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C Frostell

Publications and source records attributed to C Frostell.

At least 37 records · Page 2Linked to original sources
PubMed1994

Prolonged bleeding time during nitric oxide inhalation in the rabbit.

During a study on the modulatory effect of inhaled nitric oxide (NO) on the airway, we observed an increased bleeding tendency. Therefore, we studied bleeding time and blood rheology in rabbits during inhalation of 3, 30 and 300 parts per million (ppm) NO. The rabbits were intubated during neurolept anaesthesia and were ventilated mechanically. The bleeding time was significantly increased after 15 min of inhalation of 30 ppm NO, from 51 +/- 5 to 72 +/- 7 s (mean +/- SEM, P < 0.001, n = 7). However, there were no changes in haematocrit, whole blood or plasma viscosity, erythrocyte aggregation tendency, or erythrocyte deformability. Inhalation of 3 ppm NO increased bleeding time from 46 +/- 11 to 59 +/- 8 s (n.s., n = 4) and 300 ppm NO from 48 +/- 12 to 78 +/- 17 s (P < 0.05, n = 4). In another group of rabbits mean arterial pressure (MAP) was monitored using NO inhalation. A non-significant decrease was seen with 3 ppm and 30 ppm NO, from 63 +/- 2 to 59 +/- 3 mmHg (n = 6) and from 65 +/- 2 to 61 +/- 1 mmHg (n = 6) respectively. Inhalation with 300 ppm NO decreased MAP from 62 +/- 3 to 55 +/- 2 mmHg (P < 0.05, n = 6). We conclude from these data that inhalation of NO, 30 ppm or more exerts systemic effects.

Administration, Inhalation↗
PubMed1994

Effects of inhaled nitric oxide on methacholine-induced bronchoconstriction: a concentration response study in rabbits.

Inhaled nitric oxide (NO), at a concentration of 80 ppm, counters the increase in respiratory resistance (Rrs) induced by methacholine, but fails to prevent a reduction in lung compliance (Crs) in a rabbit model. This study reports the effects of 3, 30 and 300 ppm of inhaled NO. New Zealand White rabbits were intubated and mechanically ventilated with 30% oxygen during neurolept anaesthesia. Methacholine (3 mg.ml-1) was nebulized, with or without NO inhalation. Inhalation of 3 and 30 ppm NO had no effect on the induced bronchoconstriction, whereas 300 ppm fully blocked the increase in Rrs. The decrease in Crs due to methacholine was not countered by 3, 30 or 300 ppm NO. On the contrary, inhalation of 300 ppm NO in itself decreased Crs from 5.0 +/- 0.1 to 4.3 +/- 0.1 ml.cmH2O-1. Also, mean arterial pressure (60 +/- 7 to 54 +/- 5 mmHg), alveolar-arterial oxygen tension gradient (0.8 +/- 0.8 to 2.3 +/- 1.8 kPa) and methaemoglobin (0.5 +/- 0.2 to 1.5 +/- 0.5%) changed significantly on inhalation of NO 300 ppm prior to methacholine challenge. We conclude that 3 and 30 ppm NO inhalation does not alter methacholine-induced bronchoconstriction. Inhalation of 300 ppm NO blocks an increase in resistance but fails to counter the reduction in compliance due to methacholine. This suggests that the bronchodilating effects of NO in rabbits in vitro are confined to the large airways.

Administration, Inhalation↗
PubMed1993

Enhanced pneumonia resolution by inhalation of nitric oxide?

We present a patient with severe bacteraemic pneumococcal pneumonia associated with severe hypoxaemia, where nitric oxide (NO) 15-40 ppm was added to the inspired gas. Nitric oxide therapy improved gas exchange, reduced pulmonary vasoconstriction and peak airway pressure. The patient survived. We observed an unexpected rapid and complete disappearance of bilateral pulmonary infiltrates during the first 120 h of the 7-day NO inhalation period.

Administration, Inhalation↗
PubMed1993

Inhalation of nitric oxide modulates methacholine-induced bronchoconstriction in the rabbit.

Nitric oxide (NO) accounts for the major effects of endothelium-derived relaxing factor. We investigated whether NO, added to the inspired gas, could exert a bronchodilatory action similar to the pulmonary vasodilation described when administering NO during lung vascular constriction. New Zealand White rabbits were intubated and mechanically-ventilated with 30% oxygen during neuroleptanaesthesia. Methacholine (MCh) was nebulized at increasing concentrations from 0.5 to 4.0 mg.ml-1, with or without inhalation of 80 parts per million (ppm) NO. The technique of rapid airway occlusion during constant-flow inflation was used for measuring respiratory mechanics, i.e. resistance and compliance of the respiratory system. Methacholine nebulization without NO inhalation raised the resistance from 51 +/- 6 (mean +/- 95% confidence interval) to 107 +/- 52 cmH2O.l-1.s at Mch 4 mg.ml-1. During NO inhalation, nebulization of MCh showed no significant increase in resistance. Arterial oxygen tension (PaO2) and compliance fell to the same extent during methacholine challenge, whether NO was inhaled or not. Closure of small airways may be a mechanism that causes the decrease in PaO2 and compliance observed. This suggests that 80 ppm NO added to the inspired gas modulates the response in central airway tone to nebulized MCh in this rabbit model. However, it appears to have less effect on peripheral airways.

Administration, Inhalation↗
PubMed1992

Influence of hypertonic-hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide. 2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). 3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Oedema formation was terminated by deflating the balloon and reducing the infusion rate. 4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS+furosemide. HHS, 6 ml kg-1, was given as a bolus injection and furosemide, 1 mg kg-1, intravenously as a bolus followed by an infusion of 0.5 mg kg-1 h-1. All dogs were studied for 4 h. 5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant. 6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-1 in groups A, C and D and to 14.7 in group B (only furosemide)). 7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11.0 +/- 5.7; B, 9.7 +/- 3.3; C, 10.5 +/- 3.1 and D, 10.6 +/- 1.8 g kg-1. 8. We speculate that mechanisms other than effective Starling gradients and enhanced diuresis might define a maximal rate of pulmonary oedema clearance.

Animals↗
PubMed1992

Bronchodilator action of inhaled nitric oxide in guinea pigs.

The effects of inhaling nitric oxide (NO) on airway mechanics were studied in anesthetized and mechanically ventilated guinea pigs. In animals without induced bronchoconstriction, breathing 300 ppm NO decreased baseline pulmonary resistance (RL) from 0.138 +/- 0.004 (mean +/- SE) to 0.125 +/- 0.002 cmH2O/ml.s (P less than 0.05). When an intravenous infusion of methacholine (3.5-12 micrograms/kg.min) was used to increase RL from 0.143 +/- 0.008 to 0.474 +/- 0.041 cmH2O/ml.s (P less than 0.05), inhalation of 5-300 ppm NO-containing gas mixtures produced a dose-related, rapid, consistent, and reversible reduction of RL and an increase of dynamic lung compliance. The onset of bronchodilation was rapid, beginning within 30 s after commencing inhalation. An inhaled NO concentration of 15.0 +/- 2.1 ppm was required to reduce RL by 50% of the induced bronchoconstriction. Inhalation of 100 ppm NO for 1 h did not produce tolerance to its bronchodilator effect nor did it induce substantial methemoglobinemia (less than 2%). The bronchodilating effects of NO were additive with the effects of inhaled terbutaline, irrespective of the sequence of NO and terbutaline administration. Inhaling aerosol generated from S-nitroso-N-acetylpenicillamine also induced a rapid and profound decrease of RL from 0.453 +/- 0.022 to 0.287 +/- 0.022 cmH2O/ml.s, which lasted for over 15 min in guinea pigs broncho-constricted with methacholine. Our results indicate that low levels of inhaled gaseous NO, or an aerosolized NO-releasing compound are potent bronchodilators in guinea pigs.

Aerosols↗
PubMed1991

The effect of yoga on puborectalis paradox.

Nine patients with severe defaecation difficulties primarily considered to be due to puborectalis dysfunction (puborectalis paradox), verified by electromyography (EMG) of the striated anal sphincter muscles, were offered training in Yogic techniques of relaxation and muscle control in order to change the activity of the pelvic floor muscles during attempted defaecation. Five patients completed the training program of 20 2-hour sessions and were re-examined clinically and with EMG. One patient regained a normal EMG pattern but none of the patients improved clinically.

Adult↗
PubMed1991

Thoracic lymph drainage in the dog: evaluation of a new model.

A new model for selective sampling of thoracic lymph flow (TLF) and abdominal lymph flow (TDA) in the dog was assessed to ascertain whether there were extrathoracic contributions of lymph to the TLF. Inflating a right atrial balloon in 4 dogs and a left atrial balloon in 2 dogs indicated good separation between TLF and TDA. Data on total lymph protein and albumin clearance before and after oleic acid induced pulmonary oedema in an additional 5 dogs indicated that TLF and TDA drained two differing regions. Our data demonstrate that this lymph preparation provides a sample of thoracic lymph flow with no major extrathoracic lymph contamination. We also propose an alternative method to test for extrathoracic contributions to thoracic lymph, by the application of positive end-expiratory pressure, thereby replacing right atrial balloon inflation.

Albumins↗
PubMed1991

Inhaled nitric oxide. A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction.

Background. The gas nitric oxide (NO) is an important endothelium-derived relaxing factor, inactivated by rapid combination with heme in hemoglobin. Methods and Results. Awake spontaneously breathing lambs inhaled 5-80 ppm NO with an acutely constricted pulmonary circulation due to either infusion of the stable thromboxane endoperoxide analogue U46619 or breathing a hypoxic gas mixture. Within 3 minutes after adding 40 ppm NO or more to inspired gas, pulmonary hypertension was reversed. Systemic vasodilation did not occur. Pulmonary hypertension resumed within 3-6 minutes of ceasing NO inhalation. During U46619 infusion pulmonary vasodilation was maintained up to 1 hour without tolerance. In the normal lamb, NO inhalation produced no hemodynamic changes. Breathing 80 ppm NO for 3 hours did not increase either methemoglobin or extravascular lung water levels nor modify lung histology compared with control lambs. Conclusions. Low dose inhaled NO (5-80 ppm) is a selective pulmonary vasodilator reversing both hypoxia- and thromboxane-induced pulmonary hypertension in the awake lamb [corrected].

Administration, Inhalation↗
PubMed1991

Does PEEP facilitate the resolution of extravascular lung water after experimental hydrostatic pulmonary oedema?

The effect of mechanical ventilation with positive end-expiratory pressure on the resolution of hydrostatic pulmonary oedema created by temporary left atrial balloon inflation was studied in mechanically ventilated dogs. Immediately after the hydrostatic process was terminated, by deflating the left atrial balloon, the animals were ventilated for 4 h with zero end-expiratory pressure (ZEEP, n = 6) or with a positive end-expiratory pressure (PEEP, n = 6) of 1.0 kPa (10 cmH2O). Gas exchange and extravascular lung water content (EVLW) with the double indicator dilution technique (dye/cold) were studied and gravimetric determination of lung water was made postmortem. EVLW decreased from 31.6 +/- 7.3 mean +/- SD ml.kg.1 during maximal oedema to 14.5 +/- 2.1 ml.kg.1 (p less than 0.001) 4 h after deflation of the left atrial balloon in dogs ventilated with ZEEP. The corresponding values in dogs ventilated with PEEP were a reduction in EVLW from 28.0 +/- 4.1 to 20.7 +/- 4.0 ml.kg.1 (p less than 0.01) (mean decrease 7.3 +/- 4.0 ml.kg.1). EVLW was significantly higher after 4 h on PEEP than after ZEEP (p less than 0.01). Gravimetric values at the end of the experiment were 12.4 +/- 2.8 ml.kg.1 (ZEEP) and 14.7 +/- 4.5 ml.kg.1 (PEEP) (NS). Oxygenation improved in both groups during the resolution of oedema with a more evident and early effect in the PEEP group. It is concluded that mechanical ventilation with PEEP of 1.0 kPa (10 cmH2O) in the resolution phase after experimental hydrostatic oedema improves oxygenation but retards the resolution of oedema.

Animals↗
PubMed1990

Measurement of extravascular lung water by thermal-dye dilution technique: mechanisms of cardiac output dependence.

The extent to which extravascular lung water (EVLW) is dependent on cardiac output was analysed in anaesthetized and mechanically ventilated pigs. EVLW was measured by thermal-dye dilution technique, by a fibreoptic thermistor catheter system (system 1), and by a thermistor catheter-external optical cuvette system (system 2). During baseline conditions, at which cardiac output was 3.65 l/min, and EVLW was 11.7 and 7.7 ml/kg b.w. with systems 1 and 2 respectively. A reduction of cardiac output to a mean of 1.90 l/min by the addition of halothane to the inspired gas did not significantly affect EVLW with system 1 (-5%) but increased EVLW by 39% (p less than 0.05) with system 2. An increase of cardiac output to a mean of 4.78 l/min by intravenous infusion of isoproterenol caused a small increase in EVLW with system 1 (14%; p less than 0.05) and a decrease with system 2 (10%; p less than 0.05). The dependence on cardiac output was the same whether the catheters were positioned centrally (aortic root) or peripherally (abdominal aorta). With system 1 the CO dependence was due to different time constants in thermistor and optical systems, and with appropriate phasing the dependence could be eliminated. With system 2 a large overestimation of the mean transit time difference between the two indicators was seen when cardiac output was low, resulting in overestimation of EVLW. It is concluded that the dependence of EVLW volume on cardiac output is an artefact due to technical problems in the design of the recording equipment rather than a reflection of pulmonary or vascular effects.

Animals↗
PubMed1990

Lung fluid balance evaluated by the rate of change of extravascular lung water content.

Lung fluid balance was studied in 27 mongrel dogs by measuring changes in extravascular lung water content (EVLW). The expression delta EVLWi, which is the difference in EVLWi per kilo bodyweight per hour between two measurement occasions, was used as an estimate of the rate of change of EVLW. EVLW was measured by a double-indicator dilution technique (EVLWi) using iced glucose and indocyanine green. In addition, EVLW was determined at the end of each experiment with gravimetric technique (EVLWg), which enabled the calculation of a regression equation between EVLWi and EVLWg. Delta EVLWi was calculated repeatedly during an 8-h period of mechanical ventilation (MV) with no application of a positive end-expiratory pressure (n = 5), during an 8-h period with a positive end-expiratory pressure (PEEP) of 10 cmH2O (1.0 kPa) (n = 5), during the development of oleic acid (OA)-induced pulmonary oedema (n = 7), and hydrostatic pulmonary oedema (left atrial balloon inflation) (n = 9). An increase of EVLW was seen during PEEP 8 h (mean 35%) and after induction of OA and hydrostatic oedema (mean 300%), but no change was found during MV without PEEP. The regression equation was EVLWi = 5.5 + 0.97 x EVLWg (P = 0.001, r = 0.90). OA-induced oedema caused a mean maximum delta EVLWi of 5.1 ml/kg/h, indicating capillary leakage which, however, was self-limiting within 2 h after OA injection. In hydrostatic oedema there was a maximum delta EVLWi of 16.0 ml/kg/h. Delta EVLWi was negative after deflation of the left atrial balloon, indicating reabsorption of oedema.

Animals↗
PubMed1990

Measurement of dynamic lung fluid balance in the mechanically ventilated dog. Theory and results.

An expression (LN) is presented for the net fluid leakage from the intravascular to the extravascular space in the lung. It is based on a new dog model and is the sum of rate of change in extravascular lung water content (EVLW), thoracic lymph flow, and pleural fluid formation. The rate of change of EVLW (delta EVLW) in ml/kg/h was calculated from repeated measurements of EVLW with a double-indicator dilution technique (dye/cold) and corrected according to the relation between EVLW measured by this technique and gravimetry. LN was studied in lung-healthy mechanically ventilated dogs during a prolonged period of mechanical ventilation with and without the application of a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). During mechanical ventilation, LN was found to be 0.3 ml/kg/h in the basal condition, increasing to 0.5 ml/kg/h (P less than 0.01) after a mean period of 7 h. After the application of a positive end-expiratory pressure (PEEP) of 10 cmH2O (1 kPa) for 0.5-2 h, LN was found to increase significantly, from a mean of 0.3 ml/kg/h to 0.9 ml/kg/h (P less than 0.01). We conclude that LN is a useful quantitative expression in experimental studies on lung fluid balance.

Animals↗
PubMed1990

Net fluid leakage (LN) in experimental pulmonary oedema in the dog.

Net fluid leakage (LN) from the intravascular to the extravascular pulmonary space was estimated in anaesthetised dogs after injection of oleic acid (OA) (n = 8), or after hydrostatic pressure elevation by inflation of a left atrial balloon (n = 5). LN was calculated as the sum of: (i) rate of change in extravascular lung water (delta EVLW), (ii) thoracic lymph flow, and (iii) pleural fluid formation per time unit. Pleural fluid formation was measured in five dogs with hydrostatic or OA induced pulmonary oedema and was 1.8 +/- 0.9 ml/kg/h. In OA-induced pulmonary oedema, LN increased to a peak of 9.2 ml/kg/h within 2 h after OA injection. Thereafter LN fell and was 2-4 ml/kg/h during the succeeding 2-4 h. During hydrostatic pulmonary oedema LN was increased to as much as 13 ml/kg/h, but it became negative, -5 to -8 ml/kg/h (reabsorption of extravascular fluid) as soon as pulmonary vascular pressures returned to normal following deflation of the left atrial balloon. We conclude that in both forms of oedema there is an initial rapid leakage. In OA-induced oedema this leakage continues, although at a slower rate, whereas in hydrostatic oedema there is a considerable net fluid absorption from the pulmonary extravascular to the intravascular space as soon as vascular pressures are brought to normal levels.

Animals↗