Cardiorespiratory adjustments of homing pigeons to steady wind tunnel flight.

We made detailed cardiorespiratory measurements from homing pigeons during quiet rest and steady wind tunnel flight. Our pigeons satisfied their 17.4-fold increase in oxygen consumption during flight with a 7.4-fold increase in cardiac output (Q) and a 2.4-fold increase in blood oxygen extraction. Q was increased primarily by increasing heart rate sixfold. Comparisons between our study and those from the only other detailed cardiorespiratory study on flying birds reveal a number of similarities and important differences. Although the avian allometric equations from this earlier study accurately predicted the flight Q of our pigeons, this was primarily due to due to compensating discrepancies in their heart rate and stroke volume predictions. Additionally, the measured heart mass (MH)-specific Q (Q/MH) of our pigeons during wind tunnel flight was about 22% lower than the estimated value. Compared to running mammals in previous studies, the 1.65-fold Q of our pigeons is consistent with their larger heart mass.

Administration of adenosine receptor agonists or antagonists after controlled cortical impact in mice: effects on function and histopathology.

Adenosine is an endogenous neuroprotectant via anti-excitotoxic effects at A(1) receptors, and blood flow promoting and anti-inflammatory effects at A(2a) receptors. Previous studies showed improved motor function after fluid percussion injury (FPI) in rats treated with the broad-spectrum adenosine receptor agonist 2-chloroadenosine (2-CA). We studied the effects of 2-CA, a specific A(1) agonist (2-chloro-N(6)-cyclopentyladenosine, CCPA), and a specific A(1) antagonist (8-cyclopentyl-1,3-dipropylxanthine, DPCPX) on motor task and Morris water maze (MWM) performance, and histopathology (contusion volume, hippocampal cell counts) after controlled cortical impact (CCI) in mice. Each agent (12 nmol), or respective vehicle (saline or DMSO) was injected into dorsal hippocampus beneath the contusion immediately after CCI or craniotomy (sham). 2-CA treatment attenuated wire grip deficits after CCI (P<0.05 versus other treatments). DPCPX treatment exacerbated deficits on beam balance (P<0.05 versus sham). No treatment effect was seen on MWM performance, although there was a deleterious effect of the DMSO vehicle used for DPCPX. Contusion volume tended to be attenuated by 2-CA (P=0.08 versus saline) and increased after either DMSO or DPCPX (P<0.05 versus all groups). CA1 and CA3 counts were decreased in all groups versus sham. However, treatment with the selective A(1) agonist CCPA attenuated the CA3 cell loss (P<0.05 versus other treatment). We suggest that the beneficial effect of the broad spectrum adenosine receptor agonist 2-CA on motor function after CCI is not mediated solely by effects at the A(1) receptor.