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Biomedical subjects

J Vaage

Publications and source records attributed to J Vaage.

At least 163 records · Page 9Linked to original sources
PubMed1980

The role of platelets in post-traumatic pulmonary insufficiency.

It is suggested that pulmonary microembolism, due to intravascular platelet aggregation, is an important pathogenetic factor in the development of acute post-traumatic pulmonary insufficiency. Changes in blood flow, vessel wall injury and/or changes in the composition of the blood may all induce aggregation of the circulating platelets. Platelet aggregates are then trapped in the pulmonary microcirculation. Experimentally induced intravascular platelet aggregation causes pulmonary vasoconstriction and increases pulmonary vascular resistance. The vasoconstriction has predominantly a precapillary localization. It has also been demonstrated that intravascular platelet aggregation will increase transiently the hydraulic conductivity of pulmonary exchange vessels. Thus, edema development is facilitated, although platelet aggregation per se cannot induce fulminant lung edema. In parallel with the vascular changes, platelet aggregation causes constriction of both peripheral and central airways, as reflected in a decreased dynamic compliance and an increased pulmonary resistance. The central airways are at least partly constricted secondary to nervous reflexes mediated through bronchomotor, parasympathetic nerve fibres in the vagal nerve. If a persistent and long-lasting intravascular aggregation of platelets is induced, the changes in respiratory mechanics described will impair gas exchange and precipitate a severe respiratory insufficiency. This pulmonary insufficiency is, however, dependent on an ongoing activation and aggregation of platelets. When the experimentally induced platelet aggregation is stopped, gas exchange function returns rapidly to normal.

Animals↗
PubMed1980

Inherent changes in the in vivo growth characteristics of C3H/He mammary carcinomas.

The ability of C3H/He mammary carcinoma cells to grow in the lungs after i.v. injection was repeatedly tested with cells from tumors which were kept in serial s.c. passage in syngeneic female mice. The s.c. growth rate and the s.c. transplantation immunogenicity were also determined for each transplant generation. The ability of a tumor to grow in the lungs, which appeared in most tumors only after repeated s.c. passages, coincided mainly with increased growth rate and not with the loss of immunogenicity and/or gain of endogenous growth-stimulating factors. In each combination of cross-reactivity tested, transplantation immunogenicity was tumor specific, and growth stimulation was not tumor specific. Three of ten tumors were retested in serial passages started again from pieces of the primary tumors stored in liquid N2, and the identical changes recurred in the same, or in nearly the same, transplant generations. This indicates that certain variable neoplastic characteristics may be inherent and will appear not haphazardly, but according to a genetically predetermined schedule.

Animals↗
PubMed1979

Lack of release of prostaglandins from isolated perfused lungs during pulmonary hypertension and oedema.

1 The effects on pulmonary prostaglandin synthesis of pulmonary hypertension and oedema have been studied. 2 Seventeen isolated lungs of rabbit, cat and guinea-pig were perfused with plasma, whole blood or Krebs Ringer solution in a recirculating system. 3 The venous effluent from the lungs superfused (10 ml/min) a series of smooth muscle tissues sensitive to prostaglandins and thromboxane A2; these were: rat stomach strip, rat colon, chick rectum and rabbit aorta. 4 Left atrial pressure was increased by between 10 and 30 mmHg for periods of 3 to 59 minutes. Gross alveolar oedema eventually developed in all experiments. 5 Neither pulmonary hypertension nor subsequent oedema caused release of prostaglandins into the venous effluent.

Animals↗
PubMed1979

Release of prostaglandin-like substances during elevations of left atrial pressure in the cat.

The purpose of the present work was to measure prostaglandin (PG)-like activity in arterial blood during acute pulmonary hypertension. Anesthetized cats with the chest opened and given positive pressure ventilation were used. A balloon in the left atrium was inflated to elevate hydrostatic vascular pressure in the lungs. Blood was pumped (10 ml/min) from a carotid artery to superfuse 3 smooth muscle tissues: rat stomach strip, rat colon and chick rectum: the blood was then returned to the jugular vein by gravity. The assay tissues were pretreated with antagonists against catecholamines, histamine, serotonin and acetylcholine during the experiments. They were sensitive to calibrating doses of 2 ng/ml of PGF2 alpha and 1 ng/ml of PGE2. 18 periods with elevated left atrial pressure (P LA) (21--49 mmHg), lasting 2--26 min, were applied in 9 cats. This manoevre usually also caused systemic hypotension. 14 of these PLA elevations were accompanied by increased arterial PG-like activity, which rapidly subsided when the pressure was released or when indomethacin (2 mg/kg, n = 4) was given i.v. In 3 additional experiments it was found that pulmonary degradation of PGs was unaffected during P LA elevation. I.v. infusion of angiotensin II contracted the tissues in a pattern different from that caused by pressure elevations and the PG calibrations, and these contractions were not affected by indomethacin. This indicates that the assay tissue contractions cannot be caused by angiotensin II which alone does not increase PG-like activity in arterial blood. Consequently, acute pulmonary vascular hypertension appears to stimulate PG synthesis and release in lungs of intact cats.

Angiotensin II↗
PubMed1979

Endogenous tumor growth factor indicated by increased ornithine decarboxylase activity in malignant cells treated with host serum ascites fluid.

Ornithine decarboxylase (ODC) production was used as an indicator of mitotic activity in neoplastic cells removed from murine hosts at progressive stages of growth. Cells from three ascites cancers and one fibrosarcoma were tested and showed declining ODC production with progressive growth. The cells were incubated with serum or malignant effusion fluid taken from the murine hosts at progressive stages of growth. For 2 to 3 weeks after tumor implantation, sera and, in particular, ascites fluids increasingly stimulated ODC production in cells at all stages of growth. With advancing disease, without the malignant growth having reached a stationary phase, the collected fluids decreasingly stimulated ODC production in the cells. The stimulating factor(s) in host serum and malignant effusion fluid were not tumor specific in the one combination tested.

Animals↗
PubMed1979

Effects of combination drug therapy on the subcutaneous and pulmonary growth of a slow and a fast-growing C3H/He mammary carcinoma.

Changes in susceptibility to treatment with Cytoxan, methotrexate, 5-fluorouracil, and Adriamycin, single or in combination, have been studied during the initial and progressive stages of s.c. and pulmonary (via tail vein injection) growth of two transplanted syngeneic C3H/He mammary carcinomas. One tumor was fast growing, reaching a size of 3 mm from a 1-mm s.c. implant in 7 days; the second tumor would grow to the same size in 30 days. The tumor with the slower growth rate was more susceptible to drug treatment, manifested by delayed growth as well as by prevented growth. The slower-growing tumor also remained susceptible longer, when treatment was delayed, than did the faster-growing tumor. Pulmonary growth was more often prevented by drug treatment than was s.c. growth. Tumor implants s.c. which had reached palpable size could be reduced temporarily to impalpable size by effective drug treatment but were rarely cured. The importance of early treatment relative to the time of tumor implantation was indicated when early treatment with a single drug proved more effective than did delayed treatment with a more potent combination of drugs.

Animals↗
PubMed1978

Prostaglandin content in blood and lung tissue during alveolar hypoxia.

The aim of the present work was to investigate whether prostaglandins (PGs) are synthetized and released from isolated blood-perfused rat and cat lungs secondary to vasoconstriction induced by alveolar hypoxia. The lungs were perfused with autologous blood with constant volume inflow via the pulmonary artery in a recirculating system. They were ventilated with constant volume positive pressure, and acute alveolar hypoxia was induced by ventilation with a gas containing 2% O2. A superfusion bioassay technique was used to measure PG-like activity in the perfusate from the lungs, the blood being re-oxygenated before reaching the assay tissues. The oxygenator prevented the perfusate hypoxia induced by ventilation hypoxia to affect the bioassay tissues. The assay tissues were rat stomach strip, rat colon and chick rectum. They were sensitive to calibrating doses of 0.5--1 ng/ml PGE2 and 1--2 ng/ml PGF2alpha. In another series of experiments PGs of the F-series were measured in lung tissue from normoxic and hypoxic lungs with radioimmunoassay technique. No increase in PG-like activity could be detected in the venous effluent by means of bioassay during hypoxia, nor was the lung tissue content of immunoactive PGF increased by hypoxia. The present findings indicate that alveolar hypoxia does not stimulate PG-synthesis in lungs, refuting that PGs are important mediators of the pulmonary vasoconstrictor response to alveolar hypoxia. It is concluded that PGs play no significant role in producing the pressor response to alveolar hypoxia.

Animals↗
PubMed1978

Release of prostaglandin-like substances and lung reactions to induced intravascular platelet aggregation in cats.

Induced intravascular aggregation of blood platelets gives pulmonary vasoconstrictor and bronchoconstrictor responses, which might be mediated by bioactive substances from the platelets. The aim of the present work was to see if these lung reactions could be related to the release of prostaglandin-like substances (PGLS). Repeated episodes of platelet aggregation were induced by i.v. infusions of collagen in anaesthetized cats ventilated at a constant tidal volume. Arterial blood was pumped from a carotid artery (10 ml/min) to superfuse a series of smooth muscle organs sensitive to prostaglandins (PGs): rabbit aorta, rat stomach strip, rat colon and chick rectum. In two experiments cat jejunum replaced the rabbit aorta in order to detect kinins. All tissues were pretreated with antagonists against catecholamines, histamine, serotonin and acetylcholine. The bioassay tissues were calibrated with standard doses of PGE2 and PGF2alpha. Collagen infusions caused lung responses (as judged from the rise in peak tracheal pressure) and in most cases also a transient systemic hypotension. Simultaneously, contractions of the bioassay tissues occurred, indicating release of PGLS. Such release was only detected as long as lung responses could be elicited by i.v. collagen infusions. These findings imply that PGs and/or the various intermediates in PG synthesis might mediate the pulmonary smooth muscle constriction occurring after intravascular platelet aggregation.

Angiotensin II↗
PubMed1978

Mammary tumor virus oncogenesis and tumor immunogenicity in three sublines of the C3H mouse.

Mammary tumorigenesis and mammary tumor transplantation immunogenicity have been studied and compared in three sublines of the C3H strain: in standard mammary tumor virus (MTV-S)-infected C3H/He mice; in MTV-S-infected C3H/Ki mice; and in MTV-S-free C3Hf/He mice. The age at the appearance of the first tumor, the growth rate of the tumors in their first transplant generation, and the immunogenicity of each tumor in syngeneic female recipients have been determined for the first tumor to appear in each of 25 breeding females from each of the three sublines. Two statistically significant trends were evident among the tumor characteristics compared in the three sublines: (a) an early appearance of tumors was related to the presence of the MTV-S. The genetically dissimilar sublines, C3H/He and C3H/Ki, both infected with the MTV-S, developed mammary tumors at an average age of about 10 months, 11 months before MTV-S-free C3Hf/He mice; (b) the tumor characteristics of immunogenicity and growth stimulation were related to host genetic factors. The genetically similar sublines, C3H/He and C3Hf/He, developed similar proportions of immunogenic and growth-stimulating mammary tumors; the genetically divergent C3H/Ki subline developed tumors that were not immunogenic and tended to be strongly growth stimulating.

Age Factors↗
PubMed1978

Effect of progressive neoplastic growth on the decarboxylation of DL-[1-14C]ornithine by lymphocytes from C3H/He tumor hosts.

The reactivity of normal and tumor host lymphocytes incubated with normal serum or with serum or malignant ascites fluid from tumor hosts was measured by the ability of the lymphocytes to synthesize ornithine decarboxylase after phytohemagglutinin stimulation. Each of three tumors tested (a solid fibrosarcoma, an ascites mammary carcinoma, and an ascites ovarian carcinoma) caused increasing unresponsiveness in the lymphocytes of mice with progressing syngeneic neoplastic growth. The sera and particularly the malignant ascites fluids from mice given implants of the ascites cancers became progressively inhibitory to the activation of lymphocytes from tumor hosts as well as from normal mice. The serum from mice carrying s.c. implants of the fibrosarcoma enhanced the activation of lymphocytes from tumor hosts and from normal mice during early tumor growth before it also became inhibitory.

Animals↗
PubMed1978

Changing transplantation characteristics with serial in vivo passage of C3H/He mammary carcinomas.

The transplantation immunogenicity of spontaneous C3H/He mammary carcinomas was studied by means of the surgery-challenge procedure during serial in vivo passages in syngeneic mice. Reciprocal cross-sensitization and challenge tests between late transplant generations and early transplant generations (from liquid N2 storage) of the same tumors showed that factors responsible for transplantation resistance and factors causing stimulated tumor growth were present in the tumors at the same time as independent variables. The immunogenicity and the immunosensitivity of tumors were seen as dependent variables. The relative prominence of the characteristics of immunogenicity and growth stimulation changed with continuous in vivo passages. Transplantation immunogenicity was tumor specific in four of five tumors tested. Growth stimulation was, in each of four combinations tested, not tumor specific.

Animals↗
PubMed1977

Small airway constriction and closure after induced intravascular platelet aggregation.

The aim of this study was to investigate the function of the peripheral airways after intravascular platelet aggregation induced by i.v. infusions of collagen in open chest anesthetized cats, ventilated with constant tidal volume. Lung compliance was examined under static conditions (stat CL) and under dynamic conditions (dyn CL) at ventilation frequencies of 5, 24 and 50/min. In the control situation dyn CL 24 was approximately 90% of stat CL. Collagen infusions resulted in a pronounced frequency-dependence of lung compliance. When dyn CL 24 had decreased by approximately 40% a reduction in stat CL could also be detected. When dyn CL 24 decreased even more a concurrent reduction in stat CL was evident. These findings indicate that the initial event after induced intravascular platelet aggregation is small airway constriction. With more pronounced changes airway closure and reduction in lung volume occurs. We suggest that these functional changes in peripheral airways result in the impaired gas exchange known to occur after intra-vascular platelet aggregation.

Animals↗
PubMed1977

A time factor in the success or failure of immune rejection of transplanted tumors.

Changes in susceptibility to immune rejection have been studied and compared during the initial stages of s.c. and pulmonary establishment of a transplanted syngeneic C3H mouse mammary carcinoma. The time of immunological attack on the implanted tumor cells was varied by two experimental procedures: In one experiment, the test mice that were immunologically suppressed by the presence of a large s.c. tumor implant were surgically cured before s.c. challenge. However, the immune recovery, which normally follows directly after tumor removal, was delayed for increasing lengths of time after challenge by injections of irradiated cells of the same tumor. In another experiment, the test mice were immunologically impaired by sublethal whole-body irradiation before s.c. and i.v. challenge. Immune rejection reactivity was then introduced, by passive transfers of lymph node cells from immunized mice, at increasing delays after the challenge implantations of tumor cells. In both of the two experiments, an increase in the number of tumor "takes" was observed if tumor immunity was reduced or absent for at least 3 days after challenge. If tumor immunity was restored or provided by the third day after challenge, there was an abrupt decrease in the number of observed tumors. The reduction in the effectiveness of immunosupportive treatments about the third day after tumor implantation may indicate a reduction in the vulnerability to immune rejection that coincides with vascularization of the implants.

Animals↗