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Biomedical subjects

J Vaage

Publications and source records attributed to J Vaage.

At least 181 records · Page 10Linked to original sources
PubMed1977

Serum therapy for radiation-induced impairment of immune resistance to metastasis.

The use of serum transfusion to remedy radiation-induced damage to established antitumor resistance was investigated in female C3H mice. The mice, which had been actively immunized against a syngeneic mammary carcinoma, were injected i.v. and s.c. with suspensions of cells from the same tumor and were then given 300 R extensive-field irradiation to the abdomen two times. Tumor cells implanted outside the irradiated area grew better in irradiated mice than in unirradiated controls. Under these experimental conditions, protection could be transferred to radiation-impaired hosts with several injections of cell-free immune serum. Transfers of normal serum provided a detectable but low degree of protection. The corrective effect of serum transfers to radiation-impaired hosts was clearly expressed against pulmonary tumor growth (i.v. challenge), provided the transfusions were started no later than the first day after the injection of the tumor cells. Serum transfusions were ineffective against the growth of tumors implanted s.c. Transfers of serum from hosts carrying large (15 mm) s.c. tumor implants had a negative effect on the resistance of irradiated recipients. The results indicate that humoral resistance factors, both normal and immune, may act against metastatic spread of solid tumors.

Animals↗
PubMed1977

Intravascular platelet aggregation and acute respiratory insufficiency.

Respiratory effects of long-lasting episodes of intravascular platelet aggregation have been studied in cats. Animals in 1 group had the chest opened and were given mechanical ventilation with a constant tidal volume. Animals of another group were breathing spontaneously. Platelet aggregation was induced by intravenous infusion (for 1 hr) of a suspension of collagen fibrils. Such infusions caused acute respiratory distress in both groups. Severe arterial hypoxemia and rapid breathing as well as constriction of airways and lung vessels occurred. Most of these changes were reversed within 2 hr after collagen infusion had ended. Deep lung inflations markedly improved lung function. It is concluded that an acute, but reversible pulmonary insufficiency might be caused by pulmonary microembolization due to intravascular platelet aggregation. The arterial hypoxemia is suggested to be caused by disturbances in the ventilation-perfusion ratio secondary to airway constriction and closure. The present findings also imply that besides platelet aggregation, some additional factors are necessary for irreversible or progressive respiratory insufficiency to develop.

Animals↗
PubMed1976

Lung responses and platelet release reaction following induced intravascular platelet aggregation in the cat.

Pulmonary microembolism secondary to intravascular platelet aggregation causes a rise in pulmonary vascular resistance and a decrease in dynamic lung compliance. The relationship between these lung responses and the platelet release reaction was investigated in the cat. Repeated episodes of platelet aggregation were induced by intravenous infusions of either ADP or collagen. Platelet release was evaluated by serial determinations of the plasma concentration of platelet factor 4 (PF-4). An increased plasma concentration of PF-4 was found after the initial episode of such induced intravascular platelet aggregation. Consecutive infusions of an aggregating agent still elicited vigorous lung responses, but no further increase in the plasma concentration of PF-4 was observed. There are different possible explanations for this lack of correlation between the lung responses and the PF-4 release. It may well be that the pattern of release for PF-4 does not reflect those release events which result in pulmonary smooth muscle contraction. Alternatively, but less likely, pulmonary smooth muscle constriction and platelet release could be fully independent phenomena.

Adenosine Diphosphate↗
PubMed1976

Vagal reflexes in the bronchoconstriction occurring after induced intravascular platelet aggregation.

Intravascular platelet aggregation induced in cats by i.v. infusions of collagen caused a transient increase in pulmonary vascular resistance (PVR) and in non-elastic pulmonary resistance (RL), and a transient decrease in dynamic lung compliance (dyn CL). PVR,dyn CL and platelet aggregation after collagen infusions were unaffected by bilateral cervical vagotomy and atropinization, wheras these procedures reduced the post-infusion rise in RL by about 50 per cent. The administration of indomethacin inhibited platelet aggregation as well as bronchoconstriction after collagen infusion. The present investigation indicates that intravascular platelet aggregation will cause reflex bronchoconstriction mediated by vagal efferent fibres.

Animals↗
PubMed1976

Stimulation or inhibition of immune resistance against metastatic or local growth of a C3H mammary carcinoma.

The effects of syngeneic tumor vaccine preparations on resistance against s.c. and pulmonary implants of a spontaneous C3H mouse mammary carcinoma have been compared during progressive primary tumor growth, after surgical cure, and during declining immune resistance following complete tumor removal. Concomitant antitumor immunity reached a higher level of effectiveness in the lungs than in s.c. tissue. The concomitant immune resistance in the lungs also remained effective longer than did s.c. resistance, which was the first to decline under the increasing antigen burden of a growing tumor implant. Resistance to challenge recovered quickly after the complete removal of a large tumor burden, but recovery was impeded if killed tumor tissue was reinjected too soon after tumor removal. If injections of killed tumor tissue were given 7 days after tumor removal, the completed recovery was not affected. If injections of killed tumor tissue were given 30 days after tumor removal, immune resistance to challenge, at this time much declined, was stimulated.

Animals↗
PubMed1976

Aggregation fo blood platelets and increased hydraulic conductivity of pulmonary exchange vessels.

Pulmonary microembolization secondary to platelet aggregation has been suggested to be a pathogenetic component of the shock lung syndrome. In vitro experiments have also shown that platelets can release factors with a permeability-enhancing activity. We studied the effect of collagen-induced platelet aggregation on the hydraulic conductivity of thexchange vessels in isolated, blood-perfused rabbit lungs. The net rate of fluid filtration in each pair of lungs was determined during standardized elevations of left atrial pressure before and after platelet aggregation induced by intraarterial collagen infusions. Such infusions were followed by a significant, but transient increase in the net rate of fluid filtration. These lungs were papaverinized so that collagen infusions caused only minor increases in inflow pressure. Separate experiments indicated that the observed increase in pulmonary arterial pressure could not explain the increase in net filtration rate after collagen infusion. When platelet-poor plasma was used as a perfusate no change in the net rate of fluid filtration was observed after collagen infusion. The conclusion from these experiments is then that intravascular platelet aggregation induced by collagen infusion caused a transient increase in the permeability of the pulmonary exchange vessels.

Animals↗
PubMed1975

The release of prostaglandin-like substances during platelet aggregation and pulmonary microembolism.

During pulmonary microembolism subsequent to induced platelet aggregation in vivo, a pressor response is elicited in the lungs due to the release of vasoactive substances. During the prefusion of isolated cat lungs with whole blood, platelet aggregation induced by collagen released prostaglandin-like substances (PG-LS), and a rabbit aorta contracting substance (RCS) as measured by continuous biosassay of the venous effluent. This release occurred in parallel to the pulmonary pressor response. The same amount of PG-LS and RCS was released when the lungs were replaced by a blood filter to trap platelet aggregates. Apparently PG-LS and RCS are released from platelets during their aggregation. As E- and F-type PGs are rapidaly inactivated in the pulmonary circulation, there must either be an equal generation of PGs in the lungs themselves, or rather, the release of PGs from platelets must occur distal to the inactivation mechanism without any additional PG-release from the lungs. The exact role of PGs in the lung responses to intravascular platelet aggregation is not clear.

Animals↗
PubMed1975

The pulmonary vasoconstrictor response to hypoxia: effects of inhibitors of prostaglandin biosynthesis.

The main purpose of the present work was to determine whether prostaglandins (PGs) synthetised in the lungs mediate the vasoconstrictor response to acute alveolar hypoxia. Isolated and ventilated lungs of rats were perfused at 37 degrees C with homologous blood at constant-volume, pulsatile inflow, and pressor responses to 3 min periods of standardized ventilation hypoxia recorded. Indomethacin, sodium meclofenamate and acetylsalicylic acid (all 100 mug/ml), which are potent inhibitors of PG biosynthesis, did not reduce the hypoxic vasoconstrictor response. Sometimes they even enhanced this response. We conclude that PGs do not mediate the hypoxia-induced vasoconstriction. We suggest that vasodilatory PGs might act to reduce and modify pulmonary arterial hypertension due to hypoxia.

Animals↗