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Biomedical subjects

M Mohr

Publications and source records attributed to M Mohr.

At least 91 records · Page 5Linked to original sources
PubMed1990

Sloping alveolar plateaus of CO2, O2, and intravenously infused C2H2 and CHClF2 in the dog.

To investigate the role of the various mechanisms assumed to contribute to the slope of the alveolar plateau, two test gases exhibiting identical solubility but two-fold differing diffusivity, acetylene (C2H2) and chlorodifluoromethane (Freon 22, CHClF2), dissolved in saline were intravenously infused in 10 anesthetized, paralyzed, artificially ventilated dogs (mean body mass, 18 kg). The partial pressures of C2H2, CHClF2, CO2 and O2 during a constant-flow single-breath washout maneuver were recorded by mass spectrometry and analyzed in terms of slope of the alveolar plateau (phase III) and series (Fowler) dead space. The slope of the alveolar plateau (S) was determined as the relative alveolar slope normalized to mixed-expired partial pressure and referred to expired volume (VE), S(V) = delta PE/(PE - PI)/delta VE or expiration time (tE), S(t) = delta PE/(PE - PI)/delta tE (subscripts I, E, and E refer to inspired, instantaneous expired and mixed-expired gas, respectively). The effects of expiratory flow rate (VE), and time of breath-hold (BH) were studied with reference to control conditions (VI = 0.5 L.sec-1, VE = 0.1 L.sec-1, VI = 50% and VE = 75% of volume at FRC, BH = 0 sec). In control conditions, the following significantly different S(V) values (units: L-1), grouped in ascending order, were obtained (means +/- SD): CO2, 0.83 +/- 0.26; C2H2, 0.93 +/- 0.18; CHClF2, 1.00 +/- 0.20; O2, 1.07 +/- 0.29. The mean C2H2/CHClF2 ratio for S(V), 0.94 (SD +/- 0.03), was statistically different from unity. In line with model calculations, the experimental findings suggest that three mechanisms contribute to the sloping alveolar plateaus: 1, continuing gas exchange during expiration; 2, ventilation-perfusion inequality combined with sequential emptying; 3, intrapulmonary diffusion limitation.

Acetylene↗
PubMed1990

Pulmonary diffusing capacities for nitric oxide and carbon monoxide determined by rebreathing in dogs.

Pulmonary diffusing capacities (DL) of NO and CO were determined simultaneously from rebreathing equilibration kinetics in anesthetized paralyzed supine dogs (mean body wt 20 kg) after denitrogenation (replacement of N2 by Ar). During rebreathing the dogs were ventilated in closed circuit with a gas mixture containing 0.06% NO, 0.06% 13C18O, and 1% He in Ar for 15 s, with tidal volume of 0.5 liter and frequency of 60/min. The partial pressures of NO, 13C18O, 16O18O, N2, Ar, CO2, and He in the trachea were continuously analyzed by mass spectrometry. Measurements were performed at various O2 levels characterized by the mean end-expired PO2 during rebreathing (PE'O2). In control conditions ("normoxia," PE'O2 = 67 +/- 8 Torr) the following mean +/- SD values were obtained (in ml.min-1.Torr-1): DLNO = 52.4 +/- 11.0 and DLCO = 15.4 +/- 2.9. In hypoxia (PE'O2 = 24 +/- 7 Torr) DLNO increased by 11 +/- 8% and DLCO by 19 +/- 10%, and in hyperoxia (PE'O2 = 390 +/- 26 Torr) DLNO decreased to 87 +/- 3% and DLCO to 56 +/- 8% with respect to values in normoxia. DLNO/DLCO of 3.24 +/- 0.06 (hypoxia), 3.38 +/- 0.31 (normoxia), and 5.54 +/- 1.04 (hyperoxia) were significantly higher than the NO/CO Krogh diffusion constant ratio (1.92) predicted for simple diffusion through aqueous layers. With increasing O2 uptake elicited by 2,4-dinitrophenol, DLNO and DLCO increased and DLNO/DLCO remained close to unchanged. The results suggest that the combined effects of diffusion and chemical reaction with hemoglobin limit alveolar-capillary transport of CO. If it is assumed that reaction kinetics of NO with hemoglobin (known to be extremely fast) are not rate limiting for NO uptake, the contribution of the slow chemical reaction with hemoglobin to the total CO uptake resistance (= 1/DLCO) was estimated to be 38% in hypoxia, 41% in normoxia, and 64% in hyperoxia. The various factors expected to restrict the validity of this analysis are discussed, in particular the effects of functional inhomogeneity.

2,4-Dinitrophenol↗
PubMed1990

Alveolar slope and dead space of He and SF6 in dogs: comparison of airway and venous loading.

Series (Fowler) dead space (VD) and slope of the alveolar plateau of two inert gases (He and SF6) with similar blood-gas partition coefficients (approximately 0.01) but different diffusivities were analyzed in 10 anesthetized paralyzed mechanically ventilated dogs (mean body wt 20 kg). Single-breath constant-flow expirograms were simultaneously recorded in two conditions: 1) after equilibration of lung gas with the inert gases at tracer concentrations [airway loading (AL)] and 2) during steady-state elimination of the inert gases continuously introduced into venous blood by a membrane oxygenator and partial arteriovenous bypass [venous loading (VL)]. VD was consistently larger for SF6 than for He, but there was no difference between AL and VL. The relative alveolar slope, defined as increment of partial pressure per increment of expired volume and normalized to mixed expired-inspired partial pressure difference, was larger by a factor of two in VL than in AL for both He and SF6. The He-to-SF6 ratio of relative alveolar slope was generally smaller than unity in both VL and AL. Whereas unequal ventilation-volume distribution combined with sequential emptying of parallel lung regions appears to be responsible for the sloping alveolar plateau during AL, the steeper slope during VL is attributed to the combined effects of continuing gas exchange and ventilation-perfusion inequality coupled with sequential emptying. The differences between He and SF6 point at the contributing role of diffusion-dependent mechanisms in intrapulmonary gas mixing.

Administration, Inhalation↗
PubMed1990

Cardiogenic oscillations in He and SF6 expirograms during airway and venous loading.

Cardiogenic oscillations in the expired partial pressure profiles of two inert gases (He and SF6) were monitored in seven anesthetized paralyzed mechanically ventilated dogs. He and SF6 were administered either intravenously by a membrane oxygenator and partial arteriovenous bypass [venous loading (VL)] or by washin into lung gas [airway loading (AL)]. The single-breath expirograms obtained during constant-flow expiration after inspiration of test gas-free air displayed distinct and regular cardiogenic oscillations. The relative oscillation amplitude (ROA), calculated as oscillation amplitude divided by mixed expired-inspired partial pressure difference, was in the range of 1-8%. The ROA for both He and SF6 was approximately 4.2 times higher in VL than in AL, which indicated that among lung units that emptied sequentially in the cardiac cycle, the effects of alveolar ventilation-perfusion (VA/Q) inequality were more pronounced than those of alveolar ventilation-alveolar volume (VA/VA) inequality. In AL, He and SF6 oscillations were 180 degrees out of phase compared with CO2 and O2 oscillations and with He and SF6 oscillations in VL, which suggests that regions with low VA/VA had high VA/Q and very low Q/VA. The ROA was practically unaffected by breath holding in both AL and VL, which indicates that there was little diffusive or convective (cardiogenic) mixing between the lung units that were responsible for cardiogenic oscillations. The ROA was consistently higher for He than for SF6, and the He-to-SF6 ratio was independent of route of test gas loading, averaging 1.6 in both AL and VL. This result may be explained by laminar Taylor dispersion, whereby oscillations generated in peripheral lung regions are dissipated in inverse proportion to diffusion coefficient during transit through the proximal (larger) airways.

Administration, Inhalation↗
PubMed1990

[Isolated paralysis of the ocular motor nerve caused by infarction of fascicular fibers].

We report the case of an 80 year-old woman who developed an unilateral brainstem infarction with a lesion of the intraparenchymatous fibres of the IIIrd cranial nerve. Intraaxial lesions of this nerve are usually part of the alternate paralysis syndrome. Our case might be the second since the report of Achard and Levi in 1901. Infarction limited to the fascicular fibres of the oculomotor nerve sparing the oculomotor nuclei results in characteristic clinical manifestations. This in turn results from the highly selective distribution of the terminal arterial territories in the midbrain.

Aged↗
PubMed1989

Autoradiographic visualization of the binding sites for [125I]endothelin in rat and human brain.

Putative receptors for endothelin were localised autoradiographically in frozen sections of rat and human brain using [125I]endothelin as a ligand. In the rat brain the highest densities were in the granular layer of the cerebellum, choroid plexus, hippocampus, and habenular nucleus. Similar brain high densities were found in the human cerebellum and hippocampus. The non-vascular pattern of distribution suggests that endothelin may have a function as a modulator of neuronal function in addition to its possible involvement in the regulation of vascular tone.

Aged↗
PubMed1989

Cyclooxygenase inhibition and effects of hypoxia on pulmonary circulation and gas exchange in anesthetized dogs.

To investigate whether endogenously produced prostanoids are involved in hypoxic pulmonary vasoconstriction, pulmonary hemodynamic and gas exchange parameters and eicosanoid metabolites were measured in 5 anesthetized, artificially ventilated dogs (mean body weight 27 kg). Hypoxia elicited pulmonary vasoconstriction, but blood plasma levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F 1 alpha (6kPGF1 alpha) (stable metabolites of TXA2 and prostaglandin I2, respectively) remained unchanged. Administration of the cyclooxygenase inhibitor indomethacin blocked the synthesis of prostanoids, so that 6kPGF1 alpha and TXB2 levels decreased to values below the detection level (10 pg.ml-1) both during normoxia or hypoxia, but did not affect pulmonary vascular resistance or the alveolar-arterial PO2 difference (PAi-Pa)O2. The pulmonary vascular bed remained, however, responsive to TXA2 as evidenced by infusion of the TXA2 mimetic, U 46619, which significantly increased the pulmonary vascular resistance and (PAi-Pa)O2. Our data suggest that prostanoids are not involved in eliciting the effects of hypoxia on pulmonary hemodynamics and gas exchange efficiency.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Cardiogenic mixing: mechanisms and experimental evidence in dogs.

Cardiogenic mixing was studied in seven anaesthetized closed-chest dogs undergoing mechanical ventilation by comparing single-breath washout of two poorly soluble inert gases of widely differing diffusivities (helium (He) and sulphur hexafluoride (SF6)) in normal conditions with the heart beating (control), and during reversible temporary myocardial arrest (heart arrest). Cardiac arrest of approximately 20 s duration was induced repeatedly (8-15 times) by intracoronary injection of acetylcholine (approximately 35 mg) facilitated by a non-occluding 7-French gauge angiographic catheter maintained in the left coronary artery. After equilibration of lung gas with 1% helium and 1% SF6, single breath, constant flow expirograms were recorded in the tracheal tube by mass spectrometry after inspiration of test gas-free air. Series deadspace (VD) and relative alveolar slope (S) (increment of expired partial pressure, normalized to mixed expired-inspired partial pressure difference per increment of expired volume (S = (delta P/(PE-P1]/delta VE litre-1], were determined as indices for intrapulmonary gas mixing. The effects attributable to the action of the heart were quantified by the heart arrest: control ratio of VD and S, which were not significantly different from unity (P greater than 0.05) (VD: 0.95 (SD 0.05) for helium and 0.94 (0.07) for SF6; S:1.03 (0.10) for helium and 1.05 (0.14) for SF6. The He:SF6 ratios of VD and S (0.90 and 0.64, respectively), indicating diffusion dependent separation of gases, also were unaffected by the mechanical action of the heart. The data indicate that convective mixing by the mechanical action of the heart did not significantly enhance intrapulmonary mixing and transport.

Acetylcholine↗
PubMed1989

Elastase and papain inhibition by serum of mammals.

The protease-antiprotease imbalance concept has gained wide acceptance in reference to experimental animal models of human pulmonary emphysema. The destructive process may be induced by proteolytic enzymes such as porcine pancreas elastase (E) or papain (P), or by oxidants such as chloramine T (CT) which cause inactivation of alpha-1-antiprotease. The susceptibility to development of severe emphysema has been found to differ among animal species. We investigated the inhibition of elastase and papain by serum of seven species (rat, dog, human, rabbit, sheep, hamster, mini pig) and the effect of CT on serum inhibition. The relative inhibitor concentration of serum was expressed in terms of its inhibitor capacity for elastase and papain (EIC and PIC) defined as number of inhibited units (U) of enzyme catalysed hydrolysis of chromogenic peptide substrate (SAPNA and BAPNA) per unit of serum. The effect of CT on enzyme inhibition was quantified in terms of fractional loss of inhibition relative to control. The serum concentration of inhibitor was highest in the rat (EIC 8642 +/- 989 microU/microliter, PIC 214.2 +/- 110.3 microU/microliter; means +/- SD). Next in order of decreasing EICs were dog, human, rabbit, sheep, hamster, and mini pig exhibiting the lowest EIC (2523 +/- 184 microU/microliter) while sheep had lowest PIC (39.6 +/- 3.5 microU/microliter). The EIC/PIC ratio varied from 20 (mini pig) to about 100. The reduction of elastase inhibition after CT exposure of serum was high (80-100%) in rat, dog, human, and hamster, moderate (40%) in mini pig and rabbit, and low (10%) in sheep. Because papain was directly affected by CT the effect of CT on papain inhibition could not be analysed. The data suggest that the intrinsic antiprotease and antioxidant screen varies among experimental animals. For the purpose of animal models of emphysema, hamster appears to be most susceptible to the progressive destruction of lung parenchyma elicited by experimental burden of proteases or oxidants.

Animals↗
PubMed1987

Recognition of xenogeneic erythrocytes: the GalNAc/Gal-particle receptor of rat liver macrophages mediates or participates in recognition.

We studied mechanisms that mediate recognition of human erythrocytes (HRBC) and sheep erythrocytes (SRBC) by rat liver macrophages. We used an in vitro cell binding assay that allows spontaneous formation of cell contacts. Binding of HRBC to rat macrophages shows the following characteristics: inhibition studies with several monosaccharides and oligosaccharides yield complete inhibition of cell contacts with saccharides, which block the GalNAc/Gal-particle receptor on rat liver macrophages. We found the inhibition pattern: N-acetyl-D-galactosamine, lactose greater than D-galactose, D-fucose greater than L-fucose much greater than N-acetyl-D-glucosamine. Cell binding is dependent on the presence of calcium ions, but not influenced by heat-aggregated IgG or gangliosides. The inhibition pattern was the same after treatment of HRBC with neuraminidase. Therefore, binding of HRBC, as well as binding of neuraminidase-treated HRBC, is mediated by the GalNAc/Gal-particle receptor. Binding of SRBC is partly inhibited by galactose-related saccharides. Binding is also partly inhibited by heat-aggregated IgG, gangliosides, and L-fucose. Complete inhibition of cell contacts with SRBC is achieved by combination of all inhibitors. We therefore conclude that binding of SRBC is mediated by several different mechanisms, including the GalNAc/Gal-particle receptor. Binding of neuraminidase-treated SRBC, however, was found to be completely inhibited by saccharides, which block the GalNAc/Gal-particle receptor. We conclude that the GalNAc/Gal-particle receptor mediates or participates in recognition of non-self structures.

Animals↗
PubMed1987

Nitrous oxide and cerebrospinal fluid markers of ischaemia following cardiopulmonary bypass.

Twenty patients with good ventricular function undergoing coronary artery bypass surgery were studied to determine whether the pre-bypass use of nitrous oxide resulted in any differences in cerebrospinal fluid markers indicative of cerebral ischaemia. All patients were anaesthetised with diazepam, fentanyl and pancuronium, after which ten patients received 50-60% nitrous oxide in oxygen until commencement of bypass, and the remaining patients 100% oxygen. Because of the known effect of nitrous oxide in expanding gaseous bubbles, any neurological dysfunction of gaseous microembolic origin may be worsened in the presence of nitrous oxide. Patients were lumbar punctured 24 hours after cardiopulmonary bypass and cerebrospinal fluid analysed for the following markers of central nervous system ischaemia: creatine kinase, lactate, total protein, noradrenaline, adrenaline and adenylate kinase. There was a statistically significant difference in cerebrospinal fluid lactate between the two groups. There were no statistically significant differences in the other cerebrospinal fluid markers of ischaemia.

Adenylate Kinase↗