Regulation of brain temperature in pigeons: effects of corneal convection

1982 ◽  
Vol 242 (5) ◽  
pp. R577-R581 ◽  
Author(s):  
B. Pinshow ◽  
M. H. Bernstein ◽  
G. E. Lopez ◽  
S. Kleinhaus

The effect of direct ventilation of the eyes on cooling in the brain was investigated in domestic pigeons (Columba livia, mean mass 0.27 kg) with thermocouples chronically implanted in the hypothalamus and anterior eye chamber. During conductive heating in still air body-brain temperature difference (delta T) was 2.6 degrees C. During exclusive ventilation of ocular surfaces, with air flowing at about flight speed, delta T increased to 3.5 degrees C and returned to preventilation values on cessation of ventilation. When the eyes were sealed then ventilated, delta T was not different from that in still air. Administration of phenylephrine caused iridial vasoconstriction and a significant decrease in intraocular temperature, but no changes in brain temperature. This suggests that compensation may occur via other evaporating cranial surfaces. Our findings suggest that the eyes contribute to the control of brain temperature by dissipating heat. Blood cooled while flowing through the ocular vasculature apparently contributes to the venous flow through the ophthalmic rete, serving as a heat sink for arterial blood flowing to the brain.

2001 ◽  
Author(s):  
Liang Zhu ◽  
Maithreyi Bommadevara

Abstract In this study a theoretical model was developed to evaluate the temperature difference between the body core and the arterial blood supplied to the brain. Several factors including the local blood perfusion rate, blood vessel bifurcation in the neck, and blood vessel pairs on both sides of the neck were considered in the model. The theoretical approach was used to estimate the potential for cooling of blood in the carotid artery on its way to the brain by heat exchange with its countercurrent jugular vein and by the radial heat conduction loss to the cool neck surface. It shows that blood temperature along the common and internal carotid arteries typically decreases up to 0.86°C during hyperthermia. Selectively cooling the neck surface during hypothermia increases the heat loss from the carotid arteries and results in approximately 1.2°C in the carotid arterial temperature. This research could provide indirect evidence of the existence of selective brain cooling (SBC) in humans during hyperthermia. The simulated results can also be used to evaluate the feasibility of lowering brain temperature effectively by selectively cooling the head and neck surface during hypothermia treatment for brain injury or multiple sclerosis.


1985 ◽  
Vol 249 (6) ◽  
pp. R758-R764 ◽  
Author(s):  
B. Pinshow ◽  
M. H. Bernstein ◽  
Z. Arad

Bird heads contain paired countercurrent heat exchangers, the ophthalmic retia, which function in brain temperature regulation. Blood, cooled by evaporation from the nasal and buccal mucosa and the ocular surfaces, flows to the venous side of each rete and there gains heat from arterial blood flowing countercurrent to it. The cooled arterial blood then flows to the brain. To ascertain whether characteristics of the blood reaching the cooling surfaces and the retia favor O2 and CO2 exchange, as well as heat exchange, we studied blood O2 affinity in relation to temperature (T) and CO2 tension (PCO2) in six pigeons (Columba livia). O2 tension (PO2) at half-saturation (P50, Torr) was measured at various combinations of T and PCO2 from 36 to 44 degrees C and 9 to 33 Torr. pH was uncontrolled. O2 half-saturation of hemoglobin (P50) varied according to P50 = 1.049T + 0.573PCO2–19.444. We propose that shifts in blood O2 affinity, associated with T and PCO2 at the mucosa and eyes and in the retia, would enhance the brain O2 supply by an exchange of O2 and CO2 between air and blood at moist cephalic surfaces, thereby augmenting O2 and reducing CO2 in the venous return to the retia and diffusion of O2 from veins to arteries in the retia. This mechanism might have particular importance at high altitude; we calculate that at 7,000 m above sea level both O2 saturation and PO2 could double in blood flowing from the retia to the brain.


2007 ◽  
Vol 292 (3) ◽  
pp. R1298-R1305 ◽  
Author(s):  
Shane K. Maloney ◽  
Duncan Mitchell ◽  
Dominique Blache

The degree of variability in the temperature difference between the brain and carotid arterial blood is greater than expected from the presumed tight coupling between brain heat production and brain blood flow. In animals with a carotid rete, some of that variability arises in the rete. Using thermometric data loggers in five sheep, we have measured the temperature of arterial blood before it enters the carotid rete and after it has perfused the carotid rete, as well as hypothalamic temperature, every 2 min for between 6 and 12 days. The sheep were conscious, unrestrained, and maintained at an ambient temperature of 20–22°C. On average, carotid arterial blood and brain temperatures were the same, with a decrease in blood temperature of 0.35°C across the rete and then an increase in temperature of the same magnitude between blood leaving the rete and the brain. Rete cooling of arterial blood took place at temperatures below the threshold for selective brain cooling. All of the variability in the temperature difference between carotid artery and brain was attributable statistically to variability in the temperature difference across the rete. The temperature difference between arterial blood leaving the rete and the brain varied from −0.1 to 0.9°C. Some of this variability was related to a thermal inertia of the brain, but the majority we attribute to instability in the relationship between brain blood flow and brain heat production.


1991 ◽  
Vol 71 (2) ◽  
pp. 590-595 ◽  
Author(s):  
W. Rasch ◽  
P. Samson ◽  
J. Cote ◽  
M. Cabanac

Evaporative and convective heat loss from head skin and expired air were measured in four male subjects at rest and during incremental exercise at 5, 15, and 25 degrees C ambient temperature (Ta) to verify whether the head can function as a heat sink for selective brain cooling. The heat losses were measured with an open-circuit method. At rest the heat loss from head skin and expired air decreased with increasing Ta from 69 +/- 5 and 37 +/- 18 (SE) W (5 degrees C) to 44 +/- 25 and 26 +/- 7 W (25 degrees C). At a work load of 150 W the heat loss tended to increase with increasing Ta: 119 +/- 21 (head skin) and 82 +/- 5 W (respiratory tract) at 5 degrees C Ta to 132 +/- 27 and 103 +/- 12 W at 25 degrees C Ta. Heat loss was always higher from the head surface than from the respiratory tract. The heat losses, separately and together (total), were highly correlated to the increasing esophageal temperature at 15 and 25 degrees C Ta. At 5 degrees C Ta on correlation occurred. The results showed that the heat loss from the head was larger than the heat brought to the brain by the arterial blood during hyperthermia, estimated to be 45 W per 1 degree C increase above normal temperature, plus the heat produced by the brain, estimated to be up to 20 W. The total heat to be lost is therefore approximately 65 W during a mild hyperthermia (+1 degrees C) if brain temperature is to remain constant.(ABSTRACT TRUNCATED AT 250 WORDS)


1991 ◽  
Vol 11 (4) ◽  
pp. 611-616 ◽  
Author(s):  
John D. Michenfelder ◽  
James H. Milde ◽  
Zvonimir S. Katušić

Following complete global cerebral ischemia and reperfusion, a brief period of reactive hyperemia is followed by a prolonged period of low flow commonly referred to as the delayed postischemic hypoperfusion state. It is generally assumed that this low-flow state may be injurious because of inadequate substrate delivery, thus implying that flow is no longer coupled to metabolic needs. This relationship of CBF to CMRO2 was examined in six anesthetized dogs that were subjected to 12 min of complete ischemia induced either by CSF compression or aortic occlusion. Following reperfusion and onset of the low-flow state, which stabilized at 45 min postischemia, control normothermic (37°C) measurements of CBF and CMRO2 were determined. Thereafter, femoral arterial blood was circulated through a heat exchanger (42.5°C), and brain temperature was increased to 40°C and measurements were repeated. The brain was then cooled back to 37°C for a final set of normothermic measurements. Thereafter, brain biopsies were taken to determine the energy state of the brain. CMRO2 changed ∼6%/°C. CBF paralleled the change in CMRO2. Accordingly, the ratio of CBF to CMRO2 remained constant throughout at a value of 8 to 9, demonstrating maintained coupling. The brain energy state was normal at the end of the study. The authors conclude that postischemic CBF is modulated by the brain's metabolic needs.


1994 ◽  
Vol 267 (2) ◽  
pp. R355-R359 ◽  
Author(s):  
G. Kuhnen ◽  
C. Jessen

In species with a carotid rete, the arterial blood destined for the brain can be cooled on its passage through the rete. The temperature difference between the blood before the rete and the brain is termed selective brain cooling (SBC). The onset and degree of cooling depend on internal body temperature. The aim of this study was to determine the brain sites where the temperature signals driving SBC are generated. Thirty-six experiments were performed in three conscious goats, which were prepared with an arteriovenous shunt, carotid loops, and hypothalamic thermodes to manipulate the temperatures of the trunk (Ttr), the hypothalamus (Thyp), the extrahypothalamic brain (Texh), or the whole brain (Tbr). In all experiments, Ttr was clamped at 39.5 degrees C. The increase of SBC was 2.1 degrees C per 1 degree C increase of Tbr (gain = 2.1). The rise of Thyp at constant Texh yielded a gain of 1.6, whereas the gain of Texh at constant Thyp was 0.7. It is concluded that onset and degree of SBC are predominantly determined by temperature signals generated in the hypothalamus itself.


2006 ◽  
Vol 2 (3) ◽  
pp. 475-477 ◽  
Author(s):  
Graham Mitchell ◽  
Andrea Fuller ◽  
Shane K Maloney ◽  
Nicola Rump ◽  
Duncan Mitchell

Selective brain cooling (SBC) is defined as the lowering of brain temperature below arterial blood temperature. Artiodactyls employ a carotid rete, an anatomical heat exchanger, to cool arterial blood shortly before it enters the brain. The survival advantage of this anatomy traditionally is believed to be a protection of brain tissue from heat injury, especially during exercise. Perissodactyls such as horses do not possess a carotid rete, and it has been proposed that their guttural pouches serve the heat-exchange function of the carotid rete by cooling the blood that traverses them, thus protecting the brain from heat injury. We have tested this proposal by measuring brain and carotid artery temperature simultaneously in free-living horses. We found that despite evidence of cranial cooling, brain temperature increased by about 2.5 °C during exercise, and consistently exceeded carotid temperature by 0.2–0.5 °C. We conclude that cerebral blood flow removes heat from the brain by convection, but since SBC does not occur in horses, the guttural pouches are not surrogate carotid retes.


2020 ◽  
Vol 51 (4) ◽  
pp. 1220-1225
Author(s):  
Faraj & Al- Amery

Ascaridiosis is a very important parasitic disease of birds, it is caused by Ascaridia. This study was conducted to identify the Ascaridia species by microscopic and molecular assay in Baghdad city. One hundred and sixty fecal samples were collected from domestic pigeons during the period from 1/1/ 2019 to 31/3/ 2019.  Results showed that the rate of infection for Ascaridia spp. 15.62% by microscopic examination.  Significant difference was observed in infection rates between males and females pigeons. Fifty samples randomly selected and subjected to molecular diagnosis of Ascaridia  spp.. Molecular examination results, the total infection rate showed 16%(8/50). The eight  positive PCR products were sequenced and deposited in Gene bank data base, phylogenic analysis demonstrated that 4 sequences belongs to Ascaridia galli ( MK918635.1, MK918636.1, MK918847.1, MK919081.1), while 2 (MK919199.1, MK919200.1) belong to  Ascaridia nymphii and 2 (MK919207.1, MK919264.1)  belong to Ascaridia numidae. It is the first study in Iraq to diagnosis of  Ascaridia nymphii and Ascaridia numidae  in domesticed pigeons by using conventional PCR.


Pathogens ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 440
Author(s):  
Imron Rosyadi ◽  
Siti Isrina Oktavia Salasia ◽  
Bayanzul Argamjav ◽  
Hiroshi Sato

Pigeon haemoproteosis caused by Haemoproteus columbae (Apicomplexa: Haemosporida: Haemoproteidae) is globally prevalent in rock doves (Columba livia), although little is known regarding this disease in pigeons and doves in Indonesia. Blood samples of 35 farmed domestic pigeons (C. livia f. domestica) from four localities in Yogyakarta Special Region, Central Java, Indonesia, were collected from March to June, 2016, subjected to a hemogram, and analyzed for the presence of hemoprotozoan infections. Microscopic examination of blood smears revealed a prevalence of 62.5–100% of H. columbae at the four localities (n = 8–10 for each locality), and geometric means of 3.0–5.6% of erythrocytes were parasitized by young and mature gametocytes, suggesting that all infected pigeons were in the chronic phase of infection with repeated recurrences and/or reinfections. Nucleotide sequencing of mitochondrial cytochrome b gene (cytb) for haemosporidian species demonstrated the distribution of four major cytb lineages of H. columbae (mainly HAECOL1, accompanied by COLIV03, COQUI05, and CXNEA02 according to the MalAvi database). Hemogram analysis, involving the estimation of packed cell volume, erythrocyte counts, mean corpuscular volume, mean corpuscular hemoglobin concentration, and plasma protein and fibrinogen levels of 20 parasitized pigeons and five non-infected pigeons demonstrated significant macrocytic hypochromic anemia with hypoproteinemia and hyperfibrinogenemia in the infected pigeons. This study shows the profound impact of long-lasting subclinical pigeon haemoproteosis caused by H. columbae on the health of farmed domestic pigeons.


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