Novel vascular plexus in the head of a sea snake (Elapidae, Hydrophiinae) revealed by high-resolution computed tomography and histology

Novel phenotypes are often linked to major ecological transitions during evolution. Here, we describe for the first time an unusual network of large blood vessels in the head of the sea snake Hydrophis cyanocinctus . MicroCT imaging and histology reveal an intricate modified cephalic vascular network (MCVN) that underlies a broad area of skin between the snout and the roof of the head. It is mostly composed of large veins and sinuses and converges posterodorsally into a large vein (sometimes paired) that penetrates the skull through the parietal bone. Endocranially, this blood vessel leads into the dorsal cerebral sinus, and from there, a pair of large veins depart ventrally to enter the brain. We compare the condition observed in H. cyanocinctus with that of other elapids and discuss the possible functions of this unusual vascular network. Sea snakes have low oxygen partial pressure in their arterial blood that facilitates cutaneous respiration, potentially limiting the availability of oxygen to the brain. We conclude that this novel vascular structure draining directly to the brain is a further elaboration of the sea snakes' cutaneous respiratory anatomy, the most likely function of which is to provide the brain with an additional supply of oxygen.

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Regional blood flow in the brain and spinal cord of hypothermic rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.3.h785 ◽

1989 ◽

Vol 257 (3) ◽

pp. H785-H790

Author(s):

T. Sakamoto ◽

W. W. Monafo

Keyword(s):

Spinal Cord ◽

Blood Flow ◽

Brain Stem ◽

Regional Blood Flow ◽

Experimental Conditions ◽

Pentobarbital Sodium ◽

Arterial Blood ◽

Group A ◽

Group B ◽

The Brain

[14C]butanol tissue uptake was used to measure simultaneously regional blood flow in three regions of the brain (cerebral and cerebellar hemispheres and brain stem) and in five levels of the spinal cord in 10 normothermic rats (group A) and in 10 rats in which rectal temperature had been lowered to 27.7 +/- 0.3 degrees C by applying ice to the torso (group B). Pentobarbital sodium anesthesia was used. Mean arterial blood pressure varied minimally between groups as did arterial pH, PO2, and PCO2. In group A, regional spinal cord blood flow (rSCBF) varied from 49.7 +/- 1.6 to 62.6 +/- 2.1 ml.min-1.100 g-1; in brain, regional blood flow (rBBF) averaged 74.4 +/- 2.3 ml.min-1.100 g-1 in the whole brain and was highest in the brain stem. rSCBF in group B was elevated in all levels of the cord by 21-34% (P less than 0.05). rBBF, however, was lowered by 21% in the cerebral hemispheres (P less than 0.001) and by 14% in the brain as a whole (P less than 0.05). The changes in calculated vascular resistance tended to be inversely related to blood flow in all tissues. We conclude that rBBF is depressed in acutely hypothermic pentobarbital sodium-anesthetized rats, as has been noted before, but that rSCBF rises under these experimental conditions. The elevation of rSCBF in hypothermic rats confirms our previous observations.

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Use of 19F NMR Spectroscopy for Measurement of Cerebral Blood Flow: A Comparative Study Using Microspheres

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1989.122 ◽

1989 ◽

Vol 9 (6) ◽

pp. 886-891 ◽

Cited By ~ 31

Author(s):

David Barranco ◽

Leslie N. Sutton ◽

Sandra Florin ◽

Joel Greenberg ◽

Teresa Sinnwell ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Arterial Blood ◽

Radioactive Microsphere ◽

Low Concentrations ◽

Cat Brain ◽

Nmr Techniques ◽

High Concentrations ◽

Washout Curves ◽

The Brain

19F NMR was used to determine washout curves of an inert, diffusible gas (CHF3) from the cat brain. The cerebral blood flow was estimated from a bi- or tri-phasic fit to the deconvoluted wash-out curve, using the Kety-Schmidt approach. Cerebral blood flow values determined by 19F NMR show the expected responsiveness to alterations in Paco2, but are approximately 28% lower than cerebral blood flow values determined simultaneously by radioactive microsphere techniques. High concentrations of CHF3 have little effect on intracranial pressure, mean arterial blood pressure or Paco2, but cause small changes in the blood flow to certain regions of the brain. We conclude that 19F NMR techniques utilizing low concentrations of CHF3 have potential for the noninvasive measurement of cerebral blood flow.

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Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1979.237.3.h381 ◽

1979 ◽

Vol 237 (3) ◽

pp. H381-H385 ◽

Cited By ~ 4

Author(s):

E. F. Ellis ◽

E. P. Wei ◽

H. A. Kontos

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Arterial Blood Pressure ◽

Standard Error ◽

Arterial Blood ◽

Cerebral Arterioles ◽

The Mean ◽

Dose Dependent ◽

The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

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Vascular pressures and cortical blood flow in cavernous angioma of the brain

Journal of Neurosurgery ◽

10.3171/jns.1990.73.4.0555 ◽

1990 ◽

Vol 73 (4) ◽

pp. 555-559 ◽

Cited By ~ 69

Author(s):

John R. Little ◽

Issam A. Awad ◽

Stephen C. Jones ◽

Zeyd Y. Ebrahim

Keyword(s):

Blood Flow ◽

Cavernous Angioma ◽

Sitting Position ◽

Cortical Blood Flow ◽

Content Type ◽

Cavernous Angiomas ◽

Arterial Blood ◽

Mean Pressure ◽

Local Cortical Blood Flow ◽

The Brain

✓ This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (± standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 ± 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 ± 0.6 torr. Mean CO2 reactivity was 1.1 ± 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 ± 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.

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Incidental capture of sea-snakes (Hydrophiidae) by prawn trawlers in the Gulf of Carpentaria, Australia

Marine and Freshwater Research ◽

10.1071/mf9940429 ◽

1994 ◽

Vol 45 (3) ◽

pp. 429 ◽

Cited By ~ 15

Author(s):

TJ Wassenberg ◽

JP Salini ◽

H Heatwole ◽

JD Kerr

Keyword(s):

Survival Rate ◽

Coastal Waters ◽

Significant Interaction ◽

Catch Per Unit Effort ◽

Sea Snake ◽

Incidental Capture ◽

Seasonal Movement ◽

Sea Snakes ◽

Breeding Cycles ◽

Shallow Coastal Waters

Sea-snakes were collected from research trawlers and commercial prawn trawlers in the Gulf of Carpentaria during the period from April 1976 to December 1991. The data were analysed on the basis of CPUE (catch per unit effort) for depth, latitude and season. The research trawlers, operating in the eastern Gulf of Carpentaria, and the commercial prawn trawlers, operating in the south-western Gulf of Carpentaria, caught sea-snakes at a rate of 0.028 and 0.026 sea-snakes per metre of headrope length per hour, respectively. Lapemis hardwickii was the sea-snake most commonly caught by the research trawlers-53% of all snakes-and Hydrophis elegans was the sea-snake most commonly caught by commercial trawlers-25% of all snakes. Depth was the most significant factor affecting CPUE, with more than 70% of all sea-snakes being caught in waters less than 15 m deep. When catches of all species were combined, a significant interaction (P<0.05) existed between depth and season. L. hardwickii specimens were caught more frequently in shallow coastal waters (< 15 m deep) in spring but in deeper water further offshore in autumn. A significant interaction between latitude and depth was found for Astrotia stokesii; specimens were caught more frequently in deeper water at 14% Enhydrina schistosa is generally coastal, with 8800 of specimens being caught in water less than 10 m deep. Seasonal movement of sea-snakes between inshore and offshore waters may be linked to their breeding cycles. The estimated number of sea-snakes captured in the Gulf of Carpentaria for the 1991 prawning season ranged from 73 583 to 165 559, with a mean of 119 571. The survival rate of sea-snakes from commercial prawn trawls was about 60% and hence between 29 801 and 67 051 sea-snakes are estimated to have died.

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Abstract MP57: Chronic Inhibition Of Brain Rhomboid-like Protein 2 (irhom2) Activity Decreases Arterial Blood Pressure In Salt-sensitive Hypertension In Mice

Hypertension ◽

10.1161/hyp.78.suppl_1.mp57 ◽

2021 ◽

Vol 78 (Suppl_1) ◽

Author(s):

Mazher Mohammed ◽

Mona Elgazzaz ◽

Clara Berdasco ◽

Eric D Lazartigues

Keyword(s):

Blood Pressure ◽

Neutralizing Antibody ◽

Experimental Models ◽

Arterial Blood ◽

Artificial Cerebrospinal Fluid ◽

Tnf Α ◽

Significant Attenuation ◽

Factor Α ◽

Salt Sensitive Hypertension ◽

The Brain

We previously reported that ADAM17 (aka tumor necrosis factor-α convertase) is critical for the development of hypertension in experimental models and patients. Recent studies highlighted that ADAM17’s formation of TNF-α relies on prior maturation of this sheddase, controlled by the rhomboid-like protein 2 (iRhom2) specifically in microglia. Genetic deletion of iRhom2 in mice shows significant attenuation of TNF-α and ADAM17 activity in a tissue specific manner. Here, we hypothesized that silencing iRhom2 activity specifically in the brain would decrease blood pressure (BP) in the DOCA-salt model of hypertension, in mice. Uninephrectomized mice were implanted subcutaneously (sc) with DOCA-pellets (50 mg) and provided with 1% saline in drinking water. In addition, mice were chronically implanted with an icv cannula connected to a sc osmotic minipump for delivery of: (1) iRhom2-siRNA (9.6 μg/kg/day), (2) scrambled siRNA (SCR 0.2 μg/kg/day), (3) ADAM17 antibody (ADAM17-Ab; 23.8 μg/kg/day) or (4) artificial cerebrospinal fluid (aCSF) for 2 weeks while BP was recorded by telemetry. DOCA-salt treatment led to a significant increase in BP in the control groups (SCR: 156 ±3 mmHg and aCSF: 161 ±1 mmHg; n=3/group; p<0.001) compared to baseline values (122 ±2 mmHg; n=12). ICV infusion of iRhom2-siRNA or ADAM17 neutralizing antibody for 2-weeks in DOCA-salt-treated mice resulted in a significant attenuation of BP (iRhom2-siRNA: 152 ±2 mmHg and ADAM17-Ab: 151 ±2 mmHg n=3/group, p<0.001). These data suggest that: 1) Selective silencing of iRhom2 from microglia is as potent as ADAM17 neutralization throughout the brain in lowering BP and 2) iRhom2 is a potential new therapeutic target for the treatment of salt-sensitive hypertension.

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Abstract P790: Landiolol Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest in Mice

Stroke ◽

10.1161/str.52.suppl_1.p790 ◽

2021 ◽

Vol 52 (Suppl_1) ◽

Author(s):

Tomoyuki Iwai ◽

Shin Nakayama

Keyword(s):

Cardiac Arrest ◽

Water Content ◽

Cerebral Edema ◽

Ischemia Reperfusion ◽

Control Group ◽

P Value ◽

Brain Water Content ◽

Arterial Blood ◽

The Brain ◽

Brain Water

Introduction: Cerebral edema following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) is associated with unfavorable neurologic outcome. The Na + -K + -2Cl - water cotransporter NKCC1 is suspected to be a critical mediator of edema formation after ischemia. It is reported that β1 adrenoreceptor antagonists protect neurons following brain ischemia in rodents. β1 adrenoreceptor antagonists inhibit the Na + -K + -ATPase, which can inhibit driving force of NKCC1 that theoretically reduces cerebral edema following ischemia-reperfusion injury. In this study, we examined whether landiolol, a selective β1 adrenoreceptor antagonist, attenuates cerebral edema following CA/CPR. Methods: Isoflurane-anesthetized adult male mice (C57BL/6J, 25-30g) were randomized into landiolol group or control group. After 7-min CA followed by CPR, landiolol (0.5ml, 830μg/ml) was administered by continuous infusion intravenously for 4 hours. Animals in control group were given normal saline (0.5ml) in the same manner. Twenty-four hours after CA/CPR, the brain was removed to assess brain water content using wet-to-dry method. The primary outcome was measurement of the brain water content. Heart rate and arterial blood pressure were recorded. Measured parameters were analyzed by one-way ANOVA with post hoc Tukey-Kramer test using SPSS® statistics 25. Differences were considered statistically significant at a P value < 0.05. Results: Brain water contents was increased in control group mice after CA/CPR (n=10) compared with those in sham operated mice (n=5) (79.5±0.85% vs 78.3±0.14%, P=0.003). Compared with control group, landiolol treatment significantly reduced brain water content in mice subjected to CA/CPR (n=12) (78.9±0.51% vs 79.5±0.85%, P=0.04). Conclusion: Landiolol attenuated brain edema following CA/CPR. These results may suggest selective β1-blocker could be alternative treatment for neuroprotection in patients who suffered CA/CPR.

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Abstract 081: Reporter Mouse Strain Provides a Novel Look at Angiotensin Type-2 Receptor Distribution in Central Nervous System Cardiovascular Control Centers

Hypertension ◽

10.1161/hyp.64.suppl_1.081 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Annette D de Kloet ◽

Lei Wang ◽

Jacob A Ludin ◽

Helmut Hiller ◽

Justin A Smith ◽

...

Keyword(s):

Blood Pressure ◽

Fluid Balance ◽

Hypothalamic Nucleus ◽

Reporter Mouse ◽

Arterial Blood ◽

Egfp Reporter ◽

Angiotensin Type 2 Receptor ◽

The Brain ◽

Angiotensin Type

It is established that angiotensin-II acts at its type-1 receptor (AT1R) in the brain to increase sympathetic outflow and blood pressure, and modulate fluid balance. However, the role of the angiotensin type-2 receptor (AT2R) in the neural control of these processes has received far less attention, largely because of an inability to effectively localize these receptors at a cellular level in the brain. The present studies combine the use of a bacterial artificial chromosome transgenic AT2R-eGFP reporter mouse with recent advances in in situ hybridization (ISH) to circumvent this obstacle. Dual IHC/ ISH studies validated the AT2R-eGFP reporter mice by determining that eGFP and AT2R mRNA were highly co-localized within the nucleus of the solitary tract (NTS; 98.0 ± 0.18 %; 125 ± 3.6 of 127 ± 3.9 cells; n = 4). Analysis of eGFP immunoreactivity in the brain revealed localization to neurons within nuclei that regulate blood pressure and fluid balance (e.g., NTS and median preoptic nucleus [MnPO]). Additional IHC/ISH studies uncovered the phenotype of specific AT2R-eGFP cells. For example, within the NTS, AT2R-eGFP neurons primarily express glutamic acid decarboxylase-67 (GABAergic; 80 ± 2.8 %; 225 ± 12.5 of 280 ± 8.4 cells; n = 4), while only a subset express vesicular glutamate transporter-2 (glutamatergic; 18.2 ± 2.9 %; 50.8 ± 7.7 of 280 ± 8.4 cells) or AT1R (8.7 ± 1.0 %; 22 ± 2.2 of 256 ± 11.7 cells). No co-localization was observed with tyrosine hydroxylase in the NTS. Although AT2R-eGFP neurons were not observed within the paraventricular hypothalamic nucleus (PVN), eGFP was localized to efferents terminating in the PVN and to GABAergic neurons surrounding this nucleus. Retrograde neuronal tract tracing studies revealed that many eGFP-positive efferents to the PVN arise from neurons in the MnPO. Based on these neuroanatomical results, we hypothesized that activation of central AT2R would decrease blood pressure. Consistent with this hypothesis, chronic administration of the selective AT2R agonist, compound 21 (7.5 ng/h into the lateral cerebral ventricle) reduced baseline mean arterial blood pressure relative to control mice (103 ± 1.65 v. 110 ± 1.70 mmHg; n = 16; p = 0.02). These studies demonstrate that central AT2R are positioned to regulate blood pressure.

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Temperature Difference Between the Body Core and the Arterial Blood Supplied to the Brain During Hyperthermia or Hypothermia

10.1115/imece2001/htd-24418 ◽

2001 ◽

Author(s):

Liang Zhu ◽

Maithreyi Bommadevara

Keyword(s):

Blood Vessel ◽

Temperature Difference ◽

Carotid Arteries ◽

Brain Temperature ◽

Indirect Evidence ◽

Blood Perfusion ◽

The Body ◽

Arterial Blood ◽

Body Core ◽

The Brain

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.

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Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽

10.1542/peds.56.6.999 ◽

1975 ◽

Vol 56 (6) ◽

pp. 999-1004

Author(s):

Daniel C. Shannon ◽

Robert De Long ◽

Barry Bercu ◽

Thomas Glick ◽

John T. Herrin ◽

...

Keyword(s):

Metabolic Acidosis ◽

Venous Drainage ◽

Respiratory Alkalosis ◽

Ammonia Concentration ◽

Reye's Syndrome ◽

Acid Base ◽

Arterial Blood ◽

Cerebral Venous Drainage ◽

Acid Base Status ◽

The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

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