Biomedical subjects

L G Branco

Publications and source records attributed to L G Branco.

At least 37 records · Page 2Linked to original sources

PubMed1999

Role of nitric oxide in 2-deoxy-D-glucose-induced hypothermia in rats.

The present study was designed to test the hypothesis that nitric oxide (NO) plays a role in 2-deoxy-D-glucose (2-DG)-induced hypothermia. The body temperature of awake, unrestrained rats was measured before and after the administration of 2-DG, or N(G)-nitro-L-arginine methyl ester (L-NAME; a non-selective NOS inhibitor) or both treatments together. We observed a significant reduction in body temperature after 2-DG injection. L-NAME alone caused no significant change in body temperature. When the two treatments were combined, a reduction in the magnitude of 2-DG-induced hypothermia was observed. The neuronal NOS inhibitor 7-nitroindazole also inhibited 2-DG-induced hypothermia. The data indicate that NO, probably produced by neuronal NOS, plays a role in 2-DG-induced hypothermia.

Animals↗

PubMed1999

Atrial natriuretic peptide and oxytocin induce natriuresis by release of cGMP.

Our hypothesis is that oxytocin (OT) causes natriuresis by activation of renal NO synthase that releases NO followed by cGMP that mediates the natriuresis. To test this hypothesis, an inhibitor of NO synthase, L-nitroarginine methyl ester (NAME), was injected into male rats. Blockade of NO release by NAME had no effect on natriuresis induced by atrial natriuretic peptide (ANP). This natriuresis presumably is caused by cGMP because ANP also activates guanylyl cyclase, which synthesizes cGMP from GTP. The 18-fold increase in sodium (Na+) excretion induced by OT (1 microgram) was accompanied by an increase in urinary cGMP and preceded by 20 min a 20-fold increase in NO3- excretion. NAME almost completely inhibited OT-induced natriuresis and increased NO3- excretion; however, when the dose of OT was increased 10-fold, a dose that markedly increases plasma ANP concentrations, NAME only partly inhibited the natriuresis. We conclude that the natriuretic action of OT is caused by a dual action: generation of NO leading to increased cGMP and at higher doses release of ANP that also releases cGMP. OT-induced natriuresis is caused mainly by decreased tubular Na+ reabsorption mediated by cGMP. In contrast to ANP that releases cGMP in the renal vessels and the tubules, OT acts on its receptors on NOergic cells demonstrated in the macula densa and proximal tubules to release cGMP that closes Na+ channels. Both ANP- and OT-induced kaliuresis also appear to be mediated by cGMP. We conclude that cGMP mediates natriuresis and kaliuresis induced by both ANP and OT.

Animals↗

PubMed1999

Central thermoregulatory effects of lactate in the toad Bufo paracnemis.

Hypoxia induces a regulated decrease in body temperature (Tb; anapyrexia) in organisms ranging from protozoans to mammals, but very little is known about the mechanisms involved. Several candidates have been suggested to mediate hypoxia-induced anapyrexia, among them lactate, which is a classical compansion of hypoxic stress in vertebrates. The present study was designed to assess the central thermoregulatory effects of lactate in Bujo paracnemis. Toads equipped with a temperature probe were tested over a thermal gradient (10-40 degrees C). Lactate injected systemically (4.0 mmol kg-1) caused a significant reduction of Tb from 24.6 +/- 2.1 to 17.4 +/- 3.9 degrees C. To assess the role of central thermoregulatory mechanisms, a lower dose (0.4 mmol kg-1) of lactate was injected into the fourth cerebral ventricle or systemically. Intracerebroventricular injection of lactate caused a similar decrease in Tb, whereas systemic injection caused no change. The data indicate that lactate may play a role in hypoxia-induced anapyrexia in central rather than peripheral sites.

Animals↗

PubMed1999

Seasonal changes in the cardiorespiratory responses to hypercarbia and temperature in the bullfrog, Rana catesbeiana.

We assessed the seasonal variations in the effects of hypercarbia (3 or 5% inspired CO2) on cardiorespiratory responses in the bullfrog Rana catesbeiana at different temperatures (10, 20 and 30 degrees C). We measured breathing frequency, blood gases, acid-base status, hematocrit, heart rate, blood pressure and oxygen consumption. At 20 and 30 degrees C, the rate of oxygen consumption had a tendency to be lowest during winter and highest during summer. Hypercarbia-induced changes in breathing frequency were proportional to body temperature during summer and spring, but not during winter (20 and 30 degrees C). Moreover, during winter, the effects of CO2 on breathing frequency at 30 degrees C were smaller than during summer and spring. These facts indicate a decreased ventilatory sensitivity during winter. PaO2 and pHa showed no significant change during the year, but PaCO2 was almost twice as high during winter than in summer and spring, indicating increased plasma bicarbonate levels. The hematocrit values showed no significant changes induced by temperature, hypercarbia or season, indicating that the oxygen carrying capacity of blood is kept constant throughout the year. Decreased body temperature was accompanied by a reduction in heart rate during all four seasons, and a reduction in blood pressure during summer and spring. Blood pressure was higher during winter than during any other seasons whereas no seasonal change was observed in heart rate. This may indicate that peripheral resistance and/or stroke volume may be elevated during this season. Taken together, these results suggest that the decreased ventilatory sensitivity to hypercarbia during winter occurs while cardiovascular parameters are kept constant.

Animals↗

PubMed1999

Carbon monoxide as a novel mediator of the febrile response in the central nervous system.

Heme oxygenase catalyzes the metabolism of heme to biliverdin, free iron, and carbon monoxide (CO), which has been shown to be an important neuromodulatory agent. Recently, it has been demonstrated that lipopolysaccharide (LPS) can induce the enzyme heme oxygenase in glial cells. Therefore, the present study was designed to test the hypothesis that central CO plays a role in LPS-induced fever. Colonic body temperature (T(b)) was measured in awake, unrestrained rats (basal T(b) = 36.8 +/- 0.2 degrees C). Intracerebroventricular injection of zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG; 75 nmol), a heme oxygenase inhibitor, caused no significant change in T(b), indicating that the central heme oxygenase pathway plays no tonic role in T(b) under the experimental conditions used. Intraperitoneal injections of LPS (50-100 microgram/kg) evoked dose-dependent increases in T(b). Intracerebroventricular injection of ZnDPBG in febrile rats attenuated LPS-induced fever (thermal index with ZnDPBG = 1.1 +/- 0. 2 degrees C, thermal index with vehicle = 2.3 +/- 0.4 degrees C), suggesting that the central heme oxygenase pathway plays a role in fever generation. The antipyretic effect of ZnDPBG could be reversed by intracerebroventricular administration of heme-lysinate or CO-saturated saline. Collectively, our data indicate that CO arising from heme oxygenase may play an important role in fever generation by acting on the central nervous system.

Animals↗

PubMed1999

Endogenous vasopressin does not mediate hypoxia-induced anapyrexia in rats.

The present study was designed to test the hypothesis that arginine vasopressin (AVP) mediates hypoxia-induced anapyrexia. The rectal temperature of awake, unrestrained rats was measured before and after hypoxic hypoxia, AVP-blocker injection, or a combination of the two. Control animals received saline injections of the same volume. Basal body temperature was 36.52 +/- 0.29 degreesC. We observed a significant (P < 0.05) reduction in body temperature of 1. 45 +/- 0.33 degreesC after hypoxia (7% inspired O2), whereas systemic and central injections of AVP V1- and AVP V2-receptor blockers caused no change in body temperature. When intravenous injection of AVP blockers was combined with hypoxia, we observed a reduction in body temperature of 1.49 +/- 0.41 degreesC (V1-receptor blocker) and of 1.30 +/- 0.13 degreesC (V2-receptor blocker), similar to that obtained by application of hypoxia only. Similar results were observed when the blockers were injected intracerebroventricularly. The data indicate that endogenous AVP does not mediate hypoxia-induced anapyrexia in rats.

Animals↗

PubMed1999

Role of nitric oxide in hypoxia inhibition of fever.

Hypoxia causes a regulated decrease in body temperature (T(b)), and nitric oxide (NO) is now known to participate in hypoxia-induced hypothermia. Hypoxia also inhibits lipopolysaccharide (LPS)-induced fever. We tested the hypothesis that NO may participate in the hypoxia inhibition of fever. The rectal temperature of awake, unrestrained rats was measured before and after injection of LPS, with or without concomitant exposure to hypoxia, in an experimental group treated with N(omega)-nitro-L-arginine (L-NNA) for 4 consecutive days before the experiment and in a saline-treated group (control). L-NNA is a nonspecific NO synthase inhibitor that blocks NO production. LPS caused a dose-dependent typical biphasic rise in T(b) that was completely prevented by hypoxia (7% inspired oxygen). L-NNA caused a significant drop in T(b) during days 2-4 of treatment. When LPS was injected into L-NNA-treated rats, inhibition of fever was observed. Moreover, the effect of hypoxia during fever was significantly reduced. The data indicate that the NO pathway plays a role in hypoxia inhibition of fever.

Animals↗

PubMed1999

Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: participation of the locus coeruleus.

Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced hypothermia and hyperventilation, and works as a neuromodulator in the central nervous system, including the locus coeruleus (LC), which is a noradrenergic nucleus in the pons. The LC plays a role in a number of stress-induced responses, but its participation in the control of breathing and thermoregulation is unclear. Thus, in the present study, we tested the hypothesis that LC plays a role in the hypoxia-induced hypothermia and hyperventilation, and that NO is involved in these responses. Electrolytic lesions were performed bilaterally within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. Body temperature and pulmonary ventilation (V E) were measured. The rats were divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N = 19), and each group received a saline or an N G-nitro-L-arginine methyl ester (L-NAME, 250 microg/microl) intracerebroventricular (icv) injection. No significant difference was observed between control and sham-operated rats. Hypoxia (7% inspired O2) caused hyperventilation and hypothermia in both control (from 541.62 +/- 35.02 to 1816.18 +/- 170.7 and 36.3 +/- 0.12 to 34. 4 +/- 0.09, respectively) and LC-lesioned rats (LCLR) (from 694.65 +/- 63.17 to 2670.29 +/- 471.33 and 36 +/- 0.12 to 35.3 +/- 0.12, respectively), but the increase in V E was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused no significant change in V E or in body temperature under normoxia, but abolished both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished the hypoxia-induced hypothermia in LCLR. The present data indicate that hypoxia-induced hyperventilation and hypothermia may be related to the LC, and that NO is involved in these responses.

Animals↗

PubMed1999

Participation of nitric oxide in the nucleus isthmi in CO2-drive to breathing in toads.

The nucleus isthmi (NI) is a mesencephalic structure of the amphibian brain. It has been reported that NI plays an important role in integration of CO2 chemoreceptor information and glutamate is probably involved in this function. However, very little is known about the mechanisms involved. Recently, it has been shown that nitric oxide synthase (NOS) is expressed in the brain of the frog. Thus the gas nitric oxide (NO) may be involved in different functions in the brain of amphibians and may act as a neurotransmitter or neuromodulator. We tested the hypothesis that NO plays a role in CO2-drive to breathing, specifically in the NI comparing pulmonary ventilation, breathing frequency and tidal volume, after microinjecting 100 nmol/0.5 microl of L-NAME (a nonselective NO synthase inhibitor) into the NI of toads (Bufo paracnemis) exposed to normocapnia and hypercapnia. Control animals received microinjections of vehicle of the same volume. Under normocapnia no significant changes were observed between control and L-NAME-treated toads. Hypercapnia caused a significant (P<0.01) increase in ventilation only after intracerebral microinjection of L-NAME. Exposure to hypercapnia caused a significant increase in breathing frequency both in control and L-NAME-treated toads (P<0.01 for the control group and P<0.001 for the L-NAME group). The tidal volume of the L-NAME group tended to be higher than in the control group under hypercapnia, but the increase was not statistically significant. The data indicate that NO in the NI has an inhibitory effect only when the respiratory drive is high (hypercapnia), probably acting on tidal volume. The observations reported in the present investigation, together with other studies on the presence of NOS in amphibians, indicate a considerable degree of phylogenetic conservation of the NO pathway amongst vertebrates.

Animals↗

PubMed1998

Respiratory and metabolic responses of the spiny rats Proechimys yonenagae and P. iheringi to CO2.

The recently described burrow-dwelling Proechimys yonenagae from the Brazilian semiarid caatinga was compared to P. iheringi from the Brazilian rain forest of Mata Atlântica in terms of interactions between body temperature (Tb), ventilation (VE) and oxygen consumption (V(O2)) during hypercapnia (5 or 10% CO2). Wistar rats were also used as a control. VE was measured by plethysmography, Tb by inserting a probe into the colon, and V(O2) by a close-flow system. During air breathing, VE did not differ between the rodents, Wistar Tb was elevated compared to P. yonenagae, and the V(O2) values of P. yonenagae and P. iheringi were significantly lower than those of Wistar rats. Hypercapnia caused hyperventilation in the three rodents, hypothermia in P. yonenage and Wistar rats, but no change in V(O2) was observed in any of the rodents. The hypercapnia-induced hyperventilation may be a major factor producing heat loss. This effect was independent of V(O2). Comparisons of the two spiny rat species suggest little adaptation of P. yonenagae to hypercapnia in burrows.

Acclimatization↗

PubMed1998

Physiological significance of behavioral hypothermia in hypoglycemic frogs (Rana catesbeiana).

Hypoxia elicits a number of compensatory responses in animals, including behavioral hypothermia. The hypothesis that hypoglycemia induces hypothermia in the bullfrog Rana catesbeiana was tested and that this behavioral response would be beneficial. Frogs equipped with a temperature probe were tested in a thermal gradient (10-40 degrees C). Insulin (15 IU kg-1) caused significant reduction of body temperature, from 25.0 to 17.8 degrees C. A non-metabolizable glucose analogue, 2-deoxy-D-glucose (2-DG, 50 mg kg-1), which blocks intracellular glucose utilization, was also injected and caused a similar drop in body temperature, despite an increase in plasma glucose levels. To assess the possible benefits of hypoglycemia-induced hypothermia, the effects of insulin and 2-DG injections were measured on plasma glucose concentration and on oxygen consumption of frogs equilibrated at 10, 20 and 30 degrees C. The plasma glucose was elevated at higher temperatures and so was oxygen consumption. The insulin caused a significant reduction of plasma glucose concentration (about 1.22 muMol ml-1) whereas 2-DG caused a significant increase (about 0.70 muMol ml-1) at 30 degrees C. Both drugs caused a reduction of oxygen consumption (approximately 0.388 and 0.382 ml min-1 kg at 30 degrees C after insulin and 2-DG injection, respectively). No effect of either insulin or 2-DG was observed when the animals were equilibrated at 10 degrees C. In conclusion, hypothermia may be a beneficial response to hypoglycemia in frogs.

Animals↗

PubMed1998

Role of nitric oxide in systemic vasopressin-induced hypothermia.

It has been reported that arginine vasopressin (AVP) plays a thermoregulatory action, but very little is known about the mechanisms involved. In the present study, we tested the hypothesis that nitric oxide (NO) plays a role in systemic AVP-induced hypothermia. Rectal temperature was measured before and after AVP, AVP blocker, or NG-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) injection. Control animals received saline injections of the same volume. The basal body temperature (Tb) measured in control animals was 36.53 +/- 0.08 degreesC. We observed a significant (P < 0.05) reduction in Tb to 35.44 +/- 0.19 degreesC after intravenous injection of AVP (2 micrograms/kg) and to 35.74 +/- 0. 10 degreesC after intravenous injection of L-NAME (30 mg/kg). The systemic injection of the AVP blocker [beta-mercapto-beta, beta-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin (10 micrograms/kg) caused a significant increase in Tb to 37.33 +/- 0.23 degreesC, indicating that AVP plays a tonic role by reducing Tb. When the treatments with AVP and L-NAME were combined, systemically injected L-NAME blunted AVP-induced hypothermia. To assess the role of central thermoregulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected into the third cerebral ventricle. Intracerebroventricular injection of L-NAME caused an increase in Tb, but when intracerebroventricular L-NAME was combined with systemic AVP injection (2 micrograms/kg), no change in Tb was observed. The data indicate that central NO plays a major role mediating systemic AVP-induced hypothermia.

Animals↗

PubMed1998

Effect of nitric oxide synthase inhibition on hypercapnia-induced hypothermia and hyperventilation.

Hypercapnia elicits hypothermia in a number of vertebrates, but the mechanisms involved are not well understood. In the present study, we assessed the participation of the nitric oxide (NO) pathway in hypercapnia-induced hypothermia and hyperventilation by means of NO synthase inhibition by using Nomega-nitro-L-arginine (L-NNA). Measurements of ventilation, body temperature, and oxygen consumption were performed in awake unrestrained rats before and after L-NNA injection (intraperitoneally) and L-NNA injection followed by hypercapnia (5% CO2). Control animals received saline injections. L-NNA altered the breathing pattern during the control situation but not during hypercapnia. A significant (P < 0.05) drop in body temperature was measured after both L-NNA (40 mg/kg) and 5% inspired CO2, with a drop in oxygen consumption in the first situation but not in the second. Hypercapnia had no effect on L-NNA-induced hypothermia. The ventilatory response to hypercapnia was not changed by L-NNA, even though L-NNA caused a drop in body temperature. The present data indicate that the two responses elicited by hypercapnia, i.e., hyperventilation and hypothermia, do not share NO as a common mediator. However, the L-arginine-NO pathway participates, although in an unrelated way, in respiratory function and thermoregulation.

Animals↗

PubMed1998

Seasonal changes in the cardiovascular, respiratory and metabolic responses to temperature and hypoxia in the bullfrog Rana catesbeiana.

We assessed seasonal variations in the effects of temperature on hypoxia-induced alterations in the bullfrog Rana catesbeiana by measuring the heart rate, arterial blood pressure, breathing frequency, metabolic rate, blood gas levels, acid-base status and plasma glucose concentration. Regardless of the season, decreased body temperature was accompanied by a reduction in heart and breathing frequencies. Lower temperatures caused a significant decrease in arterial blood pressure during all four seasons. Hypoxia-induced changes in breathing frequency were proportional to body temperature and were more pronounced during winter, less so during spring and autumn and even smaller during summer. Season had no effect on the relationship between hypoxia and heart rate. At any temperature tested, the rate of oxygen consumption had a tendency to be highest during summer and lowest during winter, but the difference was significant only at 35 degrees C. The PaO2 and pH values showed no significant change during the year, but PaCO2 was almost twice as high during winter than in summer and spring, indicating increased plasma bicarbonate levels. Lower temperatures were accompanied by decreased plasma glucose levels, and this effect was greater during summer and smaller during autumn. Hypoxia-induced hyperglycaemia was influenced by temperature and season. During autumn and winter, plasma glucose level remained elevated regardless of temperature, probably to avoid dehydration and/or freezing. In winter, the bullfrog may be exposed not only to low temperatures but also to hypoxia. These animals show temperature-dependent responses that may be beneficial since at low body temperatures the set-points of most physiological responses to hypoxia are reduced, regardless of the season.

Acid-Base Equilibrium↗

PubMed1997

Participation of the nitric oxide pathway in cold-induced hypertension.

Several mechanisms are known to participate in cold-induced hypertension, but no information exist on the role of the nitric oxide (NO). In the present study, we assessed the participation of nitric oxide in cold-induced hypertension by means of inhibition of NO synthase. Experiments were performed in rats treated with N omega-nitro-L-arginine (L-NNA) injected i.p. at a dose of 25 mg/kg body weight twice a day for four consecutive days. Control animals received saline injections of the same volume. Two days before the experiment, the femoral artery was cannulated for blood pressure recording. Arterial blood pressure was measured at 25 degrees C for 30 min (control period), followed by a 3.5 hour period at 4 degrees C (cold exposure) and, eventually, a last 3 hour period after removal from cold (back to 25 degrees C). In control animals, at 25 degrees C, mean arterial blood pressure was 112.5+/-3.6 mmHg and heart rate was 380+/-3.5 bpm. L-NNA treatment caused an increase in blood pressure to 155.0+/-3.5 mmHg (P<0.01) and in heart rate to 410+/-6.0 bpm (P<0.05). Exposure to cold caused blood pressure to increase up to 131.5+/-3.6 mmHg (P<0.05) in the control group, whereas no significant change could be measured in treated animals. Recovery from cold exposure led to a decrease in blood pressure in control animals, but not in treated animals. These results indicate that NO plays a role in the development of cold-induced elevation of blood pressure.

Animals↗

PubMed1997

Effects of 2-deoxy-D-glucose and insulin on plasma glucose levels and behavioral thermoregulation of toads.

The present study was designed to test the hypothesis that hypoglycemia induces hypothermia in ectotherms and to elucidate the mechanisms responsible for behavioral hypothermia. Behavioral hypothermia is a stress response that occurs in organisms ranging from protozoans to mammals, but very little is known about the cellular mechanisms involved. Toads equipped with a temperature probe were tested in a thermal gradient (10-40 degrees C). Insulin was used to reduce plasma glucose levels, and an inhibitor of glucose utilization, 2-deoxy-D-glucose (2-DG), was used to cause intracellular glucopenia. Insulin injections into the dorsal lymph sac caused significant reductions of both plasma glucose levels and body temperature. To determine if the response was mediated by extracellular glucose receptors or an intracellular mechanism. 2-DG was also injected into the lymph sac. 2-DG caused a similar drop in body temperature and a marked increase in plasma glucose. To assess the role of central thermoregulatory mechanisms, a smaller dose of 2-DG was injected into the fourth cerebral ventricle or the lymph sac. Intracerebroventricular injection of 2-DG caused a decrease in body temperature despite elevated circulating glucose levels, whereas injection into the lymph sac caused no significant change. The data indicate that exclusion of glucose from central rather than peripheral sites plays a major role in the hypoglycemia-induced behavioral hypothermia and that intracellular mechanisms rather than extracellular glucose receptors are involved in this response. Hypothermia may be a beneficial response to hypoglycemia in toads because it dampens cellular oxidative demands during glucose deprivation.

Animals↗

PubMed1997

Role of the nitric oxide pathway in hypoxia-induced hypothermia of rats.

Hypothermia is a response to hypoxia that occurs in organisms ranging from protozoans to mammals, but very little is known about the mechanisms involved. Recently, the NO pathway has been suggested to be involved in thermoregulation. In the present study, we assessed the participation of nitric oxide in hypoxia-induced hypothermia by means of NO synthase inhibition using NG-nitro-L-arginine methyl ester (L-NAME). The rectal temperature of awake, unrestrained rats was measured before and after hypoxia or L-NAME injection or both treatments together. Control animals received saline injections of the same volume. We observed a significant (P < 0.05) reduction in body temperature of 1.32 +/- 0.36 degrees C after hypoxia (7% inspired O2) and of 0.96 +/- 0.42 degree C after L-NAME (30 mg/kg body wt) injected intravenously. When the two treatments were combined, no significant difference in body temperature was observed. To assess the role of central thermo-regulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected into the third cerebral ventricle or intravenously. Intracerebroventricular injection of L-NAME caused an increase in body temperature, but when L-NAME was combined with hypoxia (7% inspired O2) no change in body temperature was observed. Intravenous injection of 1 mg/kg L-NAME had no effect. The data indicate that NO plays a major role in hypoxia-induced hypothermia at central rather than peripheral sites.

Animals↗

PubMed1997

Cardiovascular, respiratory and metabolic responses to temperature and hypoxia of the winter frog Rana catesbeiana.

The objective of the present study was to determine the effects of hypoxia and temperature on the cardiovascular and respiratory systems and plasma glucose levels of the winter bullfrog Rana catesbeiana. Body temperature was maintained at 10, 15, 25 and 35 degrees C for measurements of breathing frequency, heart rate, arterial blood pressure, metabolic rate, plasma glucose levels, blood gases and acid-base status. Reducing body temperature from 35 to 10 degrees C decreased (P < 0.001) heart rate (bpm) from 64.0 +/- 3.1 (N = 5) to 12.5 +/- 2.5 (N = 6) and blood pressure (mmHg) (P < 0.05) from 41.9 +/- 2.1 (N = 5) to 33.1 +/- 2.1 (N = 6), whereas no significant changes were observed under hypoxia. Hypoxia-induced changes in breathing frequency and acid-base status were proportional to body temperature, being pronounced at 25 degrees C, less so at 15 degrees C, and absent at 10 degrees C. Hypoxia at 35 degrees C was lethal. Under normoxia, plasma glucose concentration (mg/dl) decreased (P < 0.01) from 53.0 +/- 3.4 (N = 6) to 35.9 +/- 1.7 (N = 6) at body temperatures of 35 and 10 degrees C, respectively. Hypoxia had no significant effect on plasma glucose concentration at 10 and 15 degrees C, but at 25 degrees C there was a significant increase under conditions of 3% inspired O2. The arterial PO2 and pH values were similar to those reported in previous studies on non-estivating Rana catesbeiana, but PaCO2 (37.5 +/- 1.9 mmHg, N = 5) was 3-fold higher, indicating increased plasma bicarbonate levels. The estivating bullfrog may be exposed not only to low temperatures but also to hypoxia. These animals show temperature-dependent responses that may be beneficial since during low body temperatures the sensitivity of most physiological systems to hypoxia is reduced.

Animals↗