Interstitial pneumonia in guinea pigs

Interstitial pneumonia was observed in 12 male guinea pigs. Grossly, the lung showed clear white areas in the parenchyma. Histological changes in the lung consisted of interstitial pneumonia and formation of granulomas accompanied by bacterial clumps. It was thought that this disorder might have occurred as a bacterial infection.     

Experimental cryptococcosis in guinea pigs

A guinea pig model was used to evaluate immune response to Cryptococcus neoformans. This model shared characteristics with cryptococcosis in humans. Twenty five guinea pigs injected intraperitoneally with 10(7) viable C. neoformans cells developed disseminated disease. Forty days after infection all guinea pigs were killed and autopsy performed. C. neoformans growth in the lungs, brains, livers and spleen of the infected animals were determined. Furthermore, the immune response was characterized by moderate degree of delayed-type hypersensitivity and humoral response. In some organs was observed neutrophil and lymphocyte infiltration with presence of cryptococci cells. The infiltration observed in the organs was probably a consequence of an immune reaction.     

Macrophage migration-inhibition in desensitized guinea pigs

The migration of peritoneal exudate cells obtained from guinea pigs with delayed skin reactivity to egg albumin (EA) and diphtheria toxoid (DT) was inhibited in the presence of antigen. A dose of 2 mg of EA given intravenously 8 days after sensitization specifically abolished the migration inhibition tested 5 weeks later. When the challenge was given into a foot pad 6 weeks after sensitization the migration inhibition was partially suppressed 3 to 28 days later.Repeated skin testing did not affect the migration results of the challenged or unchallenged guinea pigs.The demonstration in vitro of desensitization argues that the mechanism is either a reduced number or a reduced responsiveness of the specific effector cells of delayed hypersensitivity, or an inhibitory effect of cells stimulated by the specific antigen. If a humoral inhibitory factor is involved, it is either tightly bound by the cells or produced during the migration assay.     

Visual evoked potential in guinea pigs

The present study was designed to establish visual evoked potential (VEP) as one of clinical tests for veterinary medicine. Experiments were carried out on eight adult male guinea pigs weighed 350 to 750 g. We investigated influences of click sound, luminous intensity and habituation on VEP patterns. The VEP of the guinea pig was composed of primary (P 10, N 20, P 30, N 40) and secondary (P 55, N 75, P 100, N 140) components, followed by a rhythmic after-discharge. Click sound with flash produced some unclear peaks in VEP, while click sound without flash elicited clear six peaks. These different components of the response to stimulation suggested that the acoustically evoked potential induced some peaks in VEP. With the intensity used in the present study, changes in luminous intensity resulted in unrecognizable difference among the VEPs. Early components of VEP were not clearly influenced by the habituation to stimulation. As the stimulation was repeated, rhythmic after-discharge seemed to be suppressed in the half of experiments.     

Diethylaminoethoxyhexestrol causes hypertriglyceridemia in guinea pigs

Treatment of rats, monkeys and man with diethylaminoethoxyhexestrol causes phospholipid storage in liver and other tissues. However, this drug has not been reported to alter plasma lipoprotein levels. When guinea pigs were treated with diethylaminoethoxyhexestrol, the fasting plasma triacylglycerol levels increased dramatically, from 43 to 1281 mg/dl, after only five doses of 12.5 mg/kg. Diethylaminoethoxyhexestrol-treated guinea pigs had reduced postheparin lipase activity. In addition, in vitro assays showed that this agent inhibited guinea pig postheparin lipoprotein lipase. It is hypothesized that diethylaminoethoxyhexestrol causes hypertriglyceridemia in guinea pigs because these animals are known to have low levels of serum activator for lipoprotein lipase and may be unusually susceptible to agents that inhibit lipoprotein lipase activity. The ability to produce hypertriglyceridemia in guinea pigs provides an animal model in which the metabolic consequences of hypertriglyceridemia can be studied.     

Melanocytic carcinogenesis in albino guinea pigs

We describe an experimental model for the induction of cutaneous melanomas in albino guinea pigs by means of repeated topical application of 7,12-dimethyl-benzanthracene over 13 consecutive months. At the end of the experiment 87.5% of the animals presented multiple lesions of a melanocytic nature. The most frequent and the earliest detected was melanocytic hyperplasia, followed by dysplasia. These lesions occurred in 75% of animals and were observed from the 4th month onward. Nevus-type lesions appeared from the 12th month and affected 70% of animals, whilst melanomas occurred in 65%. Metastases were observed in 45% of animals, in lungs, lymph nodes, kidney, and adrenal gland.     

Histamine dose-response curves in guinea pigs

Histamine dose-response curves were performed on anesthetized tracheostomized guinea pigs that were paralyzed and mechanically ventilated at a constant tidal volume and breathing frequency. The dose was calculated by generating an aerosol of known concentration and measuring the volume delivered to the lung. Increasing the dose was accomplished by increasing the number of breaths of aerosol delivered. The response to each dose was determined by measuring the change in airway resistance (RL) and dynamic compliance (Cdyn) using the method of Von Neergaard and Wirz (Z. Klin. Med. 105: 51-82, 1927). With increasing doses of histamine, RL increased and reached a plateau at approximately five times the base-line value and Cdyn fell to approximately 20% of its initial value. The variability in the base-line and maximum response as well as the calculated sensitivity and reactivity was less than that previously reported. Propranolol pretreatment increased resting RL and shifted the dose-response curve for RL to the left of the controls, increasing reactivity but not sensitivity. Atropine shifted the dose-response curve to the right of the control, decreasing sensitivity but without changing reactivity. The data for Cdyn showed that atropine pretreatment caused a higher resting value and propranolol pretreatment a lower value at the highest histamine dose but no differences in either sensitivity or reactivity.