Topography of cat medullary ventral surface hypoxic acidification

The topographic relationship between previously identified medullary ventral surface respiratory chemosensitive regions and brain surface extracellular fluid (ECF) acid production during acute hypoxia was explored in anesthetized, paralyzed, and artificially ventilated cats. Glass pH electrodes (0.8-mm diam, sheathed in stainless steel tubing) were mounted in mechanical contact with surfaces of medullary surface or adjacent pyramids, pons, spinal cord, or parietal cortex. Isocapnic hypoxia of 5 min [at arterial O2 saturation (SaO2) = 48 +/- 10%] reduced pH over rostral (Mitchell) and caudal (Loeschcke) areas by 0.12 +/- 0.09 and 0.07 +/- 0.04, respectively (n = 10, P < 0.05). Change in pH (delta pH) was proportional to desaturation with slopes 100 delta pH/delta SaO2 of 0.45 (rostral) and 0.20 (caudal) (R = 0.91 and 0.88, respectively). pH drop usually began within 3 min of hypoxia, became stable between 5 and 15 min, began to rise within 2 min of reoxygenation, and returned to control within 10 min. During equally hypoxic tests, intermediate area (Schlafke), pons, and spinal cord surfaces showed no significant acid shift. Parietal cortex ECF pH dropped more slowly but steadily by 0.079 +/- 0.034 during 20 min at SaO2 = 50% after a small but significant initial alkaline shift, and acidification of cortical surface continued for > 5 min after reoxygenation. We conclude that medullary ventral chemosensitive regions produce more lactic acid during hypoxia than neighboring brain surfaces.(ABSTRACT TRUNCATED AT 250 WORDS)

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Anomalous hypoxic acidification of medullary ventral surface

Journal of Applied Physiology ◽

10.1152/jappl.1991.71.6.2211 ◽

1991 ◽

Vol 71 (6) ◽

pp. 2211-2217 ◽

Cited By ~ 11

Author(s):

F. D. Xu ◽

M. J. Spellman ◽

M. Sato ◽

J. E. Baumgartner ◽

S. F. Ciricillo ◽

...

Keyword(s):

Ventral Surface ◽

High Pco2 ◽

Nerve Roots ◽

Arterial Pco2 ◽

Glass Bulb ◽

Response Slope ◽

Left Posterior ◽

End Tidal ◽

Arterial O2 Saturation ◽

Ph Electrodes

In castrated male goats, two flexible catheters, one open ended for reference and the other ending in a 1-mm-diam glass bulb pH electrode, were advanced ventrally through a left posterior fossa craniotomy into the subarachnoid space between the 9th and 10th cranial nerve roots, passing medially into cerebrospinal fluid (CSF) over the medullary ventral surface (MVS). They were anchored to dura and fascia, tunneled under the scalp, and terminated in connectors on the left horn. After several days for recovery, while the animals were awake, the effects of CO2 and hypoxia on pH of the film of CSF between the pia and arachnoid (pHMVS) were recorded along with end-tidal PCO2 and PO2 (mass spectrometer), ventilation (pneumotachometer) through a permanent tracheostomy, and, when possible, ear arterial O2 saturation (SaO2). High PCO2 acidified MVS as expected: delta pH MVS/delta log PCO2. = -0.64 +/- 0.14, producing a ventilatory response slope delta VI/delta pHMVS = 372 l/min. Hypoxia resulted in acid shifts even when PCO2 was allowed to fall. The development of hypoxic acidosis was related to the location of pH electrodes determined at necropsy. In isocapnic hypoxia, pH over putative chemoreceptor surfaces fell in proportion to desaturation: delta pHMVS = 0.0033(SaO2)-0.34, r = 0.80, Sy.x = 0.025. With uncontrolled arterial PCO2, similar acidosis occurred when SaO2 fell below 85–90%: delta pHMVS = 0.0039(SaO2)-0.34, r = 0.88, Sy.x = 0.032. With constant hypoxia, pH fell (tau = 3.7 +/- 2.2 min) to a plateau after 10–20 min and showed rapid recovery (tau = 2.0 +/- 1.3 min).(ABSTRACT TRUNCATED AT 250 WORDS)

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Novel axonal projection from the caudal end of the ventrolateral medulla to the intermediolateral cell column

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00254.2006 ◽

2007 ◽

Vol 292 (2) ◽

pp. R927-R936 ◽

Cited By ~ 12

Author(s):

Kamon Iigaya ◽

Hiroo Kumagai ◽

Hiroshi Onimaru ◽

Akira Kawai ◽

Naoki Oshima ◽

...

Keyword(s):

Spinal Cord ◽

Optical Imaging ◽

Cross Sections ◽

Ventral Surface ◽

Ventrolateral Medulla ◽

Cell Column ◽

Spontaneously Hypertensive ◽

Optical Images ◽

Caudal Pressor ◽

Wistar Kyoto

We used an optical imaging technique to investigate whether axons of neurons in the caudal end of the ventrolateral medulla (CeVLM), as well as axons of neurons in the rostral ventrolateral medulla (RVLM), project to neurons in the intermediolateral cell column (IML) of the spinal cord. Brain stem-spinal cord preparations from neonatal normotensive Wistar-Kyoto and spontaneously hypertensive rats were stained with a voltage-sensitive dye, and responses to electrical stimulation of the IML at the Th2 level were detected as changes in fluorescence intensity with an optical imaging apparatus (MiCAM-01). The results were as follows: 1) depolarizing responses to IML stimulation during low-Ca high-Mg superfusion were detected on the ventral surface of the medulla at the level of the CeVLM, as well as at the level of the RVLM, 2) depolarizing responses were also detected on cross sections at the level of the CeVLM, and they had a latency of 24.0 ± 5.5 (SD) ms, 3) antidromic action potentials in response to IML stimulation were demonstrated in the CeVLM neurons where optical images were detected, and 4) glutamate application to the CeVLM increased the frequency of excitatory postsynaptic potentials (EPSPs) and induced depolarization of the IML neurons. The optical imaging findings suggested a novel axonal and functional projection from neurons in the CeVLM to the IML. The increase in EPSPs of the IML neurons in response to glutamate application suggests that the CeVLM participates in the regulation of sympathetic nerve activity and blood pressure and may correspond to the caudal pressor area.

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Identification of a subsurface area in the ventral medulla sensitive to local changes in PCO2

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.2.439 ◽

1992 ◽

Vol 72 (2) ◽

pp. 439-446 ◽

Cited By ~ 55

Author(s):

F. G. Issa ◽

J. E. Remmers

Keyword(s):

Spinal Cord ◽

Neural Activity ◽

Ventral Surface ◽

Sudden Increase ◽

Neonatal Rats ◽

Central Chemoreceptors ◽

Ventral Medulla ◽

Ventromedial Medulla ◽

Stimulation Of

The exact location of the central respiratory chemoreceptors sensitive to changes in PCO2 has not yet been determined. To avoid the confounding effects of the cerebral circulation, we used the in vitro brain stem-spinal cord of neonatal rats (1–5 days old) to identify areas within 500 microns of the ventral surface of the medulla where changes in PCO2 evoked a sudden increase in the rate of respiratory neural activity. The preparation was superfused with mock cerebrospinal fluid (CSF) while maintained at constant temperature (26 +/- 1 degrees C) and pH (7.34). Respiratory frequency increased linearly with decreases in superfusate pH (r2 = 0.92, P less than 0.001), indicating that the respiratory circuitry for the detection of CO2 and stimulation of breathing was intact in this preparation. The search for central chemoreceptors was performed with a specially designed micropipette that allowed microejection of 2–10 nl of mock CSF equilibrated with different CO2-O2 gas mixtures. The pipette was advanced in 50- to 100-microns steps by use of a microdrive to a maximum depth of 500 microns from the surface of the ventral medulla. Depending on the location of the micropipette, ejection of CO2-acidified mock CSF at depths of 100–350 microns below the ventral surface of the medulla stimulated neural respiratory output. Using this response as an indication of the location of central respiratory chemoreceptors, we found that chemoreceptive elements were located in a column in the ventromedial medulla extending from the hypoglossal rootlets caudally to an area 0.75 mm caudal to VI nerve in the rostral medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of acute hypoxia on respiration and brain stem blood flow in the piglet

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.1.251 ◽

1991 ◽

Vol 70 (1) ◽

pp. 251-259 ◽

Cited By ~ 10

Author(s):

R. A. Darnall ◽

G. Green ◽

L. Pinto ◽

N. Hart

Keyword(s):

Blood Flow ◽

Brain Stem ◽

Minute Ventilation ◽

Acute Hypoxia ◽

Extracellular Fluid ◽

Respiratory Drive ◽

Peripheral Chemoreceptor ◽

Before And After ◽

Spontaneously Breathing ◽

Local Brain

Changes in local brain stem perfusion that alter extracellular fluid Pco2 and/or [H+] near central chemoreceptors may contribute to the decrease in respiration observed during hypoxia after peripheral chemoreceptor denervation and to the delayed decrease observed during hypoxia in the newborn. In this study, we measured the changes in respiration and brain stem blood flow (BBF) during 2–4 min of hypoxic hypoxia in both intact and denervated piglets and calculated the changes in brain stem Pco2 and [H+] that would be expected to occur as a result of the changes in BBF. All animals were anesthetized, spontaneously breathing, and between 2 and 7 days of age. Respiratory and other variables were measured before and during hypoxia in all animals, and BBF (microspheres) was measured in a subgroup of intact and denervated animals at 0, 30, and 260 s and at 0 and 80 s, respectively. During hypoxia, minute ventilation increased and then decreased (biphasic response) in the intact animals but decreased only in the denervated animals. BBF increased in a near linear fashion, and calculated brain stem extracellular fluid Pco2 and [H+] decreased over the first 80 s both before and after denervation. We speculate that a rapid increase in BBF during acute hypoxia decreases brain stem extracellular fluid Pco2 and [H+], which, in turn, negatively modulate the increase in respiratory drive produced by peripheral chemoreceptor input to the central respiratory generator.

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Hypoxic pulmonary hypertension of the calf with denervation of the lungs

Journal of Applied Physiology ◽

10.1152/jappl.1964.19.5.976 ◽

1964 ◽

Vol 19 (5) ◽

pp. 976-980 ◽

Cited By ~ 6

Author(s):

John T. Reeves ◽

James E. Leathers

Keyword(s):

Spinal Cord ◽

Central Nervous System ◽

Nervous System ◽

Arterial Pressure ◽

Spinal Anesthesia ◽

Pulmonary Arterial Pressure ◽

Acute Hypoxia ◽

Pressure Rise ◽

The Central Nervous System ◽

Pulmonary Arterial

Transection of the spinal cord at the level of C2, spinal anesthesia, and/or bilateral vagotomy were done in 11 healthy young male calves. These procedures did not block the pulmonary arterial pressure rise with 12 or 9% oxygen, but they did block the increase in heart rate and systemic arterial pressure which accompanied hypoxia when the central nervous system was intact. The central nervous system, therefore, appeared to mediate the response to acute hypoxia of the systemic circulation, but not the pulmonary arterial pressure rise. hypoxia; pulmonary circulation; spinal cord section; spinal anesthesia; vagotomy Submitted on February 19, 1964

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Extracellular pH Changes during Spreading Depression and Cerebral Ischemia: Mechanisms of Brain pH Regulation

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1984.3 ◽

1984 ◽

Vol 4 (1) ◽

pp. 17-27 ◽

Cited By ~ 211

Author(s):

W. A. C. Mutch ◽

A. J. Hansen

Keyword(s):

Cerebral Ischemia ◽

Parietal Cortex ◽

Spreading Depression ◽

Rapid Change ◽

Extracellular Ph ◽

Disulfonic Acid ◽

Mammalian Brain ◽

Negative Deflection ◽

Alkaline Shift ◽

Complete Cerebral Ischemia

We have examined the extracellular pH (pHe) during spreading depression and complete cerebral ischemia in rat parietal cortex utilizing double-barrelled H+ liquid ion exchanger microelectrodes. The baseline pHe of the parietal cortex was 7.33 at a mean arterial Pco2 of 38 mm Hg. Following spreading depression and cerebral ischemia, highly reproducible triphasic changes in pHe occurred, which were intimately related to the negative deflection in tissue potential (Ve). The changes in pHe for spreading depression (n = 23) were a small initial acidic shift, beginning before the rapid change in Ve, followed by a rapid transient alkaline shift of 0.16 pH units, the onset of which coincided with the negative deflection in Ve. A prolonged acidic shift of 0.42 pH units then occurred. The maximal decrease in pHe was to 6.97 and the mean duration of the triphasic pHe change was 7.8 min. The lactate concentration in brain cortex increased from baseline 1.2 m M to 7.0 m M (n = 6) during the maximal acidic change in spreading depression. In addition, lactate levels correlated well with resolution of the pHe changes during spreading depression. The triphasic pHe changes following complete cerebral ischemia were an initial acidic shift of 0.43 pH units which developed over 2 min, then an alkaline shift of 0.10 pH units coincident with the negative deflection in Ve, and a final acidic shift of 0.26 pH units. The terminal pHe was 6.75. Superfusion of the cortex with inhibitors of carbonic anhydrase (acetazolamide), Na+/H+ counter transport (amiloride), and Cl−/HCO3− countertransport (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid) altered the triphasic pHe changes in a similar fashion for both spreading depression and cerebral ischemia, providing insights into the pHe regulatory mechanisms in mammalian brain.

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Microangioarchitecture of the feline spinal cord

Journal of Neurosurgery ◽

10.3171/jns.1987.66.3.0447 ◽

1987 ◽

Vol 66 (3) ◽

pp. 447-452 ◽

Cited By ~ 15

Author(s):

Yutaka Naka ◽

Toru Itakura ◽

Kunio Nakai ◽

Kazuo Nakakita ◽

Harumichi Imai ◽

...

Keyword(s):

Spinal Cord ◽

Dorsal Surface ◽

Ventral Surface ◽

Anterior Spinal Artery ◽

Corrosion Casts ◽

Thoracic Spinal Cord ◽

Content Type ◽

Thoracic Spinal ◽

Fine Print ◽

Anterior Median

✓ The microangioarchitecture of corrosion casts of the cat spinal cord was studied by scanning electron microscopy. On the ventral surface of the spinal cord, the anterior spinal artery and the anterior spinal vein ran parallel along the anterior median fissure. Many central arteries branching from the anterior spinal artery coursed in a wavelike manner in the anterior median fissure. The number of central arteries was lowest in the thoracic spinal cord. Central arteries at some spinal cord levels revealed well-developed anastomoses with other central arteries in the anterior median fissure. These well-developed anastomotic central arteries were frequently observed in the thoracic spinal cord, in which the number of central arteries was lowest. On the dorsal surface of the spinal cord, the posterior spinal vein ran longitudinally at the midline and was drained by circumferential veins and posterior central veins. This vein formed a characteristic anastomotic plexus. Small arterioles (20 µm in diameter) in the spinal parenchyma revealed a ring-like compression at the branching site.

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Influence of hypoxic ventilatory response on arterial O2 saturation during maximal exercise in acute hypoxia

European Journal of Applied Physiology and Occupational Physiology ◽

10.1007/bf00964122 ◽

1995 ◽

Vol 72 (1-2) ◽

pp. 101-105 ◽

Cited By ~ 20

Author(s):

Henri Benoit ◽

Thierry Busso ◽

Josiane Castells ◽

Christian Denis ◽

Andr� Geyssant

Keyword(s):

Maximal Exercise ◽

Ventilatory Response ◽

Acute Hypoxia ◽

Hypoxic Ventilatory Response ◽

Arterial O2 Saturation

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Anatomy of the human spinal cord arachnoid cisterns: applications for spinal cord surgery

Journal of Neurosurgery Spine ◽

10.3171/2019.4.spine19404 ◽

2019 ◽

Vol 31 (5) ◽

pp. 756-763 ◽

Cited By ~ 1

Author(s):

Corentin Dauleac ◽

Timothée Jacquesson ◽

Patrick Mertens

Keyword(s):

Spinal Cord ◽

Cauda Equina ◽

Ventral Surface ◽

Conus Medullaris ◽

Pia Mater ◽

Axial Section ◽

Human Spinal Cord ◽

Spinal Subarachnoid Space ◽

Subarachnoid Spaces ◽

Arachnoid Mater

OBJECTIVEThe goal in this study was to describe the overall organization of the spinal arachnoid mater and spinal subarachnoid space (SSAS) as well as its relationship with surrounding structures, in order to highlight spinal cord arachnoid cisterns.METHODSFifteen spinal cords were extracted from embalmed adult cadavers. The organization of the spinal cord arachnoid and SSAS was described via macroscopic observations, optical microscopic views, and scanning electron microscope (SEM) studies. Gelatin injections were also performed to study separated dorsal subarachnoid compartments.RESULTSCompartmentalization of SSAS was studied on 3 levels of axial sections. On an axial section passing through the tips of the denticulate ligament anchored to the dura, 3 subarachnoid cisterns were observed: 2 dorsolateral and 1 ventral. On an axial section passing through dural exit/entrance of rootlets, 5 subarachnoid cisterns were observed: 2 dorsolateral, 2 lateral formed by dorsal and ventral rootlets, and 1 ventral. On an axial section passing between the two previous ones, only 1 subarachnoid cistern was observed around the spinal cord. This compartmentalization resulted in the anatomical description of 3 elements: the median dorsal septum, the arachnoid anchorage to the tip of the denticulate ligament, and the arachnoid anchorage to the dural exit/entrance of rootlets. The median dorsal septum already separated dorsal left and right subarachnoid spaces and was described from C1 level to 3 cm above the conus medullaris. This septum was anchored to the dorsal septal vein. No discontinuation was observed in the median dorsal arachnoid septum. At the entrance point of dorsal rootlets in the spinal cord, arachnoid trabeculations were described. Using the SEM, numerous arachnoid adhesions between the ventral surface of the dorsal rootlets and the pia mater over the spinal cord were observed. At the ventral part of the SSAS, no septum was found, but some arachnoid trabeculations between the arachnoid and the pia mater were present and more frequent than in the dorsal part. Laterally, arachnoid was firmly anchored to the denticulate ligaments’ fixation at dural points, and dural exit/entrance of rootlets made a fibrous ring of arachnoidodural adhesions. At the level of the cauda equina, the arachnoid mater surrounded all rootlets together—as a sac and not individually.CONCLUSIONSArachnoid cisterns are organized on each side of a median dorsal septum and compartmentalized in relation with the attachments of denticulate ligament and exit/entrance of rootlets.

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