Endogenous NO does not regulate baseline pulmonary pressure, but reduces acute pulmonary hypertension in dogs.

UNLABELLED: It has remained unclear whether endogenous production of nitric oxide (NO) plays an important role in the regulation of physiologically normal pulmonary pressures. Severe alveolar hypoxia is accompanied by decreased pulmonary NO production, which could contribute to the development of hypoxic pulmonary hypertension. On the other hand, pharmacological NO inhibition further augments this hypertensive response. AIMS: The aims of the present study were to test: (a) whether NO contributes importantly in the maintenance of baseline pulmonary pressure; and (b) to which degree NO is involved in the pulmonary haemodynamic adjustments to alveolar hypoxia. METHODS: In anaesthetized dogs (n=37), the systemic and pulmonary haemodynamic effects of the NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME, 20 mg kg(-1)) and substrate, L-arginine (200-500 mg kg(-1)), were determined at baseline and during alveolar hypoxia. Constant blood flows were accomplished by biventricular bypass, and systemic normoxaemia was maintained by extracorporeal oxygenation. RESULTS: The primary findings were: (a) L-NAME failed to increase baseline mean pulmonary arterial pressure (10.1 +/- 0.7 vs. 10.5 +/- 0.5 mmHg, P=ns), despite effective NO synthase inhibition as evidenced by robust increases in systemic arterial pressures; (b) L-NAME augmented the pulmonary hypertensive response to alveolar hypoxia (10.2 +/- 0.7 to 19.5 +/- 1.7 with L-NAME vs. 9.9 +/- 1.1 to 15.5 +/- 1.0 mmHg without L-NAME, P<0.05); and (c) L-arginine failed to decrease baseline or elevated pulmonary pressures. Instead, prolonged L-arginine caused increases in pulmonary pressure. CONCLUSION: These findings suggest that NO plays no significant role in the tonic physiological control of pulmonary pressure, but endogenous NO becomes an important vasodilatory modulator during elevated pulmonary pressure.

[Lung volume reduction surgery. A new surgical therapeutic possibility for patients with emphysema]. / Lungevolumenreducerende kirurgi. Et nyt kirurgisk behandlingstilbud til patienter med emfysem.

Lung volume reduction surgery is a new surgical procedure for treatment of patients with pulmonary emphysema. At the operation the most peripheral parts of the lung are resected. Only 15-20% of the patients admitted for lung volume reduction surgery are suitable for operation. The preliminary results have demonstrated improvement in lung function in the majority of the patients. Most of the reports comprise small numbers of patients and have a short time of observation. The longest reported period of observation for a larger number of patients is 24 months and shows a continuing improvement in lung function, dyspnoea and six minute walk test. Because of the high incidence of emphysema, lung volume reduction is a procedure that could reach large extension in the future. However, better definition of criteria of inclusion and better evaluation of the operative procedures are needed.

Effect of alveolar hypoxia on segmental pulmonary vascular resistance and lung fluid balance in dogs.

In a biventricular bypass preparation with constant-flow perfusion, pulmonary arterial pressure (Ppa), average pulmonary capillary pressure (Ppc), venous pressure (Pv), extravascular lung water volume (EVWd) and capillary permeability-surface area product for urea (PS) were determined in control animals and in animals subjected to alveolar hypoxia. During hypoxia, Ppa increased in a biphasic manner, the site of hypoxic pulmonary vasoconstriction being located in the arterial upstream segment. At baseline, Ppc values were identical in control and experimental animals (3.4 +/- 0.4 vs. 3.6 +/- 0.2 mmHg). During 150 min of airway hypoxia, the rise in Ppc (5.1 +/- 0.3 mmHg) did not exceed the rise in Ppc (4.9 +/- 0.5 mmHg) recorded in control animals at same time interval during normoxic ventilation. EVWd increased during hypoxia to values significantly higher than those obtained in control animals (0.559 +/- 0.036 vs. 0.466 +/- 0.027 mL water g-1 lung). PS remained unchanged at baseline level throughout experiments in both groups of animals. Present data suggest that lung oedema formation during alveolar hypoxia may be caused by increased transcapillary fluid loss preferentially through transcellular hydraulic pathways in capillary endothelial cells.

Effect of prolonged alveolar hypoxia on pulmonary arterial pressure and segmental vascular resistance.

The time course of hypoxic pulmonary vasoconstriction and its segmental distribution were studied during prolonged (150 min) alveolar hypoxia in in vivo dog lungs at constant-flow perfusion. With the pulmonary and the systemic circulations separated by two extracorporeal circuits, adequate systemic oxygenation was achieved throughout the experiments. The pulmonary circulation exhibited a time-related biphasic hypoxic vasoconstrictor response: an initial rapid contraction [79 +/- 11% (SE) above control level] was followed by a partial relaxation when a second slow and sustained vasoconstriction (92 +/- 13% above control level) superseded. We partitioned the pulmonary circulation into two segments by arterial occlusion: an upstream arterial segment and a downstream segment consisting of a middle and a venous segment. Measurements were performed at baseline and during the late sustained vasoconstrictor response. Prolonged alveolar hypoxia increased pulmonary capillary pressure by 90 +/- 18%, the site of pulmonary vasomotion being the arterial upstream and downstream middle and venous segments.

Proprioception at the ankle: the effect of anaesthetic blockade of ligament receptors.

Seven subjects with normal joints were tested for active and passive position sense of ankle inversion, peroneal reflex reaction time to sudden ankle inversion, and postural stability during single-leg stance. The tests were performed before and after regional block of the ankle and foot with local anaesthetic. Passive position sense, assessed with the muscles relaxed, was greatly impaired by anaesthesia but active position sense, with the calf muscles activated, was preserved, and the peroneal reaction time to sudden ankle inversion was not altered. The magnitude of postural sway during single-leg stance was also unchanged by anaesthesia of the ankle and foot. The results suggest that the afferent input from intact lateral ankle ligaments is important in sensing correct placement of the foot at heel-strike, but that this input can be replaced by afferent information from active calf muscles. Afferent input from these muscles seems also to be responsible for dynamic ankle protection against sudden ankle inversion and is adequate to allow stable single-leg stance.

Prolonged peroneal reaction time in ankle instability.

The peroneal reflex time to sudden ankle inversion and the postural control of 15 athletes with functionally instable ankles were compared with 15 stable controls. A trapdoor produced sudden ankle inversion. Surface electrodes recorded electromyographic activity of the peroneal muscles. Postural sway was expressed by a transverse sway value obtained during single limb stance on a force plate. Increased postural sway was found in subjects with functional instability (p less than 0.01). This is in accordance with previous studies. Functionally instable subjects also displayed an increased peroneal reaction time (p less than 0.01) supporting the theory that functional instability is induced by a proprioceptive reflex defect. Nine of the 15 instable subjects were unilaterally instable and showed lower peroneal reaction time and postural sway values for the stable ankle, but the difference was not significant. There was a high degree of correlation between postural sway and peroneal reaction time (Spearman's rho = .92). In ten functionally instable athletes tested with and without ankle taping, it could not be verified that a reflex enhancing effect of taping occurs through stimulation of cutaneous afferents.

Ankle instability caused by prolonged peroneal reaction time.

The reaction of 15 functionally unstable ankles to sudden inversion was described by monitoring muscle activity, joint motion, and alternation of the body center of pressure. The results were compared with those of 15 stable controls. Stable and unstable subjects showed a similar reaction pattern to sudden inversion: first, a peripheral reflex action, namely, a contraction of the peronei counteracting the ankle inverting momentum, and, then, a centrally elicited pattern, namely, a flexion of the hip, knee, and ankle relieving the vertical pressure on the ankle and producing ankle eversion. Unstable subjects did not show a defect in their central processing of afferent input. In contrast, a prolonged reaction time (median 84 msec compared with 69 msec in stable subjects) suggested a partial deafferentation of the reflex stabilization of the ankle and substantiated the theory of a proprioceptive deficit being responsible for ankle instability.

[Cannulation of the radial artery. Risks, effective examination methods and monitoring of the circulation in the hand during the procedure]. / Kanylering af a. radialis. Risici, relevante undersøgelsesmetoder og monitorering af håndens kredsløb i forbindelse med proceduren.

Cannulization of the radial artery with the object of continuous measurement of the blood pressure or repeated analyses of the arterial blood gases is an easy and relatively safe procedure. Thrombosis is observed in 25-40% of the cases. The frequency depends upon the condition of the patient, the cannula and technique of cannulization and duration of this. Permanent ischaemic damage resulting from thrombosis is, however, rare. Other complications of clinical significance are infections and vascular lesions which are, similarly, rare. Allen's test for assessing the collateral circulation of the hand has a high negative predictive value while the positive predictive value is so low that a positive test result does not exclude cannulization. In these cases, better assessment of the perfusion of the hand may be obtained by combining the test with pletysmography. After cannulization, it should be possible to monitor perfusion distal to the site of cannulization employing more recent pulse oximeters with the aid of the pletysmographic curve.