Systematization, distribution and territory of the caudal cerebral artery on the brain's surface of the turkey (Meleagris gallopavo)

Thirty Meleagris gallopavo heads with their neck segments were used. Animals were contained and euthanized with the association of mebezonium iodide, embutramide and tetracaine hydrochloride (T 61, Intervet ) by intravenous injection. The arterial system was rinsed with cold saline solution (15°C), with 5000IU heparin and filled with red-colored latex. The samples were fixed in 20% formaldehyde for seven days. The brains were removed with a segment of cervical spinal cord and after, the dura-mater was removed and the arteries dissected. The cerebral carotid arteries, after the intercarotid anastomosis, were projected around the hypophysis, until they reached the tuber cinereum and divided into their terminal branches, the caudal branch and the rostral branch. The rostral branch was projected rostrolateralwards and gave off, in sequence, two collateral branches, the caudal cerebral and the middle cerebral arteries and the terminal branch was as cerebroethmoidal artery. The caudal cerebral artery of one antimere formed the interhemispheric artery, which gave off dorsal hemispheric branches to the convex surface of both antimeres. Its dorsal tectal mesencephalic branch, of only one antimere, originated the dorsal cerebellar artery. In the interior of the cerebral transverse fissure, after the origin of the dorsal tectal mesencephalic artery, the caudal cerebral artery emitted occipital hemispheric branches, pineal branches and medial hemispheric branches, on both antimeres. The caudal cerebral artery's territory comprehended the entire surface of the dorsal hemioptic lobe, the rostral surface of the cerebellum, the diencephalic structures, the caudal pole and the medial surface of the cerebral hemisphere and in the convex surface, the sagittal eminence except for its most rostral third. Due to the asymmetry found in the caudal cerebral arteries' ramifications, the models were classified into three types and their respective subtypes.

Is there any influence of breastfeeding on the cerebral blood flow? A review of 256 healthy newborns

OBJECTIVE: To investigate whether breastfeeding influence the cerebral blood-flow velocity. MATERIALS AND METHODS: The present study included 256 healthy term neonates, all of them with appropriate weight for gestational age, 50.8% being female. Pulsatility index, resistance index and mean velocity were measured during breastfeeding or resting in the anterior cerebral artery, in the left middle cerebral artery, and in the right middle cerebral artery of the neonates between their first 10 and 48 hours of life. The data were analyzed by means of a paired t-test, Brieger's f-test for analysis of variance and linear regression, with p < 0.01 being accepted as statistically significant. RESULTS: Mean resistance index decreased as the mean velocity increased significantly during breastfeeding. Pulsatility index values decreased as much as the resistance index, but in the right middle cerebral artery it was not statistically significant. CONCLUSION: Breastfeeding influences the cerebral blood flow velocities.

Systematization, description and territory of the caudal cerebral artery of the brain in broad-snouted Caiman (Caiman latirostris)

Thirty heads with the neck segment of Caiman latirostris were used. The animals were provided from a creation center called Mister Caiman, under the authorization of the Brazilian Institute of Environment and Renewable Natural Resources (Ibama). Animals were sacrificed according to the slaughtering routine of the abattoir, and the heads were sectioned at the level of the third cervical vertebra. The arterial system was washed with cold saline solution, with drainage through jugular veins. Subsequently, the system was filled with red colored latex injection. Pieces were than fixed in 20% formaldehyde, for seven days. The brains were removed, with a spinal cord segment, the duramater removed and the arteries dissected. At the level of the hypophysis, the internal carotid artery gave off a rostral branch, and a short caudal branch, continuing, naturally, as the caudal cerebral artery. This artery projected laterodorsalwards and, as it overpassed the optic tract, gave off its I (the first) central branch. Penetrated in the cerebral transverse fissure, emitting the diencephalic artery and next its II (second) central branch. Still inside the fissure, originated occipital hemispheric branches and a pineal branch. Emerged from the cerebral transverse fissure, over the occipital pole of the cerebral hemisphere. Projected rostralwards, sagital to the cerebral longitudinal fissure, as interhemispheric artery. This artery gave off medial and convex hemispheric branches to the respective surfaces of the cerebral hemispheres, anastomosed with its contralateral homologous, forming the common ethmoidal artery. This artery entered the fissure between the olfactory peduncles, emerging ventrally and dividing into ethmoidal arteries, right and left, which progressed towards the nasal cavities, vascularizing them. The territory of the caudal cerebral artery included the most caudal area of the base of the cerebral hemisphere, its convex surface, the olfactory peduncles and bulbs, the choroid plexuses and the diencephalus with its parietal organs.

Retinal protective effects of topically administered agmatine on ischemic ocular injury caused by transient occlusion of the ophthalmic artery

Agmatine, an endogenous polyamine and putative neuromodulator, is known to have neuroprotective effects on various neurons in the central nervous system. We determined whether or not topically administered agmatine could reduce ischemic retinal injury. Transient ocular ischemia was achieved by intraluminal occlusion of the middle cerebral artery of ddY mice (30-35 g) for 2 h, which is known to also induce occlusion of the ophthalmic artery. In the agmatine group (N = 6), a 1.0 mM agmatine-containing ophthalmic solution was administered four times daily for 2 weeks before occlusion. In the control group (N = 6), a 0.1% hyaluronic acid ophthalmic solution was instilled at the same times. At 22 h after reperfusion, the eyeballs were enucleated and the retinal sections were stained by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Transient ocular ischemia induced apoptosis of retinal cells in the entire retinal layer, and topically administered agmatine can significantly reduce this ischemic retinal injury. The proportion of apoptotic cells was definitely decreased (P < 0.001; Kruskal-Wallis test). Overall, we determined that topical agmatine application effectively decreases retinal damage in an in vivo ocular ischemic injury model. This implies that agmatine is a good candidate as a direct neuroprotective agent for eyes with ocular ischemic diseases.

A systematic study of the brain base arteries in the turkey (Meleagris gallopavo)

Thirty heads with neck segments of turkeys (Meleagris gallopavo) were dissected for a systematic study of the arteries. The frequency of the arteries found was: Cerebral carotid artery, intercarotid anastomosis and internal ophthalmic artery (100%). Caudal branch of the cerebral carotid artery to the right (R) vestigial artery (70%) and developed (30%) and to the left (L) developed (70%) and vestigial artery (30%). Ventral tectal mesencephalic artery in (70%) to R and (30%) to L was the direct branch of the cerebral carotid artery to L (70%) and to R (30%) collateral branch of the developed caudal branch. Basilar artery to L in (70%) and to R (30%) formed from the developed caudal branch; rostral ventral cerebellar artery present (86.7%) and absent (13.3%) to R and L. Caudal ventral cerebellar artery to R single (73.3%), double (23.3%) and triple (3.3%); caudal ventral cerebellar artery to L single (73.3%) and double (26.7%). Dorsal spinal artery branch of caudal ventral cerebellar artery to R (80%) and to L (73.3%). The rostral branch of cerebral carotid artery showed as collateral branches the single caudal cerebral artery to R (100%) and to L (96.7%) while in (3.3%) it was double. The middle cerebral artery was single to R and L (100%). Cerebroethmoidal artery to R and L (100%) with its collateral branch to single rostral cerebral artery (90%) to R and (86.7%) to L and double (10%) to R and (13.3%) to L. Ethmoidal artery to R and to L (100%) single. The cerebral arterial circle was rostrally and caudally opened, so that the cerebral blood supply was exclusively made by the carotid system.

A systematic study of the brain base arteries in the rabbit (Oryctolagus cuniculus)

The brains of 30 New Zealand rabbits (Oryctolagus cuniculus) were injected with red stained latex. The arteries of the ventral surface of the brain were systematized on the right (R) and on the left (L) side with the respective percentage of appearance: the aortic arch emitted the braquicephalic trunk and the left subclavian artery (83.3%); or the braquicephalic trunk, the left common carotid artery and the left subclavian artery (16.7%). The braquicephalic trunk emitted the right and the left common carotid arteries and the right subclavian artery (83.3%); or the right common carotid artery and the right subclavian artery (16.7%). The common carotid arteries were divided into external and internal carotid arteries (96.7% on the R, 100% on the L.). The internal carotid artery to the R was present (96.7%) and absent (3.3%), and to the L, was present (100%). The rostral choroidal artery to the R was collateral branch of the rostral branch of the internal carotid artery (83.3%), collateral branch of caudal branch of the internal carotid artery (16.7%), and to the L was collateral branch of the rostral branch of the internal carotid artery (93.3%), collateral branch of the caudal branch of the internal carotid artery (6.7%). The middle cerebral artery to the R and to the L was single (80%) and double (20%). The rostral cerebral artery to the R had middle caliber (90%), thin caliber (6.7%) and too thin caliber (3.3%), and to the L had middle caliber (76.7%), thin caliber (16.7%) and too thin caliber (6.7%). The internal ethmoidal artery was absent (73.3%), present and single (26.7%). The caudal cerebral artery to the R was single (66.7%), double (26.7%) and triple (6.7%), and to the L was single (63.3%) and double (36.7%). The terminal branches of the right and left vertebral arteries were present (100%, and formed the basilar artery (100%). The ventral spinal artery was present (100%). The caudal cerebellar artery, to the R was single (43.3%), single with labyrinthic artery isolated (26.7%) and double (30%), and to the L was single (50%), single with labyrinthic artery isolated (6.7%), double (40%) and triple (3.3%). The trigeminal artery to the R and to the L was present (100%). The rostral cerebellar artery to the R was single (53.3%) and double (46,7%), and to the L was single (63.3%) and double (36.7%). The rabbit's cerebral arterial circle was caudally closed (100%) and rostrally closed (93.3%) or opened (6.7%). The brain was supplied by the vertebral-basilar and carotid systems.

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5°C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 ± 1.14 to 73.62 ± 8.99%, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 ± 5.02 vs 63.26 ± 11.97%, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.

A forced running wheel system with a microcontroller that provides high-intensity exercise training in an animal ischemic stroke model

We developed a forced non-electric-shock running wheel (FNESRW) system that provides rats with high-intensity exercise training using automatic exercise training patterns that are controlled by a microcontroller. The proposed system successfully makes a breakthrough in the traditional motorized running wheel to allow rats to perform high-intensity training and to enable comparisons with the treadmill at the same exercise intensity without any electric shock. A polyvinyl chloride runway with a rough rubber surface was coated on the periphery of the wheel so as to permit automatic acceleration training, and which allowed the rats to run consistently at high speeds (30 m/min for 1 h). An animal ischemic stroke model was used to validate the proposed system. FNESRW, treadmill, control, and sham groups were studied. The FNESRW and treadmill groups underwent 3 weeks of endurance running training. After 3 weeks, the experiments of middle cerebral artery occlusion, the modified neurological severity score (mNSS), an inclined plane test, and triphenyltetrazolium chloride were performed to evaluate the effectiveness of the proposed platform. The proposed platform showed that enhancement of motor function, mNSS, and infarct volumes was significantly stronger in the FNESRW group than the control group (P<0.05) and similar to the treadmill group. The experimental data demonstrated that the proposed platform can be applied to test the benefit of exercise-preconditioning-induced neuroprotection using the animal stroke model. Additional advantages of the FNESRW system include stand-alone capability, independence of subjective human adjustment, and ease of use.

Endothelium-dependent and -independent hepatic artery vasodilatation is not impaired in a canine model of liver ischemia-reperfusion injury

We investigated whether hepatic artery endothelium may be the earliest site of injury consequent to liver ischemia and reperfusion. Twenty-four heartworm-free mongrel dogs of either sex exposed to liver ischemia/reperfusion in vivo were randomized into four experimental groups (N = 6): a) control, sham-operated dogs, b) dogs subjected to 60 min of ischemia, c) dogs subjected to 30 min of ischemia and 60 min of reperfusion, and d) animals subjected to 45 min of ischemia and 120 min of reperfusion. The nitric oxide endothelium-dependent relaxation of hepatic artery rings contracted with prostaglandin F2a and exposed to increasing concentrations of acetylcholine, calcium ionophore A23187, sodium fluoride, phospholipase-C, poly-L-arginine, isoproterenol, and sodium nitroprusside was evaluated in organ-chamber experiments. Lipid peroxidation was estimated by malondialdehyde activity in liver tissue samples and by blood lactic dehydrogenase (LDH), serum aspartate aminotransferase (AST) and serum alanine aminotransferase (ALT) activities. No changes were observed in hepatic artery relaxation for any agonist tested. The group subjected to 45 min of ischemia and 120 min of reperfusion presented marked increases of serum aminotransferases (ALT = 2989 ± 1056 U/L and AST = 1268 ± 371 U/L; P < 0.01), LDH = 2887 ± 1213 IU/L; P < 0.01) and malondialdehyde in liver samples (0.360 ± 0.020 nmol/mgPT; P < 0.05). Under the experimental conditions utilized, no abnormal changes in hepatic arterial vasoreactivity were observed: endothelium-dependent and independent hepatic artery vasodilation were not impaired in this canine model of ischemia/reperfusion injury. In contrast to other vital organs and in the ischemia/reperfusion injury environment, dysfunction of the main artery endothelium is not the first site of reperfusion injury.

Bilateral carotid endarterectomy combined with myocardial revascularization during the same surgical act

The best surgical approach for the treatment of patients with severe cerebral artery disease and simultaneous serious coronary artery disease still remains controversial. In this report we present a case of a 72-year-old female patient admitted to the hospital with unstable angina. Triple coronary artery obstructive disease and severe bilateral carotid artery stenosis were diagnosed. A combined, simultaneous surgical procedure was performed. After total circulatory by-pass with a membrane oxygenator, the patient's body temperature was lowered to 32°C. During the cool-down period, three proximal anastomoses of segments of autologous saphenous veins were performed in the ascending aorta. Immediately afterwards, bilateral carotid endarterectomy was performed, followed by three distal anastomoses to coronary arteries. The patient showed a satisfactory post-operative outcome. It was concluded that the combination of moderate hypothermia, hemodilution with appropriate hemodynamic control, as used in this patient, was an effective method of cerebral protection. The simultaneous approach of carotid endarterectomy and coronary artery by-pass surgery should be seen as a safe option for the treatment of this type of patient.

Atropine and ODQ antagonize tetanic fade induced by L-arginine in cats

Although it has been demonstrated that nitric oxide (NO) released from sodium nitrite induces tetanic fade in the cat neuromuscular preparations, the effect of L-arginine on tetanic fade and its origin induced by NO have not been studied in these preparations. Furthermore, atropine reduces tetanic fade induced by several cholinergic and anticholinergic drugs in these preparations, whose mechanism is suggested to be mediated by the interaction of acetylcholine with inhibitory presynaptic muscarinic receptors. The present study was conducted in cats to determine the effects of L-arginine alone or after pretreatment with atropine or 1H-[1,2,4]oxadiazole [4,3-a]quinoxalin-1-one (ODQ) on neuromuscular preparations indirectly stimulated at high frequency. Drugs were injected into the middle genicular artery. L-arginine (2 mg/kg) and S-nitroso-N-acetylpenicillamine (SNAP; 16 µg/kg) induced tetanic fade. The Nw-nitro-L-arginine (L-NOARG; 2 mg/kg) alone did not produce any effect, but reduced the tetanic fade induced by L-arginine. D-arginine (2 mg/kg) did not induce changes in tetanic fade. The tetanic fade induced by L-arginine or SNAP was reduced by previous injection of atropine (1.0 µg/kg) or ODQ (15 µg/kg). ODQ alone did not change tetanic fade. The data suggest that the NO-synthase-GC pathway participates in the L-arginine-induced tetanic fade in cat neuromuscular preparations. The tetanic fade induced by L-arginine probably depends on the action of NO at the presynaptic level. NO may stimulate guanylate cyclase increasing acetylcholine release and thereby stimulating presynaptic muscarinic receptors.

Validation of a simple and inexpensive method for the quantitation of infarct in the rat brain

A gravimetric method was evaluated as a simple, sensitive, reproducible, low-cost alternative to quantify the extent of brain infarct after occlusion of the medial cerebral artery in rats. In ether-anesthetized rats, the left medial cerebral artery was occluded for 1, 1.5 or 2 h by inserting a 4-0 nylon monofilament suture into the internal carotid artery. Twenty-four hours later, the brains were processed for histochemical triphenyltetrazolium chloride (TTC) staining and quantitation of the schemic infarct. In each TTC-stained brain section, the ischemic tissue was dissected with a scalpel and fixed in 10% formalin at 0ºC until its total mass could be estimated. The mass (mg) of the ischemic tissue was weighed on an analytical balance and compared to its volume (mm³), estimated either by plethysmometry using platinum electrodes or by computer-assisted image analysis. Infarct size as measured by the weighing method (mg), and reported as a percent (%) of the affected (left) hemisphere, correlated closely with volume (mm³, also reported as %) estimated by computerized image analysis (r = 0.88; P < 0.001; N = 10) or by plethysmography (r = 0.97-0.98; P < 0.0001; N = 41). This degree of correlation was maintained between different experimenters. The method was also sensitive for detecting the effect of different ischemia durations on infarct size (P < 0.005; N = 23), and the effect of drug treatments in reducing the extent of brain damage (P < 0.005; N = 24). The data suggest that, in addition to being simple and low cost, the weighing method is a reliable alternative for quantifying brain infarct in animal models of stroke.

Ionic radiocontrast inhibits endothelium-dependent vasodilation of the canine renal artery in vitro: possible mechanism of renal failure following contrast medium infusion

To determine if radiocontrast impairs vascular relaxation of the renal artery, segments (4-5 mm in length) of canine renal artery were suspended in vitro in organ chambers to measure isometric force (95% O2/5% CO2, at 37ºC). Arterial segments with and without endothelium were placed at the optimal point of their length-tension relation and incubated with 10 µM indomethacin to prevent synthesis of endogenous prostanoids. The presence of nonionic radiocontrast (iohexol, Omnipaque 350, 1 ml in 25 ml control solution, 4% (v/v)) did not alter endothelium-dependent relaxation to acetylcholine in rings precontracted with both norepinephrine and prostaglandin F2alpha (N = 6). When the rings were precontracted with prostaglandin F2alpha, the presence of ionic contrast did not inhibit the relaxation of the arteries. However, in canine renal arteries contracted with norepinephrine, the presence of ionic radiocontrast (diatrizoate meglumine and diatrizoate sodium, MD-76, 1 ml in 25 ml control solution, 4% (v/v)) inhibited relaxation in response to acetylcholine, sodium nitroprusside (N = 6 in each group), and isoproterenol (N = 5; P < 0.05). Rings were relaxed less than 50% of norepinephrine contraction. Following removal of the contrast, vascular relaxation in response to the agonists returned to normal. These results indicate that ionic radiocontrast nonspecifically inhibits vasodilation (both cAMP-mediated and cGMP-mediated) of canine renal arteries contracted with norepinephrine. This reversible impairment of vasodilation could inhibit normal renal perfusion and act as a mechanism of renal failure following radiocontrast infusion. In the adopted experimental protocol the isoproterenol-induced relaxation of renal arteries precontracted with norepinephrine was more affected, suggesting a pivotal role of the cAMP system.

Radiographic aspects and angioarchitectural arrangements in corrosion casts of the blood supply to the human sternocleidomastoid muscle by the sternocleidomastoid branch of the occipital artery

The contribution of the sternocleidomastoid branch of the occipital artery (superior arterial pedicle - SAP) to the irrigation of the sternocleidomastoid muscle (SCM) was evaluated in fresh human cadavers by injecting radiological dye and a resin for microvasculature corrosion casts. From its insertion in the mastoid process of the temporal bone, the SCM was divided into superior, medium, and inferior thirds. In most of the SCM, The SAP are formed by two longitudinal parallel branches. In all specimens, the radiological dye injected into the SAP reached or trespassed the middle part of the studied SCM. The SAP was poorly distributed in the lowermost region of the inferior third of the SCM, suggesting the contribution of other arteries or pedicles. The corrosion casts of the microvasculature showed a profuse network of microscopic vessels in those levels where the SAP was detected.

Myocardial Bridges and their Relationship to the Anterior Interventricular Branch of the Left Coronary Artery

OBJECTIVE: To analyze the relationship between myocardial bridges and the anterior interventricular branch (anterior descending) of the left coronary artery. METHODS: The study was carried out with postmortem material, and methods of dissection and observation were used. We assessed the perimeter of the anterior interventricular branch of the left coronary artery using a pachymeter, calculated its proximal and distal diameters in relation to the myocardial bridge, and also its diameter under the myocardial bridge in 30 hearts. We also observed the position of the myocardial bridge in relation to the origin of the anterior interventricular branch. RESULTS: The diameters of the anterior interventricular branch were as follows: the mean proximal diameter was 2.76±0.76 mm; the mean diameter under the myocardial bridge was 2.08±0.54 mm; and the mean distal diameter was 1.98±0.59 mm. In 33.33% (10/30) of the cases, the diameter of the anterior interventricular branch under the myocardial bridge was lower than the diameter of the anterior interventricular branch distal to the myocardial bridge. In 3.33% (1/30) of the cases, an atherosclerotic plaque was found in the segment under the myocardial bridge. The myocardial bridge was located in the middle third of the anterior interventricular branch in 86.66% (26/30) of the cases. CONCLUSION: Myocardial bridges are more frequently found in the middle third of the anterior interventricular branch of the left coronary artery. The diameter of the anterior interventricular branch of the left coronary artery under the myocardial bridge may be smaller than after the bridge. Myocardial bridges may not provide protection against the formation of atherosclerotic plaque inside the anterior interventricular branch of the left coronary artery.