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At least 37 records · Page 2Linked to original sources
PubMed1988

Viral strain dependent differences in experimental Argentine hemorrhagic fever (Junin virus) infection of guinea pigs.

Guinea pigs infected with low-passage Junin virus of human origin showed viral strain dependent differences in mortality, LD50, time to death, and in viral spread and distribution. Different Junin strains appeared to cause at least two broad patterns of Argentine hemorrhagic fever in guinea pigs. A number of strains of Junin virus caused a viscerotropic type of illness in which virus replicated predominantly in lymph nodes, spleen, and bone marrow. With the most severe visceral forms of Argentine hemorrhagic fever, the guinea pigs became viremic, developed necrosis of spleen, lymph nodes, and bone marrow, showed gastric hemorrhages, and all animals died within 13-15 days. Other Junin strains induced a neurological type of illness with transient viral replication in and lymphocyte depletion of spleen and lymph nodes, with no detectable viremia or viral replication in bone marrow. Subsequently, virus was found in the brain with varying severities of polioencephalitis, and the guinea pigs frequently showed rear leg paralysis before death occurred 28-34 days after inoculation. Not all animals infected with a neurotropic strain developed all these signs. One viral strain induced some signs characteristic of both patterns of illness. Although the disease forms in the guinea pig model did not strictly correlate with those observed in the humans from which these strains were obtained, the different strains of Junin virus consistently caused very different patterns of illness in infected guinea pigs.

Animals↗
PubMed1998

Sex differences in immune responses to cephalothin in guinea pigs.

Guinea pigs of two strains, outbred Hartley and inbred Strain 2, were immunized subcutaneously with cephalothin (CET, 20 mg/body) alone, without adjuvant. Immune responses to the antibiotic were assessed by guinea-pig passive cutaneous anaphylaxis (GP-PCA) and active systemic anaphylaxis (GP-ASA) reactions. The immune response to CET in the female Hartley guinea pigs was higher than that in the males. In contrast, no difference in response to CET in Strain 2 guinea pigs was observed between males and females. These results suggested that female Hartley guinea pigs possessing a higher response should be employed in antigenicity studies involving the beta-lactam antibiotics.

Animals↗
PubMed1990

Ursodeoxycholic acid, chenodeoxycholic acid, and 7-ketolithocholic acid are primary bile acids of the guinea pig.

Guinea pig gallbladder bile contains chenodeoxycholic acid (62 +/- 5%), ursodeoxycholic acid (8 +/- 5%), and 7-ketolithocholic acid (30 +/- 5%). All three bile acids became labeled to the same specific activity within 30 min after [3H]cholesterol was injected into bile fistula guinea pigs. When a mixture of [3H]ursodeoxycholic acid and [14C]chenodeoxycholic acid was infused into another bile fistula guinea pig, little 3H could be detected in either chenodeoxycholic acid or 7-ketolithocholic acid. But, 14C was efficiently incorporated into ursodeoxycholic and 7-ketolithocholic acids. Monohydroxylated bile acids make up 51% and ursodeoxycholic acid 38% of fecal bile acids. After 3 weeks of antibiotic therapy, lithocholic acid was reduced to 6% of the total, but ursodeoxycholic acid (5-11%) and 7-ketolithocholic (15-21%) acid persisted in bile. Lathosterol constituted 19% of skin sterols and was detected in the feces of an antibiotic-fed animal. After one bile fistula guinea pig suffered a partial biliary obstruction, ursodeoxycholic and 7-ketolithocholic acids increased to 46% and 22% of total bile acids, respectively. These results demonstrate that chenodeoxycholic acid, ursodeoxycholic acid, and 7-ketolithocholic acid can all be made in the liver of the guinea pig.

Animals↗
PubMed1977

The effects of cholesterol/fat feeding on lipid levels and morphological structures in liver, kidney and spleen in guinea pigs.

Guinea pigs were fed a semisynthetic diet containing 10 per cent (by weight) cottonseed oil with or without 1 per cent cholesterol. In the animals fed fat, the lipid levels and the morphology remained normal in all tissues studied. Concomitantly with a marked accumulation of cholesteryl ester (CE) in the liver, however, many microscopical changes occurred in guinea pigs fed cholesterol/fat. A prominent deposition of lipids in vacuoles, mostly without delimitating membranes, where observed at centrilobular sites. Multivacuolated, secondary lysosomes, membrane bound lipid vacuoles (lipolysosomes) and myelin figures were found both in hepatocytes and Kupffer cells. Myelin figures and crystalline clefts were observed more often in Kupffer cells than in hepatocytes. The granular endoplasmic reticulum in the Kupffer cells was grossly dilated and filled with an amorphous material. Both the biochemical and the morphological findings in hepatocytes and Kupffer cells are very similar to those observed in cholesteryl ester storage disease and in Wolman's disease. These two lipid storage diseases are both related to deficiency of an acid lipase in the liver. Measurement of the acid liver CE hydrolase in guinea pigs fed fat and in those fed cholesterol/fat showed similar activity. A relative deficiency of this enzyme activity could be the reason for the development of the enormous CE storage in guinea pig livers. These findings suggest that guinea pigs fed cholesterol/fat, in some respects, can be used as a model for Wolman's disease and cholesteryl ester storage disease. We did not find any microscopical changes in the kidneys from animals fed cholesterol/fat, thus indicating that the experimental condition it not useful as a model for studies of the kidney changes in lecithin:cholesterol acyltransferase (LCAT) deficiency.

Animals↗
PubMed1975

Vaccination against bovine brucellosis with a low dose of strain 19 administered by the conjunctival route. I.--Protection demonstrated in guinea pigs.

Guinea pigs were vaccinated with different doses of strain Brucella abortus B 19, subcutaneously (SC) or by the conjunctival route (C), once or a second time three months later. Agglutination and complement fixation titers were determined on sera of guinea pigs taken at random at intervals from each vaccine group. Protection afforded by the vaccination was determined by intramuscular injection of the challenge strain, B. abortus 544 (5 X 10(3) bacteria) three months after the last vaccination. Forty days later the guinea pigs were killed and Brucella looked for and counted in the spleen and lymph nodes. After conjunctival vaccination with 10(6) or 10(7) bacteria, seriological responses were weak and transient even after the re-vaccination, and were lower than after subcutaneous vaccination with the 10(6) dose, and much lower than after the standard vaccination dose of 7 X 10(9) given subcutaneously. Protection, expressed as percentage of guinea pigs free of infection at autopsy (table 4) was 40 p. 100 in the standard vaccination group (SC, 7 X 10(9)) and 57 p. 100 in groups receiving successively 7 X 10(9) (SC) and 10(6) or 10(7) (C). Two successive conjunctival vaccinations with the 10(6) to 10(9) doses gave 47 to 60 p. 100 protection; two SC vaccinations with the 10(6) dose gave 75 p. 100 protection. All the control guinea pigs were heavily infected. The differences in protection rate among the groups vaccinated twice were not significant. Since vaccination through the conjunctiva with two successive instillations of 10(7) bacteria induced only a weak antibody response and protection equivalent to that of standard subcutaneous vaccination, the method appears worthy of application in cattle.

Animals↗
PubMed1985

Xenopsylla cheopis: cellular expression of hypersensitivity in guinea pigs.

Guinea pigs multiply exposed to Xenopsylla cheopis adult fleas exhibited marked blood basophil responses to challenge infestation with only minor changes in blood eosinophil levels. Dermal responses to flea feeding were marked by dominant neutrophil (52% of the infiltrate) and eosinophil (32%) accumulations 24 hr after primary feeding, with a weak basophil response (11%). However, after challenge feeding 14 days later, eosinophils dominated, representing 59% of the infiltrate with basophils comprising 30% of the cellular response; neutrophils were rare (7%). Mast cells did not exhibit any increases in density during either the primary or secondary infestation, representing 4-7% of the infiltrate. These results demonstrate that flea feeding induces systemic and local basophil responses as demonstrated for all hematophagous arthropods examined so far. Flea feeding success was not adversely affected by feeding on homologously hypersensitized guinea pigs or guinea pigs sensitized by Ornithodoros parkeri feeding. However, basophil responses at flea feeding sites in heterologous (tick) sensitized animals were more basophilic (26 +/- 4 cells/0.03-mm2 area) than feeding sites in homologous (flea) sensitized hosts (9 +/- 6 cells). Furthermore, primary tick feeding sites become erythematous and indurated after flea feeding on the opposite flank, and were marked histologically by strong basophil abscess (276 +/- 56 cells/0.03-mm2 area); primary flea feeding sites were not activated by tick challenge feeding. These cross-generic challenge feeding experiments suggest antigen cross-reactivity, resulting in activation of feeding sites of a heterologous arthropod.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Activity of alkaline phosphatase in the serum of normal and ascorbic-acid-deficient guinea pigs.

Guinea pigs well supplied with vitamin C show a linear relation between serum alkaline phosphatase activity and body weight. Investigations in guinea pigs induced to low ascorbic-acid levels by two different procedures (complete and partial deprivation of vitamin C) demonstrated that the activity of the alkaline phosphatase is not generally decreased in the serum of ascorbic-acid-deficient guinea pigs. Decreases of the serum enzyme levels reported in guinea pigs completely deprived of vitamin C, i.e. in acute deficiency, may be due to stress factors.

Aging↗
PubMed1991

[Bronchial hyperresponsiveness to histamine following antigen challenges in actively sensitized guinea pigs].

Guinea pigs were actively sensitized by intraperitoneally administered ovalbumin and challenged by intravenous injections of ovalbumin. Respiratory resistance and dynamic compliance were measured by pulmonary mechanics analyzer Buxco Model 6. Changes in resistance (delta R) and compliance (delta C) induced by intravenously administered histamine were investigated before and after the challenge. Responses to the histamine in sensitized guinea pigs were also compared with those in naive guinea pigs. The following results were obtained. 1) A significant increase in delta R by histamine administration was observed following the antigen challenge. delta C by histamine administration showed a tendency to increase after the challenge. 2) A significant increase of delta R by 7.2 micrograms/kg histamine administration was observed in actively sensitized guinea pigs. However, delta C by the histamine administration did not change in the sensitized animals.

Airway Resistance↗
PubMed1979

Cell-mediated cytotoxicity and humoral immune response in ascorbic acid-deficient guinea pigs.

Guinea pigs were divided into three dietary groups: ascorbic-acid deficient, pair-fed, and ad libitum control. Two weeks later guinea pigs were immunized intradermally with 5 x 10(8) chicken erythrocytes in Freund's complete adjuvant. Hemagglutinating antibody titers to chicken erythrocytes 2 weeks after immunization were comparable in all three dietary groups. In vitro 51Cr release from labeled chicken erythrocyte target cells incubated with lymphoid cells from spleens of ascorbic acid-deficient guinea pigs was significantly less than with spleen cells from pair-fed and ad libitum control guinea pigs. The percentage of splenic lymphoid cells that formed rosettes with rabbit erythrocytes, a T cell marker, was the same in all three dietary groups. The defect of ascorbic acid deficiency may reflect an impairment of T lymphocytes function in cell-mediated cytotoxicity or a change in number or function of another cell type.

Animals↗
PubMed1990

[Changes in contraction-relaxation coupling in experimental cardiac hypertrophy in the guinea pig].

Guinea pig myocardium resembles human myocardium with respect to the mechanisms which regulate contractility (enzymatic activity of myosine, functional activity of the sarcoplasmic reticulum). Guinea pig left ventricular hypertrophy (LVH) is therefore a good experimental model for the study of human LVH. The mechanical properties of 5 months old female guinea pigs' left ventricular papillary muscle, 3 weeks after constriction of the abdominal aorta (N = 10), were investigated. Ten papillary muscles of operated control animals and eight of normal guinea pigs submitted to 20 minutes hypoxia were also studied. The animals had no signs of cardiac failure after constriction of the abdominal aorta but the increase in the ratio of heart to body weight (p less than 0.001) confirmed the LVH. When compared with the operated controls, there was a decrease of the maximum velocity of contraction at zero load, of the velocity of contraction with preload alone (Vc), of the total isometric force normalized for the section of the muscle(s) and of the positive peak of the derivative of the isometric force normalized for section (+ dF/s) (p less than 0.001 for each parameter). The parameters of relaxation were also abnormal: decreased velocity of isotonic relaxation with preload only (Vr) and of the negative peak of the derivative of the isometric force normalized for section (- dF/s) (p less than 0.001 for each parameter), and an increase in the half relaxation time (t1/2) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Pathophysiologic features of Q fever-infected guinea pigs.

Guinea pigs infected with 9-mile phase I strain of Coxiella burnetii had increased blood glucose concentrations; alkaline phosphatase (ALP), glutamic-oxalacetic transaminase (GOT), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), and creatine phosphokinase (CPK) activities; and bilirubin value. Hypocalcemia and hypophosphatemia were evident in the latter days of infection. At necropsy of the guinea pigs, necrotic foci were in liver, spleen, and heart. Seemingly, the major pathophysiologic changes in infected guinea pigs were the direct result of lesions in liver, spleen, and heart in which rickettsial bodies were readily observable with histologic staining procedures. The guinea pig may serve as an animal disease model for Q fever.

Alkaline Phosphatase↗