Resistance Of Guinea Pigs Research Articles

Role of nitrous acid in the association between nitrogen dioxide and asthma symptoms: effect of nitrous acid exposure on specific airway resistance in guinea pigs

Epidemiological evidence regarding the effects of nitrogen dioxide (NO2) on asthma and chronic obstructive pulmonary disease (COPD) is inconclusive because NO2 assays measure nitrous acid (HONO) as NO2. Epidemiological study using separate measurements of indoor HONO and NO2 suggests that indoor HONO levels are associated with decrease in lung function, and HONO exposure experiment in rats suggests that HONO adversely affects respiratory function more than NO2. Effects of NO2 on respiratory tract resistance have not been observed in rats but have been observed in guinea pigs, including baseline specific airway resistance (sRaw). The present study aimed to investigate the effects of HONO exposure on baseline sRaw in guinea pigs. Eighteen male Hartley guinea pigs were divided into Groups C, M, and H (n = 6 per group) and exposed to HONO at three concentrations, respectively, 24 h/d for 7 weeks. Double-flow plethysmography was used to measure the sRaw once a week and grade respiratory waveforms, indicating increased airway resistance. The experiment was performed twice. Mean HONO concentrations of two experiments in Groups C, M, and H were 0.02, 0.66, and 3.43 parts per million (ppm). The sRaw increased significantly in Groups H and M compared with sRaw in Group C, and in a concentration-dependent manner after the 4th week of HONO exposure. Increased airway resistance was observed in 50% of animals in Group M and 100% of animals in Group H in some weeks. However, in some animals from Group M, increased airway resistance was observed earlier than the airway resistance increases observed in all animals in Group H. These sRaw results suggest that HONO affects asthma symptoms or COPD, at a lowest observed adverse effect level (LOAEL) of < 0.66 ppm. HONO may affect baseline sRaw after shorter exposure periods and at lower concentrations compared with the reported effects of NO2. The present results suggest that HONO is the most important nitrogen oxide affecting asthma and COPD indoors, and that HONO may be the causative agent in the association between NO2 and asthma symptoms in epidemiological studies.

Sex-specific programming of adult insulin resistance in guinea pigs by variable perinatal growth induced by spontaneous variation in litter size.

Intrauterine growth restriction (IUGR) and subsequent neonatal catch-up growth are implicated in programming of insulin resistance later in life. Spontaneous IUGR in the guinea pig, due to natural variation in litter size, produces offspring with asymmetric IUGR and neonatal catch-up growth. We hypothesized that spontaneous IUGR and/or accelerated neonatal growth would impair insulin sensitivity in adult guinea pigs. Insulin sensitivity of glucose metabolism was determined by hyperinsulinemic-euglycemic clamp (HEC) in 38 (21 male, 17 female) young adult guinea pigs from litters of two-to-four pups. A subset (10 male, 8 female) were infused with d-[3-3H]glucose before and during the HEC to determine rates of basal and insulin-stimulated glucose utilization, storage, glycolysis, and endogenous glucose production. n males, the insulin sensitivity of whole body glucose uptake ( r = 0.657, P = 0.002) and glucose utilization ( r = 0.884, P = 0.004) correlated positively and independently with birth weight, but not with neonatal fractional growth rate (FGR10-28). In females, the insulin sensitivity of whole body and partitioned glucose metabolism was not related to birth weight, but that of endogenous glucose production correlated negatively and independently with FGR10-28 ( r = -0.815, P = 0.025). Thus, perinatal growth programs insulin sensitivity of glucose metabolism in the young adult guinea pig and in a sex-specific manner; impaired insulin sensitivity, including glucose utilization, occurs after IUGR in males and impaired hepatic insulin sensitivity after rapid neonatal growth in females.

The resistance of guinea-pigs to cortisone ulcerogenesis.

The resistance of guinea-pigs to cortisone ulcerogenesis.

Effects of Yanggan Lidan Granule on insulin resistance in guinea pigs with induced cholesterol gallstones

To observe the effects of Yanggan Lidan Granule (YGLDG), a compound traditional Chinese herbal medicine, on insulin resistance in guinea pigs with induced cholesterol gallstones. Eighty guinea pigs were randomly divided into normal control group, untreated group, YGLDG group and ursodeoxycholic acid (UDCA) group, with 20 guinea pigs in each group. Except the normal control group, gallstones were induced by high-cholesterol diet in the guinea pigs. The guinea pigs in the normal control group and the untreated group were administered with normal saline. UDCA and YGLDG were given to the guinea pigs in the corresponding groups for seven weeks. Eight guinea pigs of each group were used to measure the glucose infusion rate (GIR) by using hyperinsulinemic-euglycemic clamp technique. At the end the guinea pigs were killed and their gallstone formation was observed. The gallstones in guinea pigs were identified as cholesterol stones by qualitative analysis through infrared spectrum. The incidence rate of cholelithiasis of the untreated group was 82.35% . The GIR of guinea pigs in the untreated group was obviously lowered down as compared with the normal control group. Compared with the untreated group, the GIRs of the YGLDG group and the UDCA group were obviously increased, especially in the YGLDG group. YGLDG may improve insulin resistance in guinea pigs with cholesterol gallstones by elevating GIR obviously.

Guinea Pigs Develop Cutaneous Basophilia after Repeated Infestations by Nymphs of the Tick Amblyomma triste

This study investigated the development of resistance in guinea pigs to nymphs of Amblyomma triste ticks after repeated infestations. Guinea pigs were infested thrice, at 30-day intervals, with 30 nymphs of A. triste per animal per infestation. Acquisition of resistance was evaluated by determining: nymph yielding rate, engorgement period, and weight. Skin biopsies of tick bite sites were collected at 24, 48, and 96 h after tick attachment for inflammatory cell counts. Engorged nymphs weighed 5.53 mg +/- 1.9 in re-infested hosts (56.6% less than in primary infestation) and took 6.9 days +/- 2.16 to feed in the third infestation (14.5% more than in the first infestation). Guinea pigs yielded 78%+/- 7.2 of nymphs in the re-infestation (11.6% less than in the primary infestation). In addition, a marked increase in basophil influx was observed from the first infestation onward; 69% of infiltrated cells were basophils in re-infested hosts 24 h after tick attachment. No basophils were seen at this time in primary infested animals. That number increased to 84.7% 48 h post attachment in re-infested hosts (73.2% more than in the primary infested ones) and decreased markedly 96 h post attachment in both groups (2.6% and 1% of basophils in the third and first infestation, respectively). We conclude that guinea pigs acquire resistance against nymphs of A. triste ticks after repeated infestations and that a cutaneous basophilia must play a crucial role in such a mechanism.

Neurogenic insulin resistance in guinea-pigs with cisplatin-induced neuropathy

The aim of the present work was to study whether neurotoxicity produced by cisplatin modified tissue insulin sensitivity in guinea-pigs. One week after selective sensory denervation of the anterior hepatic plexus by means of perineurial 2% capsaicin treatment, hyperinsulinaemic euglycaemic glucose clamp were performed to estimate insulin sensitivity in male guinea-pigs. The guinea-pigs underwent regional sensory denervation of the anterior hepatic plexus exhibited insulin resistance, whereas systemic capsaicin desensitization increased insulin sensitivity. Intraportal administration of l-nitro-arginine methyl esther (L-NAME decreased, whereas capsaicin increased insulin sensitivity. Neither atropine nor acetylcholine produced any significant effect. In animals with preceding regional capsaicin desensitization, none of the pharmacological maneuvers modified the resulting insulin resistant state. Cisplatin pretreatment induced sensory neuropathy and decreased insulin sensitivity. Insulin sensitivity did not change after either regional or systemic capsaicin desensitization in the cisplatin-treated animals. CGRP 8–37, a nonselective calcitonin gene-related peptide (CGRP) antagonist (50 μg/kg i.v.), significantly increased insulin sensitivity in normal animals but only a tendency to insulin sensitization was seen after cisplatin treatment. Cisplatin treatment, similar to regional capsaicin desensitization of the anterior hepatic plexus, produced a significant decrease in insulin-stimulated uptake of 2-deoxy- d [ l- 14C] glucose in cardiac and gastrocnemius muscle with no effect on percentage suppression of endogenous glucose production by hyperinsulinaemia. We conclude that the majority of cisplatin-induced insulin resistance is related to functional deterioration of the hepatic insulin sensitizing substance (HISS) mechanism.

Effect of in vitro and in vivo aerosolized treatment with geniposide on tracheal permeability in ovalbumin-induced guinea pigs

The primary objective of this study was to investigate the effect of geniposide, a potent anti-inflammatory, on ovalbumin-antigen-induced tracheal permeability and transepithelial electrical resistance in guinea pigs. Two weeks after sensitization with ovalbumin (100 mg/ml), the permeability of guinea-pig tracheas was evaluated by flux measurements using the transcellular tracer, [ 14C]estradiol, and the paracellular tracer, [ 14C]mannitol. The effect of extracellular Ca 2+ with geniposide was also studied, using deletion of Ca 2+ in the donor chamber. The in vivo treatment effect of aerosolized geniposide on tracheal permeability in the ovalbumin-sensitized guinea pigs was also evaluated. The results indicate that tight junction permeability of ovalbumin-sensitized trachea was significantly dose dependent and decreased by geniposide (1–10 mM), as evidenced by substantial recovery of transepithelial electrical resistance and decreased transepithelial permeability of [ 14C]mannitol at (1.32±0.12)×10 −5 cm/s. The effect of combination of the removal of extracellular Ca 2+ with geniposide had no effect on tight junction permeability of ovalbumin-sensitized trachea and revealed that transepithelial electrical resistance and junction permeability did not recover. In addition, the cAMP levels and phosphodiesterase activity were not significantly influenced in ovalbumin-sensitized tracheal tissues after geniposide treatment. Inhaled geniposide (50 mM, 30 min after ovalbumin sensitization) significantly restored junction permeability induced by ovalbumin (100 mg/ml, 2 min). Junction permeability did not recover on pretreatment with geniposide (50 mM for 30 min over 16 days consecutive before ovalbumin sensitization) after exposure of conscious guinea pigs to aerosol ovalbumin. In conclusion, geniposide has inhibitory effects on ovalbumin-induced junction permeability and recovery of transepithelial electrical resistance in guinea pig trachea, showing its potential as anti-asthma therapy.

Effect of combined leukotriene D 4 and thromboxane A 2 receptor antagonist on mediator-controlled resistance in guinea pigs

The effects of YM158 (3-[(4- tert-butylthiazol-2-yl)methoxy]-5′-[3-(4-chlorobenzenesulfonyl)propyl]-2′-(1 H-tetrazol-5-ylmethoxy)benzanilide monosodium salt monohydrate), a new dual antagonist for leukotriene D 4 and thromboxane A 2 receptors, on antigen-induced increases in airway resistance were investigated in mediator-controlled novel asthmatic models using actively sensitized guinea pigs. While the predominant mediator was thromboxane A 2, complete inhibition of cyclooxygenase induced mediation by cysteinyl-leukotrienes. About 1-mg/kg indomethacin induced a state where both mediators participated equally. YM158 inhibited increases in resistance whether only one or both mediators were involved. When leukotriene D 4 and thromboxane A 2 equally participated, ED 50 values for 4-oxo-8-[4-(4-phenylbutoxy)benzoylamino]-2-(tetrazol-5-yl)-4 H-1-benzopyran hemihydrate (pranlukast; 3.9 mg/kg) and 7-(3,5,6-trimethyl-1,4-benzoquinon-2-yl)-7-phenylheptanoic acid (seratrodast; 2.1 mg/kg) were similar to that for YM158 (8.3 mg/kg), although those effects on the corresponding mediator-induced reaction were 10 times stronger than those of YM158. Additionally, the maximum inhibition of YM158 was stronger than those of either single receptor antagonist. In conclusion, YM158 has a potentially greater efficacy in wider types of experimental asthmatic models than single receptor antagonists.

Accuracy of measurement of acoustic rhinometry applied to small experimental animals.

Nasal obstruction is one of the major symptoms of allergic rhinitis. In the study of the mechanism of nasal obstruction, experiments on animal are useful. In adult humans, acoustic rhinometry has been used to evaluate nasal obstruction by determining nasal cavity dimensions in terms of cross-sectional areas as a function of the distance from the nostril. We modified the equipment used on humans to assess dimensions of nasal airway geometry of small experimental animals. The purpose of this study was to investigate the accuracy of measurement of the modified acoustic rhinometry applied to small experimental animals using nasal cavity models and guinea pigs. Measurement of the nasal cavity models (made of cylindrical silicone tubes) showed that the acoustic rhinometry estimated 85.5% of actual area and 79.0% of actual volume. In guinea pigs, nasal cavity volume determined by the acoustic rhinometry was 73.7 +/- 20.0% of actual volume. The actual volume was estimated by impression material instilled into the nasal cavity of the animals (IM volume), and volume determined by acoustic rhinometry significantly correlated with IM volume. Furthermore, there was a significant negative correlation between the volume and nasal airway resistance in guinea pigs. Measurement of the nasal airway resistance is the method frequently used in the evaluation of the nasal obstruction in guinea pigs. These results suggest that acoustic rhinometry is useful in evaluating nasal obstruction in small experimental animals.

Sequential histopathology at the Rhipicephalus sanguineus tick feeding site on dogs and guinea pigs.

The tick Rhipicephalus sanguineus is a very common parasite of dogs worldwide. Dogs seem unable to acquire resistance against this tick species, whereas guinea pigs demonstrate a very strong resistance following primary infestation. We studied the inflammatory reaction at the R. sanguineus tick feeding site on dogs and guinea pigs during primary and tertiary infestations at different time intervals after attachment. Biopsies were collected after 4, 24, 48 and 96 hours. Changes that were found in all experimental groups included a cone of cement around the mouthparts of the tick, epidermal hyperplasia, edema and inflammatory cell infiltration in the dermis directly underneath the tick attachment site. Dogs reacted to ticks mainly with neutrophils, particularly after repeated exposure. Mast cells and mononuclear leukocytes were also present. Guinea pigs reacted to R. sanguineus mainly with mononuclear cells, eosinophils and basophils. These cells were particularly numerous after repeated exposure to R. sanguineus. Our results suggest that basophils and eosinophils are involved in resistance of guinea pigs to R. sanguineus and that neutrophils in dogs have little effect against this tick species.

Immunisation of dogs and guinea pigs against Rhipicephalus sanguineus ticks using gut extract

Tick-bite naive guinea pigs were inoculated three times with Rhipicephalus sanguineus gut or salivary gland extracts and saponin as adjuvant. Dogs were inoculated three times with gut extract only as this fraction induced a more efficient resistance in guinea pigs (lower tick recovery and lower engorged female weights). Freund's adjuvant and saponin were used as adjuvants for the immunisation of dogs. Freund's adjuvant was used to enhance cellular immunity. The highest level of resistance in dogs was induced by the immunisation with gut extract and Freund's adjuvant. Many female ticks from dogs immunised this way engorged fully but died prior to oviposition. Resistant guinea pigs and dogs seemed to trigger different immune mechanisms against R. sanguineus ticks as damage to parasites also differed. A major role for cellular immunity in the resistance of dogs against R. sanguineus ticks in suggested. Resistance mechanisms against R. sanguineus ticks is discussed.

Effects of lisinopril on intercellular resistance of guinea pig ventricular myocytes

Effects of lisinopril on intercellular resistance of guinea pig ventricular myocytes

Increase of a guinea pig natural killer cell (Kurloff cell) during leukemogenesis

The guinea pig Kurloff cell (KC) is an estradiol-dependent circulating mononuclear cell that has natural killer cytotoxic activity in vitro. We studied the variation of KC number during the development of transplanted leukemia in inbred strain 2 (S2) leukemia-sensitive guinea pigs. Grafts of leukemic cells (L2C) produced a significant increase in the number of KC. Leukemia occurred in 35.5% of non-estrogenized animals and in 18.3% of estrogenized guinea pigs. The increased number of KC seems to have antileukemia activity in vivo. This could be part of the general phenomenon of cancer resistance in guinea pigs.

The effect of a thromboxane A 2 receptor antagonist BAY-u-3405 on experimental allergic reactions

The effect of a novel thromboxane A2 receptor antagonist, BAY-u-3405, on experimental allergic airway and skin reactions was studied in vivo. At doses of 3–30 mg/kg BAY-u-3405 clearly inhibited the U-46619-induced increase in respiratory resistance (Rrs) in guinea pigs. BAY-u-3405 at doses of 3 and 30 mg/kg inhibited the aerosolized antigen-induced biphasic increase in respiratory resistance in guinea pigs. Moreover, BAY-u-3405 inhibited repeated aeroantigen-induced airway hyperreactivity and airway inflammation in mice. In IgE antibody-mediated biphasic skin reactions in mice, both immediate and late-phase reactions were inhibited by 10 mg/kg of BAY-u-3405. These results demonstrate the efficacy of BAY-u-3405 on the antigen-induced late-phase reactions in the airway and skin in guinea pigs and mice, and antigen-induced airway hyperreactivity in mice.

The effect of host resistance on the metabolic rate of engorged females of Rhipicephalus evertsi evertsi

This study investigated the effect of acquired resistance in guinea-pigs on the metabolic rate of adult females of the tick Rhipicephalus evertsi evertsi. Guinea-pigs were subjected to three successive infestations of ticks and the rate of CO2 production (VCO2) measured in first and third infestation engorged females. Ticks which fed on resistant hosts showed a 52% decrease in mass compared to ticks that fed on naive animals. Reduction in mass was accompanied by a decrease in VCO2 (mlh-1) per tick but an increase in mass specific VCO2 (mlg-1h-1). However, both groups shared a single allometric relationship between body mass and metabolic rate (VCO2). We suggest that the differences in size rather than any factor directly relating to the mechanism of acquired resistance account for the differences in metabolic rate between ticks fed on naive and resistant guinea-pigs.

Studies on anti-allergic action of AH 21-132, a novel isozyme-selective phosphodiesterase inhibitor in airways.

The effects of AH 21-132, a type III and IV phosphodiesterase (PDE) inhibitor, on allergic reactions in the airway were studied by comparing them with the effects of rolipram, a type IV PDE inhibitor, and aminophylline, a non-selective PDE inhibitor. The following results were obtained: 1) AH 21-132, rolipram and aminophylline inhibited the antigen-induced contraction of isolated guinea pig tracheal muscle in vitro. 2) AH 21-132 and aminophylline inhibited antigen-induced histamine release from human lung tissue fragments. 3) Antigen-induced accumulation of inflammatory cells including eosinophils and macrophages in mice bronchoalveolar lavage fluid was clearly inhibited by AH 21-132 and rolipram, but not by aminophylline. 4) AH 21-132, rolipram and aminophylline inhibited immediate phase bronchocostriction induced by either an intravenous or an aerosol challenge of antigen in guinea pigs. 5) AH 21-132 and rolipram inhibited the aeroantigen challenge-induced late phase increase in the airway resistance in guinea pigs, but aminophylline did not. These results suggest that AH 21-132 has an anti-allergic effect in the airway and that these actions may be beneficial for the treatment of allergic bronchial asthma.

The 5-lipoxygenase inhibitors ZD2138 and ZM230487 are potent and selective inhibitors of several antigen-induced guinea-pig pulmonary responses

The non-redox 5-lipoxygenase inhibitor Zeneca ZD2138 (6-[(3-fluoro-5-[4-methoxy-3,4,5,6-tetrahydro-2 H-pyran-4-yl])phenoxymethyl]-1-methyl-2-quinolone) was evaluated for its ability to inhibit antigen-induced leukotriene release from guinea-pig lung in vitro and antigen-induced increases in pulmonary resistance in guinea pigs in vivo. ZD2138 inhibited antigen-induced release of leukotriene D 4 and leukotriene B 4 with IC 50 values of 0.3±0.06 μM and 0.4±0.09 μM, respectively. At about ten times higher concentrations, ZD2138 had no effect on antigen-induced release of thromboxane B 2, indicating selectivity for inhibition of 5-lipoxygenase vs. phospholipase A 2, cyclooxygenase, or thromboxane synthetase. Similarly, ZD2138 did not inhibit histamine release, indicating that the compound did not have a generalized effect on the mediator release processes. Zeneca ZM230487 (6-[(3-fluoro-5-[4-methoxy-3,4,5,6-tetrahydro-2 H-pyran-4-yl])phenoxymethyl]-1-ethyl-2-quinolone), the N-ethyl analog of ZD2138, was approximately equipotent toward inhibition of antigen-induced leukotriene D 4 release, with an IC 50 of 0.2 ± 0.08 μM. The so-called 5-lipoxygenase activating protein (FLAP) inhibitor, MK-886 (3-[1-( p-chlorobenzyl)-5-(isopropyl)-3- tert-butylthioindol-2-yl]-2, 2-dimethylpropanoic acid), and the iron ligand 5-lipoxygenase inhibitor zileuton ( N-(1-benzo[ b]thien-2-ylethyl)- N-hydroxyurea) were also active, but less potent than ZD2138 with IC 50 values for inhibition of antigen-induced leukotriene release in vitro of 9.3±3.2 μM and 14.8±1.8 μM, respectively. In the guinea-pig in vivo model, ZD2138 and ZM230487, at 1 mg/kg i.v., significantly inhibited aerosol antigen-induced increases in pulmonary resistance. In contrast, MK-886 and zileuton had no significant effect at 1 mg/kg, but at 10 mg/kg significantly inhibited antigen-induced changes in pulmonary resistance. These results demonstrate that ZD2138 and ZM230487 are potent inhibitors of 5-lipoxygenase.

Capsaicin Increases Airflow Resistance in Guinea PigsIn Vivoby Activating both NK2and NK1Tachykinin Receptors

The role of NK1 tachykinin receptors in the increase in total pulmonary resistance (RL) produced by release of endogenous tachykinins was investigated in anesthetized guinea pigs pretreated intravenously with atropine (1 mumol/kg) by using the novel nonpeptide antagonists of NK1 (CP-96,345) and NK2 (SR 48968) tachykinin receptors. SR 48968 (0.3 mumol/kg) and CP-96,345 (2 mumol/kg) given intravenously completely blocked the response to the selective NK2 receptor agonist [beta Ala8]neurokinin A(4-10) and NK1 receptor agonist [Sar9,Met(O2)11]substance P, respectively. The response to neurokinin A was reduced dose-dependently, but not abolished, by SR 48968, and it was completely prevented by a combination of SR 48968 and CP-96,345. The response to capsaicin was reduced, but not blocked, by SR 48968, and it was completely abolished by the combination of the two antagonists. The combination of SR 48968 and CP-96,345 did not affect the increase in RL evoked by histamine. Thus, NK1, as well as NK2, receptor activation contributes to the noncholinergic increase in RL evoked by capsaicin and ascribed to release of endogenous tachykinins from sensory nerves.

Protective effect of dihydroheptaprenol in combination with vaccine to experimental Actinobacillus pleuropneumoniae infection in guinea pigs and pigs.

We investigated the effects of dihydroheptaprenol (DHP) on resistance of guinea pigs and pigs inoculated with Actinobacillus pleuropneumoniae (Apn) vaccine to subsequent challenge with Apn. Guinea pigs with complement-fixation (CF) antibody titers of 1:8 and 1:16 after intramuscular (i.m.) inoculation with inactivated Apn vaccine showed enhanced resistance to intraperitoneal (i.p.) infection with a homologous Apn strain (5 x 10(10) CFU/animal) when injected with DHP (20 mg/kg, i.m.) on the day before infection. The survival rates of the control, vehicle (lecithin solution without DHP), and DHP groups were 33%, 37%, and 63%, respectively, and that of the DHP group was significantly higher than the rates of the other groups (P < 0.05). Pigs with CF antibody titers of 1:8 and 1:16 after i.m. inoculation with inactivated Apn vaccine showed enhanced resistance to intratracheal infection with 5 x 10(10) CFU of Apn when injected with DHP (1, 2.5, or 5 mg/kg, i.m.) on the day before infection. The survival rates of the control, vehicle, DHP 1 mg/kg, DHP 2.5 mg/kg, and DHP 5 mg/kg groups were 37%, 38%, 47%, 60%, and 73%, respectively, and pigs given DHP at a dose of 5 mg/kg showed a significantly higher survival rate than the vaccinated control pigs (P < 0.05). The protective effect of DHP in vaccinated guinea pigs and pigs suggests that phagocytosis and bactericidal activity may be enhanced by this agent, depending on some opsonification effect on Apn antibody.

Acquired immunity to larvae of Amblyomma marmoreum and A.hebraeum by tortoises, guinea-pigs and guinea-fowl.

A study of acquired resistance in guinea-pigs, guinea-fowl and tortoises to larvae of the ticks Amblyomma hebraeum Koch and A.marmoreum Koch (Acari: Ixodidae) showed that repeated infestations of the laboratory host resulted in a 29.3-49.4% reduction respectively in weight of engorged larvae. No resistance was induced in guinea-fowl, the natural host for larvae of both species. A small decline in the mean weight of engorged larvae was observed for both species of ticks after three successive infestations on tortoises. The reduction in weight was more pronounced in A.hebraeum (14.5%) which does not naturally feed on tortoises than for A.marmoreum (8.4%), a common tick on this host. The occurrence of acquired resistance in natural tick host relationships as opposed to unnatural tick host relationships is discussed.