Hypoxic Pulmonary Vasoconstriction in Man: Effects of Hyperventilation

The pulmonary vasoconstriction response to hypoxia was studied in eight anaesthetized supine subjects. One lung was made hypoxic while the other was ventilated with 100% oxygen. This was achieved by separating the tidal gas-distribution to the lungs by means of a double-lumen tracheal catheter. The hypoxic pulmonary vasoconstriction (HPV) response was estimated from the blood flow diversion away from the hypoxic lung. Blood flow distribution between the lungs was calculated from the regional expired carbon dioxide production, assuming regional carbon dioxide production to be proportional to blood flow. The subjects were studied during six different conditions. Firstly, when ventilated with 100% oxygen to both lungs at a PaCO2 of about 6 kPa. Secondly, with 100% oxygen to the left lung and 5% oxygen in nitrogen to the right (test) lung. The ratio between carbon dioxide output from right and left lung was calculated. These measurements were repeated during two states of hyperventilation (PaCO2 of about 4.5 kPa and 3.5 kPa, respectively) with and without hypoxia (conditions 3-6). During normoventilation, blood flow distribution between the lungs was equal. During hypoxia, blood flow distribution to the hypoxic lung decreased by 35% of the pre-hypoxic value. Furthermore, a decrease in arterial oxygen tension from 51.5 +/- 4.5 to 11.5 +/- 2.1 kPa was observed. During excessive hyperventilation (PaCO2 3.2 +/- 0.2 kPa), blood flow distribution to the hypoxic right lung decreased by only 10% of its pre-hypoxic value. A further decrease in arterial oxygen tension to 8.5 +/- 1.8 kPa was observed. This decrease in PaO2 was possibly due to an increased venous admixture caused by an abolished HPV response. It is concluded that hyperventilation counteracts hypoxic pulmonary vasoconstriction in man.     

Buccal mucosa fibroblasts and periodontal ligament cells perturbed by tensile stimuli in vitro

Abstract – Human buccal mucosa fibroblasts and periodontal ligament cells grown in tissue culture were subjected to tensile forces approximating those used for orthodontic bodily tooth movement. The cells were synchronized into pre S phase and positively tested for response to nonmechanical physical stimuli. Two-dimensional gel analysis and immunohistochemical analysis of the three cytoskeletal components showed a lack of response. Similar negative results were found when the cells were perturbed in the presence of substance P. We hypothesize that perhaps these cells respond more readily to injury, a secondary effect of the forces of tooth movement, than to tensile forces.     

REVERSAL OF NITROUS OXIDE-INDUCED DEPRESSION OF HYPOXIC PULMONARY VASOCONSTRICTION BY LIGNOCAINE HYDROCHLORIDE DURING COLLAPSE AND VENTILATION HYPOXIA OF THE LEFT LOWER LOBE

The blood flow to the left lower lobe (L), and total (T) pulmonary blood flow, were measured in 10 open-chest dogs usingelectromagnetic flowmeters. Ventilation of the left lower lobewith 7% oxygen in nitrogen produced a greater reduction in L/T (41%) than lobar ventilation with 7% oxygen in nitrous oxide(33%). Lobar collapse reduced QL/QT by 65%, but there was nochange in L/T when 50% nitrous oxide was administered to theright lung. The i.v. infusion of lignocaine hydrochloride duringventilation of the lobe with 7% oxygen in nitrogen producedno change in L/T. However, lignocaine infusion during lobar ventilationwith 7% oxygen in nitrous oxide produced a further reductionin L/T to a value which was not significantly differentfrom that observed during ventilation with 7% oxygen in nitrogen.Lignocaine had no effect on L/T during lobar collapse whether theright lung was ventilated with 50% oxygen in nitrogen or 50%oxygen in nitrous oxide. It is concluded that lignocaine reversesthe depression of hypoxic pulmonary vasoconstriction producedby lobar ventilation with nitrous oxide.     

EFFECT OF LIGNOCAINE AND NITROUS OXIDE ON HYPOXIC PULMONARY VASOCONSTRICTION IN THE DOG CONSTANT-FLOW PERFUSED LEFT LOWER LOBE PREPARATION

The effects of lignocaine hydrochloride on hypoxic pulmonaryvasoconstriction in the presence and absence of nitrous oxidewere examined during constant-flow perfusion of the left lowerlobe. Lignocaine had no effect on lobar pulmonary vascular resistanceduring lobar ventilation with oxygen or 7% oxygen in nitrogen.The substitution of nitrous oxide for nitrogen diminished thehypoxic vasoconstrictor response, whilst the subsequent infusionof lignocaine during 7% oxygen in nitrous oxide increased theresponse to a value which was not significantly different fromthat produced by 7% oxygen in nitrogen alone. *Department of Anesthesia, Karolinska Hospital, 1041 Stockholm,Sweden.     

Monkey pulp reactions to restorative materials

Abstract — Deep buccal cavities in 99 teeth in eight young monkeys were filled with the following combination of materials: a light-cured microfilled composite with or without a base, a chemically cured composite with a base, a silicate cement, and a zinc oxide-eugenol cement. The acid etch technique and intermediate layer of resin was used in the composite group. Pulp reactions and presence and location of bacteria were studied after 8 days and after 90 days. In the short observation period the inflammatory reactions were more pronounced when unlined composite fillings were evaluated compared with silicate cement fillings and with lined fillings. Bacteria were seen in all unilined cavities and a significant association between presence of bacteria and moderate to severe inflammatory responses was found. The most severe inflammatory reactions were seen when bacteria were found in the dentinal tubules. After 90 days slight inflammatory changes prevailed in all groups. A significant correlation between bacteria and inflammatory reactions could still be observed.     

A retrospective analysis of nitric oxide inhalation in patients with severe acute lung injury in Sweden and Norway 1991–1994

Background: Patients with severe acute lung injury (ALI) have been treated compassionately on doctors' initiative with inhaled nitric oxide (INO) in Sweden and Norway since 1991. In 1994 the previously used technical grade nitric oxide was replaced by medical grade nitric oxide.
Methods: We have carried out a retrospective data collection all identified adult patients treated with IN0 for >4 h during the period 1991-1994 focusing on safety aspects and patient outcome. We used the following exclusion criteria (1) Age <18 years, Simultaneous treatment with extracorporeal removal of CO2 NO inhalation period <4 h, (4) Incomplete or missing patient charts, (5) Use of IN0 in order to treat pulmonary hypertension following cardiac surgery, with little or no acute lung injury.
Results: Inclusion criteria were met by 56 out of 73 identified patients. Mean age was 48219 years and the median duration of IN0 treatment was 102 h. PaOz/FIOz ratio at start of treatment was 85233 mm Hg with a lung injury score (LIS) of 3.2t0.8. The aetiology of the lung injury was pneumonia (n=27), sepsis (n=12) and trauma (n=8). Survival to hospital discharge was 41% and survival after 180 d was 38%. Three serious adverse events were identified, two from technical failures of the IN0 delivery device and one withdrawal reaction necessitating slow weaning from INO. No methaemoglobin values >5% were reported during treatment.
Conclusion: The overall mortality did not differ dramatically from historical controls with high mortality. Only a randomised study may determine whether IN0 as an adjunct to treatment alters the outcome in severe ALL One cannot at present advocate the routine use of IN0 in patients with ALI outside such studies.