Respiratory hypersensitivity to Ascaris antigens is carried out on 9 dogs. The participation of vagus reflex on this respiratory distress is studied in 4 of these dogs. The dogs were exposed initially to Ascaris aerosol, then to egg albumin and NaCl aerosol for control, and once more to Ascaris aerosol after bilateral vagi blockade and lavage, respectively. The principal parameters studied were ΔPoes (mm Hg)/100 ml TV as a measurement of flow resistance in the airways, and respiratory rates (Poes=changes of oesophagus pressure; TV=tidal volume). All the animals presented a significant respiratory distress with Ascaris aerosol, which could be clearly avoided with the central bilateral blockade of nervus vagus.
In anesthetized, spontaneously breathing rabbits, intratracheally administered isotonic saline, acetylcholine (Ach) and histamine (His) induced an increase of airway resistance up to 183, 571, and 312%, respectively, compared with untreated controls. This was accompanied by a decrease of the arterial pO2. Bilateral cervical vagotomy led to nearly complete inhibition of the saline- and Ach-induced bronchoconstriction, whereas the His effect was only reduced to 202%. Vagotomy did not improve the arterial pO2. While the bronchoconstrictive effects of isotonic saline and Ach revealed a significant linear correlation with the increased cGMP/cAMP ratio, His did not cause an alteration of the cGMP/ cAMP ratio to a degree that corresponds to its bronchoconstrictive activity. These data indicate that (1) bronchoconstriction-inducing agents may act (a) by stimulation of the parasympathetic nerve or (b) by contracting smooth muscles directly; (2) alveolar ventilation is not regulated by the parasympathetic nerve, and (3) bronchoconstriction induced by parasympathetic stimulation is associated with or mediated by an increase of the cGMP/ cAMP ratio
The effects of 5 mg pindolol and 100 mg propranolol on the airway resistance were compared with a placebo in an inter-individual double blind trial in eight patients with chronic obstructive lung disease. Six hours after drug administration the patients inhaled two puffs of fenoterol (0.4 mg) from a metered aerosol to test the reversibility of the bronchoconstrictive effect. Airway resistance and intrathoracic gas volume were measured by body plethysmography. Propranolol increased the airway resistance significantly (P less than 0.01). The highest increase with a mean of 44% was measured two hours after ingestion. After six hours the mean increase was still 18%. Pindolol showed a barely detectable, statistically insignificant bronchoconstrictive effect in comparison with the placebo. With regard to the circulatory effects 5 mg pindolol and 100 mg propranolol were aequipotent, propranolol had a more pronounced effect in lowering the pulse rate, pindolol in lowering the blood pressure. Fenoterol can reduce airway resistance even after beta-blockade, but the effect was more profound after the placebo than after the beta-blocker.
The influence of Dopamine on microcirculation during hemorrhagic shock was investigated by means of the pancreas chamber technique (HEISIG, 1967). Parameter of microcirculation was the corpuscular flow velocity measured with the "flying spot" method. Simultaneously arterial and venous blood pressure, heart rate, blood gases and pH-status were registered. While a Dopamine-dosage of 5 mug/kg/min did not markedly effect perfusion of the pancreas, application of 10 as well as 20 mug/kg/min Dopamine caused a significant improvement of microcirculation. There was no difference between 10 and 20 mug/kg/min Dopamine. The increase of capillary perfusion can certainly not be explained by the small rise of blood pressure that was found under treatment with Dopamine. The results support the statement of the existence of Dopamine-specific receptors in pancreatic vessels. Compared to a group of animals treated with 5 mug/kg/min Dopamine and an untreated control group, survival rate of animals treated with 10 as well as 20 mug/kg/min Dopamine was significantly increased.
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