Two experiments were conducted to evaluate the effects of arginine, vitamin E, and their combination on cardiopulmonary performance and nitric oxide synthase (NOS) activity in broilers undergoing cold-induced ascites (pulmonary hypertension) after an acute challenge with epinephrine. One day-old male broilers ( n = 25/treatment) were supplemented with arginine (0.3% water supplementation), vitamin E (400 IU/L or kg, water or feed supplementation; experiment 1 and 2 respectively) or both compounds, above NRC (1994) recommendations. From day 28 to 42, a catheterization was performed (n = 8/treatment) to evaluate pulmonary and mean arterial pressures, and heart rate. After recording baseline values, two injections of epinephrine (1 or 0.5 mg/kg body weight, experiment 1 and 2, respectively) were administered in a 20 min interval. The NOS activity was estimated through the conversion of 14C-arginine to 14C-citrulline in isolated pulmonary arteries ( n = 8/treatment). Overall, the time taken for pulmonary arterial pressure to return to values no different from initial baseline levels was longer for the birds consuming high levels of vitamin E (alone or in combination with arginine) compared to birds supplemented only with arginine. Although NOS activity was highly variable, birds fed with high arginine levels tended to have the lowest NOS activity. These results showed that vitamin E supplementation at the levels used in these experiments has detrimental effects on cardiopulmonary performance, and does not improve NOS activity in isolated pulmonary arteries.

No description available.

The contribution of the cardiovascular system. to organophosphate-induced delayed neuropathy (OPIDN) was examined using in situ and in vitro models for demonstration of response to vasoactive agents (e.g., the cholinergic agonist, acetylcholine; the α1 agonist, phenylephrine; and the β2 agonist, salbutamol). These responses were compared before and 1, 3, 7, and 21 days after hens were administered cyclic phenyl saligenin phosphate (PSP, 2.5 mg/kg i.m.), an OP that induces OPIDN but does not significantly inhibit acetylcholinesterase activity, and paraoxon (PXN, 0.1 mg/kg i.m.), an OP that inhibits acetylcholinesterase activity but does not induce OPIDN. The capability of verapamil, a calcium channel blocker, to attenuate these responses was examined, as this agent ameliorates OPIDN. For the in situ study, the ischiadic artery was cannulated and alterations in pressure measured at a constant flow used to indicate changes in vascular resistance. Changes in vascular resistance in response to acetylcholine, phenylephrine, and salbutamol that were different from those in control and PXN-treated hens were noted 1 and 3 days after administration of PSP. These changes were attenuated in hens given PSP and verapamil. Vascular segments from the ischiadic artery were used to provide an in vitro model to determine if OPs caused direct vascular damage that was responsible for effects seen in the in situ model. In the in vitro model, however, responses of PSP and PXN were similar and not modified in vascular segments from hens given verapamil as well as the OPs. This indicated that the contribution of the cardiovascular system to OPIDN was due to more than a direct effect on relatively large caliber vessels. The contribution of the cardiovascular system to OPIDN also did not appear to relate to morphological changes induced by administration of OPs, as no changes in vascular morphology were noted. An OP-induced effect that could contribute to vascular effects noted are levels of plasma catecholamines. These levels were altered in hens given PSP or PXN, with increases seen after administration of PSP and decreases seen after administration of PXN. These alterations in plasma catecholamine levels were attenuated in hens given both verapamil and OP. / Ph. D.

In adult vertebrates, cardiovascular regulation is accomplished by numerous systems with neural, hormonal and local components responsible for the majority of regulation. These regulatory components work in concert to maintain the essential function of blood perfusion to adult tissues. Given the essential nature of this function it is therefore surprising that the development of cardiovascular regulation during gestation is poorly understood. The majority of what is known is based on a single vertebrate model, the fetal lamb. The fetal lamb has been used in multiple studies due to the clear clinical applications and has been pivotal in understanding the onset of regulation in developing vertebrates. However, study on the fetal lamb is limited to the latter 40% of gestation and has the added complication of an in-utero developmental strategy. Therefore the primary focus of this dissertation was to characterize basic cardiovascular regulation in the chicken embryo to provided the needed information for it's use an alternative to the fetal lamb. Developing chicken embryos rely on both alpha and beta adrenergic tones to maintain normal heart rate and arterial blood pressure during incubation. However, on day 21, just prior to hatch, these animals lose both tones on arterial pressure suggesting the onset of adult regulation. Cholinergic tone, however, was absent throughout chicken development indicating that it must mature during the neonatal life. Adult cardiovascular reflexes become apparent late in chicken development with a clear baroreflex specifically operating initially on day. However, an adult response to changes in ambient gas tension was absent during incubation suggesting embryos possess unique regulatory systems that are absent in adult chickens. This mechanism is comprised entirely of adrenergic systems with no cholinergic action during change in ambient gas tension. Similar developmental patterns were determined in embryos of the desert tortoise suggesting fundamental differences between in-utero and ex-utero developing vertebrates.

Two identical experiments were conducted to evaluate the combined effects of arginine (AR), vitamin E (VE) and vitamin C (VC) on cardiopulmonary performance and ascites parameters of broilers reared under cold environmental temperature. One d old male broilers were fed a basal corn-soybean meal diet (CTL, 1.2 % AR and 40 IU VE), the basal diet supplemented with 1% AR and either 200 IU VE (AE group), or 500 mg of VC (AC group), or a combination of VE and VC (AEC group) at the same level per kg of feed. Pulmonary arterial pressure (PAP) and mean arterial pressure (MAP) were recorded in clinically healthy anesthetized birds (28-42 d old) before and after an epinephrine challenge (EPI, 0.5 mg/kg BW i.v.), Amino-guanidine Hemisulphate (AG, 100 mg/kg BW i.v.) and N-Nitro L-Arginine Methyl Ester (L-NAME 50 mg/kg BW, i.v.) at 20 min intervals. The PAP increased 30 s after EPI in all birds, but the peak PAP was lower in the AEC group than in all the other birds. After 120 s of challenge the PAP was lower in AEC birds compared to the other birds. The PAP returned to pre-EPI levels within 300 s in all groups. The PAP was increased ( P< 0.05) within 60 s after the AG and L-NAME challenge in all groups, but no differences were found among groups. Plasma nitric oxide (NO) was higher in the AEC birds than in all the other groups before and after challenge. Our results showed that birds fed AEC maintained a lower PAP than the CTL birds after EPI elicited an increase in cardiac output and this can be explained by a higher production of NO. A combination of AR, VE, and VC may have complementary effects against oxidative stress, protecting the endothelium and preserving NO function.

The goal of this study was to build on the historic use of the avian model of development and also to further the knowledge of autonomic nervous system (ANS) regulation of cardiovascular function in vertebrates. Vasoactive drugs sodium nitroprusside, a vasodilator and phenylephrine, a vasoconstrictor were used to study the correlation of cardiovascular function relationship with nerve activity, both sympathetic and parasympathetic (vagal). Additionally, ANG II was used to assess its effects on vagal inhibition. The present study shows that pharmacologically-induced hypertension is associated with a fall in mSNA, indicating that the capacity for sympathetic autonomic cardiovascular regulation is established by late incubation however, late-stage embryonic chickens did not show a significant increase in mSNA during hypotension. The hypotensive response of the embryo was not accompanied by the expected inhibition of vagal discharge; however a slight but insignificant reduction in vagal discharge was noted. When vagal efferent output was isolated, a significant drop in vagal efferent activity was noted in response to hypotension. The present study showed late-stage embryonic chickens lack a vagal response to hypertension in both efferent and sensory limbs. In this study, vagal discharge was reduced from baseline levels in response to Ang II. Collectively, the present study indicates that the lack of a decreased heart rate, in response to increases in Pm caused by Ang II, is due to a central inhibitory action of Ang II on the vagus. Data from the present study suggests that although autonomic interaction with the cardiovascular system in present in late-stage chicken embryos, it is still underdeveloped and possesses a limited capacity.

No description available.