (11.7 +/- 4.5 mm Hg and 23.0 +/- 8.9 mm Hg), PCW (11.6 +/- 5.1 mm Hg and 24.1 +/- 11.9 mm Hg) and LVPpreA (12.5 +/- 5.5 and 21.5 +/- 7.7 mm Hg) at rest and during exercise. LVEDP could be estimated with sufficient accuracy only from the PAPM (18.9 +/- 6.5 and 35.7 +/- 10.8 mm Hg). The increase in LVEDP (14.7 +/- 7.7 mm Hg) with exercise was not significantly different from the increase in PAPM (16.8 +/- 7.1 mm Hg). There were highly significant correlations (p less than 0.001) between LVEDP and PADP (r = 0.85) as well as PAPM (r = 0.86) at rest and during exercise with the regressionline being closest to the line of identity for LVEDP and PAPM. The pressure gradient between LVEDP and PADP (LVEDP - PADP = 6.3 mm Hg with exercise) equaled the pressure increase in LV by atrial contraction (LVEDP - LVPpreA = 6.3 and 13.3 mm Hg). The pressure difference between PADP or PAPM and LVEDP remained constant despite marked variation of other hemodynamic parameters, e.g. stroke volume index (SVI), heart rate (HR) and cardiac index(CI). These data suggest that an elevated LVEDP is caused mainly by an augmented atrial contraction in patients with LV dysfunction at rest and with exercise. This mechanism precludes an enddiastolic pressure equilibrium between pulmonary artery and left ventricel. PAPM allows the best estimation of LVEDP independent from other hemodynamic variables.

Adult↗
PubMed1978

Hemodynamic and respiratory response to varying gradients between end-expiratory pressure and end-inspiratory pressure in patients breathing on continuous positive airway pressure.

Nine patients on intermittent mandatory ventilation (IMV) and continuous positive airway pressure (CPAP) were allowed to breathe spontaneously at varying end expiratory pressure-end inspiratory pressure (EEP-EIP) gradients up to 10 cm H2O. There was no change in the mean cardiac output and oxygen delivery despite a lowered mean airway pressure (MAWP) when the gradient was increased. Three patients were uncomfortable at the higher gradients and another manifested evidence of fatigue of the muscles of respiration by raising her arterial PCO2 (PaCO2) and intrapulmonary shunt (Qs/Qt). In view of the difficulty experienced by some patients and lack of improvement in cardiac outputs (CO) during spontaneous inspiration when the EEP-EIP gradient is raised from zero to 5 and 10 cm H2O, it is recommended that the variation in airway pressure during spontaneous breaths while a patient is on CPAP be minimized.

Hemodynamics↗
PubMed1978

A comparison of the cardiorespiratory effects of continuous positive airway pressure breathing and continuous positive pressure ventilation in dogs.

Five patterns of ventilation have been compared in dogs: (1) spontaneous ventilation at ambient pressure (SV); (2) intermittent positive pressure ventilation (IPPV); (3) spontaneous ventilation at 0.98 kPa positive airway pressure, delivered from a non-rebreathing circuit incorporating a 5-litre reservoir bag and fresh-gas flow of twice the minute volume (CPAP (bag)); (4) spontaneous ventilation at 0.98 kPa positive airway pressure, with the reservoir bag replaced by a weighted bellows (CPAP (bellows)) and (5) IPPV with 0.98 kPa positive end-expiratory pressure (CPPV). CPAP significantly decreased the rate of respiration compared with SV. CPAP (bellows) resulted in a significant increase in tidal volume. Mean oesophageal pressure, right atrial pressure, pulmonary wedge pressure and pulmonary artery pressure increased during IPPV, CPAP (bag), CPAP (bellows), and CPPV compared with SV. There were no significant changes in mean systemic arterial pressure, cardiac output, PaO2, PaCO2, CaO2, (CaO2-CVO2), PAO2-PAO2) or pulmonary venous admixture. Under the conditions of this study oxygen transport was not altered by positive airway pressure ventilation.

Animals↗
PubMed1977

[The influence of vasodilatators on intraocular pressure and blood pressure (author's transl)].

The influence of different vasodilatators on blood pressure and intraocular pressure has been tested in animal experiments. For that purpose substances with alphasympathicolytic effect (Hydergin, Trental) have been tested as well as substances which are of direct influence on the muscles. In all cases a decrease of the blood pressure was noticed. Furthermore in most of the cases an increase of the intraocular pressure could be seen. This is due to a direct dilatation of ocular vessels. The effects were short-lived and reversible. We tried to find an explanation for the variations of intraocular pressure during the decrease of blood pressure. The low transmural pressure (PTM) and the corresponding low starting point of the muscle tonus seemed to be responsible for this phenomenon. Without doubt the starting point of the blood pressure, the dose, and the cardiac ability for compensation are of great influence in the development of the curve. Only a sufficiently high blood pressure is able to dilate the ocular vessels, so that one has to draw therapeutic conclusions from the constellation blood pressure/intraocular pressure before deciding on treatment.

Animals↗
PubMed1977

Mucopolysaccharide osmotic pressure in the measurement of interstitial pressure.

Subatmospheric pressures were recorded from cotton wicks inserted into Wharton's jelly of human umbilical cords (mean=-7.6+/-5.0 (SD) cmH2O; n=10). Hyaluronate concentrations (mean=0.69+/-0.30 g/100 g) and wick pressures correlated negatively (r=-0.825; P less than 0.01) but calculated hyaluronate osmotic pressures (mean=4.0+/-2.7 cmH2O) were insufficient to explain the full wick pressure. In model systems composed of asbestos fibers (mean radius=0.5 micron) and 0.9% saline, subatmospheric pressures were recorded which varied with the volume of saline added. When hyaluronate (1 g/100 g) was substituted for saline, lower wick pressures were recorded at each volume. The pressure lowering effect of hyaluronate was not seen in a matrix of glass fibers (mean radius=1.0 micron). It is suggested that the effect of hyaluronate in asbestos fibers is due to its immobilization by the matrix and the consequent development of osmotic pressure recorded via the wick. In the coarser glass-fiber matrix, hyaluronate was not immobilized and therefore had no osmotic effect. These experiments support the hypothesis that subatmospheric interstitial pressures result from osmotic pressure of immobilized mucopolysaccharide macromolecules.

Asbestos↗
PubMed1977

Skin perfusion pressure measured as the external pressure required to stop isotope washout. Methodological considerations and normal values on the legs.

The skin perfusion pressure was measured as the external pressure required to stop blood flow, as evidenced by cessation of the washout of an intracutaneous depot of [131I-]antipyrine mixed with histamine. The external pressure on the skin was measured by an 11 x 11 cm slack air-filled plastic cushion connected to a mercury manometer and interposed between the labelled area and a blood pressure cuff. The 'flow cessation external pressure' (FCEP) varied parallel to the intra-arterial femoral mean blood pressure, but was on the average 10.8 mmHg (SD 6.4) lower. FCEP was measured on twenty normal subjects at four different segments of the leg. The average differences between auscultatory brachial mean blood pressure and FCEP were: thigh 12.0 mmHg (SD 7.6); calf 10.4 mmHg (SD 7.4); ankle 12.9 mmHG (SD 10.1); foot 20.2 mmHg (SD 12.1). The SD of the difference between measurements on two different days, performed in forty-four patients with different degrees of occlusive arterial disease, varied between 5.6 and 8.3 mmHg at the different levels. The present data indicate that the skin perfusion pressure on the legs in normal subjects lies approximately 10 mmHg lower than the systemic mean arterial blood pressure.

Arterial Occlusive Diseases↗
PubMed1979

Diastolic pressure-volume relations and distribution of pressure and fiber extension across the wall of a model left ventricle.

A model for left ventricular diastolic mechanics is formulated that takes into account noneligible wall thickness, incompressibility, finite deformation, nonlinear elastic effects, and the known fiber architecture of the ventricular wall. The model consists of a hollow cylindrical mass of muscle bound between two plates of negligible mass. The wall contains fiber elements that follow a helical course and carry only axial tension. The fiber angle (i.e., helical pitch) is constant along the length of each fiber but varies through the wall in accordance with the known distribution of fiber orientations in the canine left ventricle. To simplify the analysis and reduce the number of degrees of freedom, the anatomic distribution of fiber orientations is divided into a clockwise and counterclockwise system. The reference configuration for the model corresponds to a state in which, by hypothesis, the transmural pressure gradient is zero, the tension is zero for all fibers across the wall, and all fibers are assumed to have a sarcomere length of 1.9 micrometer. This choice of reference configuration is based on the empirical evidence that canine ventricles, fixed in a state of zero transmural pressure gradient and dissected, demonstrate sarcomere lengths between 1.9 and 2.0 micrometer in inner, middle, and outer wall layers, while isolated ventricular muscle bundles are observed to have zero resting tension when the sarcomere length ranges from 1.9 to 2.0 micrometer. An equation representing the global condition for equilibrium is derived and solved numerically. It is found that the model's pressure-volume relation is representative of diastolic filling in vivo over a wide range of filling pressures, and the calculated midwall sarcomere lengths in the model compare favorably with published experimental data. Subendocardial fibers are stretched beyond Lmax even at low filling pressures, i.e., 5 mm Hg, while fibers located between 60-80% of wall thickness extend minimally between 5 and 12 mm Hg. The hydrostatic pressure field within the wall is highly nonlinear. The pressure rises steeply in the subendocardial layers so that the net gain in pressure in the inner third of the wall is 85% of the filling pressure. It is demonstrated that these results are independent of heart size for a family of heart models that are scale models of each other. They are, however, critically dependent on the existence of longitudinally oriented fibers in the endocardial and epicardial regions of heart wall.

Animals↗
PubMed1977

[Measurements of cuff pressure of different low pressure cuffed endotracheal tubes under mechanical ventilation (author's transl)].

Three different low pressure cuffed endotracheal tubes (Lanz, Portex soft-seal, Kamen-Wilkinson) were studied in cadaver tracheas and patients in our intensive care unit during ventilation. In the air filled low pressure cuffs without controlled pressure system the cuff pressure and the ventilation pressure are almost identical. Rises of intrathoracic pressure during mechanical ventilation are reflected by increased cuff pressure. Tubes with controlled pressure system or foam-filled cuffs have lower peak cuff pressures, especially during sighing, coughing and suctioning.

Airway Resistance↗
PubMed1979

Lung expansion, airway pressure transmission, and positive end-expiratory pressure.

Transmission of airway pressure to the intrapleural space and change in functional residual capacity by positive end-expiratory pressure (PEEP) were measured in ten anesthetized swine. Measurements and calculations were performed with varying lung and chest wall compliances. When both compliances were normal, approximately half of the applied airway pressure was transmitted. Aspiration of hydrochloric acid reduced lung compliance approximately fourfold and decreased airway pressure transmission. Increased thoracic compliance also reduced airway pressure transmission. When acid aspiration reduced lung compliance and sternotomy simultaneously increased thoracic compliance, pressure transmission was maximally reduced. Decreases in either thoracic or lung compliance reduced the volume-expanding effects of PEEP. Positive end-expiratory pressure was least effective when thoracic and lung compliances were reduced simultaneously. Careful assessment of both lung and thoracic compliances may be helpful in treating patients requiring elevated airway pressure.

Animals↗
PubMed1977

Influence of abdominal pressure and sympathetic vasoconstriction on the cardiovascular response to positive end-expiratory pressure.

The role of changes in abdominal pressure and sympathetically mediated vasoconstriction in the cardiovascular response to positive end-expiratory pressure was evaluated in 9 mongrel dogs. When the abdomen was widely opened, the decrease in cardiac output caused by positive end-expiratory pressure was the same as that found during control studies. When the abdomen was tightly bound, cardiac output was higher at any positive end-expiratory pressure than in control state (P less than 0.01), but the percent decrease produced by increasing positive end-expiratory pressure was the same. alpha-Adrenergic blockade with phenoxybenzamine produced a significantly greater decrease in cardiac output at any given positive end-expiratory pressure and thus appeared to inhibit the previously operative peripheral vascular adjustments to positive end-expiratory pressure. The major compensatory mechanism in the cardiovascular response to positive end-expiratory pressure thus appears to be mediated via alpha-adrenergic sympathetic factors.

Abdomen↗
PubMed2026

Reassessment of the effect of oral l-arginine on blood pressure: A systematic review and meta-analysis based on ambulatory blood pressure monitoring.

OBJECTIVE: This meta-analysis aimed to evaluate the effect of oral l-arginine supplementation on ambulatory blood pressure (ABP). METHODS: A systematic search of PubMed, Cochrane Library, Embase, and Web of Science databases was conducted from their inception through March 1, 2026. Randomized controlled trials (RCTs) assessing the effects of oral l-arginine intervention were included. Outcome measures included 24-h systolic blood pressure (24h SBP), 24-h diastolic blood pressure (24h DBP), daytime systolic blood pressure (dSBP), daytime diastolic blood pressure (dDBP), nighttime systolic blood pressure (nSBP), and nighttime diastolic blood pressure (nDBP). Meta-analysis was performed using Stata 17.0. The weighted mean difference (WMD) was used as the effect size, and the results were pooled with 95% confidence intervals (CIs). RESULTS: A total of 5 RCTs comprising 202 participants were included. Meta-analysis results demonstrated that oral l-arginine significantly reduced 24h SBP (WMD&#x202f;=&#x202f;-4.23&#x202f;mmHg, 95% CI [-5.87, -2.58]; P&#x202f;<&#x202f;0.01) and 24h DBP (WMD&#x202f;=&#x202f;-3.04&#x202f;mmHg, 95% CI [-4.48, -1.59]; P&#x202f;<&#x202f;0.01). Significant reductions were also observed for dSBP (WMD&#x202f;=&#x202f;-4.16&#x202f;mmHg, 95% CI [-5.90, -2.41]; P&#x202f;<&#x202f;0.01) and dDBP (WMD&#x202f;=&#x202f;-4.25&#x202f;mmHg, 95% CI [-5.85, -2.66]; P&#x202f;<&#x202f;0.01). Furthermore, oral l-arginine significantly lowered nSBP (WMD&#x202f;=&#x202f;-5.70&#x202f;mmHg, 95% CI [-7.81, -3.58]; P&#x202f;<&#x202f;0.01) and nDBP (WMD&#x202f;=&#x202f;-4.18&#x202f;mmHg, 95% CI [-6.27, -2.09]; P&#x202f;<&#x202f;0.01). CONCLUSION: Oral l-arginine supplementation significantly reduces ABP. However, the number of included studies was limited, and further validation through additional relevant research is warranted.

Arginine↗
PubMed1979

Relation between voice sound pressure and subglottal pressure as a diagnostic cue.

Voice sound pressure and esophageal pressure amplitudes are measured for 120 subjects with and without laryngeal status. The esophageal pressure amplitudes are taken as a approximation of the subglottal pressure. The dependency of sound pressure on subglottal pressure is approximated by a nonlinear function. The slope of the function represents the pressure transformation from subglottal pressure to sound pressure at fixed vocal tract configuration. Therefore, the slope is taken as a characterization of the efficiency of the voice organ. This quantity allows rough statement about the efficiency of the voice organ (differentiation of normal, trained normal, and pathologic larynx) but does not separates voice disorders.

Adolescent↗