Search

Hormonal regulation of thermogenesis in goslings. The effects of blockade with thiouracil and propranolol. Acta Physiol. Pol. 1977, 28 (1): 51-60. The experiments were carried out on 90 male goslings of White Italian breed. In goslings 5 to 7 and 18 to 21-day-old thiouracil (6 mg/100 g i.p., for 3 consecutive days) diminished the cold-induced increase in the metabolic rate. At the end of 1.5 h exposure to 5 degrees C a small but statistically significant drop of body temperature in the thiouracil-treated goslings was noted. Propranolol treatment (2 mg/kg s.c.) had no clear effect neither on body temperature of cold exposed goslings nor on the cold-induced increase in the metabolic rate. The drug caused a significant decrease in the plasma free fatty acid (FFA) levels only in the goslings kept at thermoneutrality. In those exposed to 5 degrees C the plasma FFA levels rose both in the control and propranolol-treated goslings. This suggests that the cold-induced lipolysis in the goslings may be accomplished without mediation of noradrenaline.

1. Effects of general body cooling on heat production: an intravascular heat exchanger was used to alter total body temperature. Heat production increased with decreasing body temperature at an average rate of -12W/kg x degree C. The rate of rise was independent of air temperature. The threshold body temperature below which heat production rose was lower at higher air temperature. 2. Effects of spinal cord cooling: heat production increased with decreasing spinal temperature at an average rate of -0.3 W/kg x degree C. The rate of rise was not clearly affected by air temperature. The spinal threshold temperature was lower at warm ambient conditions. The results suggest that spinal thermosensitivity in the goose represents only a minor fraction of total body thermosensitivity. 3. Effects of head cooling: heat exchangers closing the carotid arteries were used to alter the temperature of the blood supplied to the head. Cooling increased heat production. When the thermosensitivity of the area, which was affected by heat exchanger, was calculated from the relationship between changes of heat production and brain temperature, values between -0.74 and -1.65 W/kg x degree C were obtained. Measurements of brain, spinal cord and head skin temperatures suggest that the thermosensitive structures which mediated the responses, were predominantly situated in the brain.

The central localisation of responses to stimulation of different peripheral somatic areas was studied in anaesthetised geese of the Landes breed. Natural (light touch, tap) and electrical stimuli were applied. In the first experiments the changes in the spontaneous activity following natural stimuli were recorded systematically from different brain regions. In the following experiments evoked potentials were recorded from responsive sites. The majority of the somatic responses were localised in the paleostriatum augmentatum, the neostriatum and the neostriatum caudale. Stimulation of the bill and the head elicited responses in tractus quinto-frontalis, paleostriatum augmentatum, neostriatum and neostriatum caudale while activation from the body were mainly localised in neostriatum caudale and paleostriatum augmentatum. Responses to photic stimulation were recorded from the visual wulst, the stratum opticum and the nucleus rotundus. Auditory stimuli were found to be ineffective under our recording conditions. These results are discussed and compared with previous data obtained in other species.

To investigate possible physiologic mechanisms that allow the bar-headed goose to perform strenuous physical activity when flying at high altitude (e.g., above 9,000 m), we measured cardiopulmonary variables during running exercise (treadmill; 0.6 m.sec-1; 2 degrees incline) while the bird breathed either normoxic (21% O2) or hypoxic (7% O2) gases via a face mask. 1. During normoxic exercise, O2 uptake rate doubled and both ventilation and cardiac output increased. Blood gases and pH in arterial, mixed venous and blood from the leg, however, remained virtually unaltered. 2. Hypoxia at rest stimulated ventilation to rise but not cardiac output. The birds reached a steady state with virtually unaltered O2 uptake. 3. Exercise during hypoxia further stimulated ventilation, resulting in elevated arterial PO2 and O2 content compared to hypoxia at rest. However, O2 uptake increased only slightly, and cardiac output did not rise over the resting hypoxic value. The hyperventilation resulted in respiratory alkalosis and increased CO2 output, with R values being as high as 2.0. 4. It is concluded that neither ventilation nor pulmonary gas transfer were the limiting step in supplying O2 to the working muscles during hypoxic exercise in our experiments. It is more likely that muscle blood flow or diffusion from muscle capillaries to mitochondria, or both, determined the aerobic capacity under these conditions.

We studied gas exchange in anesthetized ducks and geese artificially ventilated at normal tidal volumes (VT) and respiratory frequencies (fR) with a Harvard respirator (control ventilation, CV) or at low VT-high fR using an oscillating pump across a bias flow with mean airway opening pressure regulated at 0 cmH2O (high-frequency ventilation, HFV). VT was normalized to anatomic plus instrument dead space (VT/VD) for analysis. Arterial PCO2 was maintained at or below CV levels by HFV with VT/VD less than 0.5 and fR = 9 and 12 s-1 but not at fR = 6 s-1. For 0.4 less than or equal to VT/VD less than or equal to 0.85 and 3 s-1. less than or equal to fR less than or equal to 12 s-1, increased VT/VD was twice as effective as increased fR at decreasing arterial PCO2, consistent with oscillatory dispersion in a branching network being an important gas transport mechanism in birds on HFV. Ventilation of proximal exchange units with fresh gas due to laminar flow is not the necessary mechanism supporting gas exchange in HFV, since exchange could be maintained with VT/VD less than 0.5. Interclavicular and posterior thoracic air sac ventilation measured by helium washout did not change as much as expired minute ventilation during HFV. PCO2 was equal in both air sacs during HFV. These results could be explained by alterations in aerodynamic valving and flow patterns with HFV. Ventilation-perfusion distributions measured by the multiple inert gas elimination technique show increased inhomogeneity with HFV. Elimination of soluble gases was also enhanced in HFV as reported for mammals.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurements of plasma GLI and IRI in normal fasting geese, before and during constant I.V. infusion of saline, gave GLI/I ratios of 1.32 +/- .07 and 1.34 +/- .03 (w/w). As total pancreatectomy markedly reduces the pancreatic hormone level, leading to a mortal hypoglycaemia, we attempted to maintain plasma glucose within the normal range by constant I.V. infusion of glucagon and insulin into operated animals. The results as follows: 1. Blood glucose levels can be maintained within the normal range during experiments lasting 6 or more hours with a constant G/I ratio. 2. The G/I ratio obtained in operated animals (.96 +/- .12) is near to, but significantly lower (p less than .005) than, the GLI/I ratio measured in normal animals. This difference may be explained by the presence of a small amount of circulating gut GLI in the 2nd group.

1. The nature and location of the receptors which stimulate salt-gland secretion in the goose have been investigated.2. The rapid injection of homologous blood (sufficient to raise the blood volume by 16 and 9%) into the right atrium failed to induce secretion. In contrast, hypertonic sucrose, Na(2)SO(4) and LiCl initiated secretion.3. These results support the theory that osmoreceptors initiate secretion by detecting an increase in plasma tonicity.4. The minimal amount of hypertonic NaCl required to initiate secretion when infusions were made into a carotid artery or into various arteries and veins in the splanchnic region was not less than that required by an I.V. route.5. Cross-circulation and perfusion studies also showed that a raised [NaCl] in the blood perfusing the head was ineffective in evoking secretion and thus that plasma tonicity must be raised elsewhere in the body.6. Secretion in response to salt-loading was abolished or prevented by cutting the vagus nerves or blocking them with local anaesthetic. Stimulation of the cephalic end of the cut vagi in an isolated, perfused decerebrate head induced secretion, indicating that the afferent fibres from the receptors to the C.N.S. lie in the vagus nerves. Cutting the vagi below the heart, however, had no effect on the secretory response.7. Blocking nerves in the crop with local anaesthetic had no effect on secretion induced by salt-loading but when local anaesthetic was injected into the pericardial sac, secretion decreased immediately, stopped, and recovered with a time course similar to that seen after blocking the vagus nerves.8. Section of the vagi in the neck abolished the tachycardia observed in response to the injection of hypertonic NaCl into the right atrium.9. As in other species, stimulation of the ;secretory nerve' induced secretion in anaesthetized or decerebrate geese.10. Hexamethonium given I.V. or applied topically to the ;secretory nerve ganglion' blocked secretion in response to salt-loading or to secretory nerve stimulation.11. It appears that the receptors for salt-gland secretion are located in or near the heart and that afferent fibres from these receptors travel in the vagus nerves to the C.N.S.12. A possible scheme of the secretory reflex which initiates and maintains salt-gland activity is proposed.