Profound Arterial Hypotension Research Articles

The role of methylene blue in the management of vasoplegic syndrome: a narrative review

Vasoplegic syndrome is an important clinical entity characterized by profound arterial hypotension refractory to vasopressor therapy. The underlying pathophysiology is characterized by a complex and multifactorial dysregulation of both vasodilatory and vasoconstrictive mechanisms. During the last decades, there is growing interest in using methylene blue as an adjunct therapy to treat vasodilatory shock. The present review evaluates the safety and efficacy of methylene blue in cardiac and transplant surgery, severe sepsis and septic shock, severe burn injury, paediatric intensive care, and intoxications. Although most of the currently available evidence reports a benefit in haemodynamic parameters and a decrease in vasopressor requirements following the administration of methylene blue, study designs are heterogeneous, and the overall level of evidence is low. Moreover, a clear and consistent benefit in morbidity and mortality is lacking. Large prospective randomized controlled trials are needed to evaluate the exact role and timing of methylene blue in the treatment of vasopressor refractory vasoplegia.

Massive pulmonary embolism in patients with extreme bleeding risk: a case series on the successful use of ultrasound-assisted, catheter directed thrombolysis in a district general hospital

Massive pulmonary embolism (PE), characterised by profound arterial hypotension, is a life-threatening emergency with a 90-day mortality of over 50%. Systemic thrombolysis can significantly reduce the risk of death or cardiovascular collapse in these patients, by around 50%, but these benefits are offset by a fivefold increased risk of intracranial haemorrhage and major bleeding, which may limit its use in patients at high risk of catastrophic haemorrhage. We describe a case series of 3 patients presenting with massive PE, each with extreme risk of bleeding and contra-indication to systemic thrombolysis, treated successfully with ultrasound-assisted, catheter directed thrombolysis (U-ACDT). Our experience of this novel technique using the EkoSonic Endovascular System (Ekos, BTG, London, UK) on carefully selected patients has demonstrated the potential to improve clinical status in shocked patients, with minimal bleed risk. There have been several clinical studies evaluating the Ekos system. Both the ULTIMA and SEATTLE II studies have shown significant reductions in RV/LV ratio by CT scanning when compared to standard anticoagulation in patients with intermediate-risk PE, with minimal bleeding complications. However, there is a pressing need for a randomised trial demonstrating improvement in robust clinical outcomes when comparing U-ACDT to simple anticoagulation. We believe that this case series adds new insight and highlights the potential of catheter directed thrombolysis in this high-risk patient cohort and consideration should be made to its use in cases where systemic thrombolysis is felt to be too high risk.

Aspiracija tromba tokom primarne perkutane koronarne intervencije - gde smo sada?

Introduction. thrombus aspiration is not recommended as a routine procedure considering the results of large randomised trials. It is necessary to define new indications for thrombus aspiration in myocardial infarction and to conduct appropriate trials. The aim of this paper was to report a patient with successful aspiration of large thrombus mass from right coronary artery made after primary balloon angioplasty, and to consider which patients could benefit with this procedure. Case report. a male, 80 years old, has been admitted to a catheterisation laboratory with clinical, biochemical and electrocardiographic signs of acute myocardial infarction with ST segment elevation (STEMI) of inferoposterolateral localisation along with sinus bradycardia and profound arterial hypotension, which all are characteristic for inferior myocardial wall infarction with right ventricular involvement. Two hours after pain onset the patient was admitted to hospital in Bijeljina and sent to catheterisation laboratory straight after. All branches of left coronary artery were well visualized and without significant stenosis. Right coronary artery was occluded in proximal segment. Predilatation was performed with SC Sprinter legend 2,0x20mm balloon. After predilatation thrombus burden is still large, blood flow was slow with significant residual stenosis. Than, BMS Pro-kinetic energy 3,5x20mm stent was implanted. After stent implantation thrombus burden existed and there was no flow in PLV branch. Thrombus mass was 2 cm long and successfully aspirated with Export aspiration catheter. Control coronarography showed no residual stenosis and normal blood flow was restored through branches of right coronary artery. Conclusion. Procedure must be gradual, carefully planned and aspiration of thrombus should be taken only after initial balloon angioplasty with flow evaluation. Large thrombus burden or several smaller thrombi with clear flow obstruction and poor peripheral flow could be the reason for aspiration of thrombus along with possible intracoronary administration of GP IIbIIIa inhibitors. If conducted cautiously, aspiration of thrombus may still be considered as a valuable technique in selected patients with a large angiographic thrombus burden.

Anaphylactic shock and mitochondria

Introduction Anaphylactic shock (AS) is a rare but potentially lethal complication during anaesthesia even in previously apparently healthy individuals. While anaphylaxis is a clear trigger for activation of multiple downstream pathways, the precise mechanisms underlying the development of organ failure, shock and death remain elusive. Our team observed that muscle partial pressure in oxygen (PtiO2) decreased rapidly after AS. This rapid drop in skeletal muscle PtiO2 was unexpected since muscles were at rest and was unusual as against the other types of shock. Mitochondrial oxidative capacities have not been investigated during AS. The aim of this study was to assess mitochondrial oxidative capacity during anaphylactic shock in skeletal muscle and in other organs. Methods Ovalbumin-sensitized anaphylactic shock rats (n = 7) were compared to control rats (n = 7) for systemic hemodynamics. Mitochondrial oxidative capacity was assessed in 6 different organs or tissues: we used isolated mitochondria for the brain, the lung and the liver and permeabilized fibers for 3 different muscles (gastrocnemius, soleus skeletal muscles and heart left ventricle). Free radical leak (H2O2 production/O2 consumption) was also calculated in the 3 muscles. Results AS provoked an early and profound arterial hypotension. Mitochondrial oxidative capacities were not altered in the liver, the lung, the brain and in the soleus. Maximal mitochondrial oxidative capacities significantly decreased in the heart (−36%, 399 ± 131 vs. 144 ± 33 O2 μmol/min/mg, P = 0.04) and increased in the gastrocnemius (+24%, 99 ± 55 vs. 173 ± 45 O2 μmol/min/mg, P = 0.03) during AS. The free radical leak was not modified by AS in left ventricle and in soleus muscle but was significantly decreased in gastrocnemius (−50%: 8/10,000 vs. 16/10,000, P = 0.046). Discussion Heart mitochondria were significantly altered, this mitochondrial dysfunction could participate to the myocardial dysfunction observed during AS. Gastrocnemius paradoxical mitochondria behaviour can directly participate to the rapidity and the severity of AS. Conclusion In our model of AS, mitochondrial oxidative capacity was not altered in most of the organs studied but was separate in 2 different types of muscle.

Insignificant response of the fetal placental circulation to arterial hypotension in sheep

Infusion of the angiotensin-converting enzyme inhibitor enalaprilat into fetal sheep caused a profound arterial hypotension within days. Five fetal lambs were infused with enalaprilat for 8 days starting at day 128 of gestation. Total accumulated dose was 0.30 ± 0.11 mg/kg. Arterial pressure decreased from 43.6 to 25.6 mmHg; venous pressure did not change. Biventricular output was not statistically significantly changed; placental blood flow decreased almost in proportion to the decrease in pressure but the increase in somatic flow was not statistically significant. There were no significant changes in pressure 30 min after the initial 50-μg loading dose of enalaprilat. However, the arterial pressure responses to test doses of ANG I were largely abolished. After 1 day, however, there was a significant decrease in somatic vascular resistance, which became stronger with time, but almost no decrease in the placental resistance. We conclude that the fetal somatic circulation exhibits a slow but strong decrease in resistance but that the response to hypotension is weak or absent in the fetal placenta, possibly because it is already fully relaxed.

Can matrix metalloproteinases be targeted in hepatic ischemia/reperfusion injury?

Can matrix metalloproteinases be targeted in hepatic ischemia/reperfusion injury?

Myocardic extended ischemia after scombroid syndrome

We describe a case of a healthy woman, presenting to the emergency department because of sudden onset of diffuse pruriginous erythema, profound arterial hypotension and anginal chest pain, just after consuing a meal with cooked fresh tuna fish. She developed progressive ECG signs of myocardial ischemia suggesting subendocardial infarction and increased serum level of troponin I. After vigourous fluid resuscitation with iv fluids and treatment with anti-hystamine drugs, corticosteroids, beta-blockers and calcium-channell blockers she progressively recovered. A clinical diagnosis of sgombroid syndrome was established: it is a syndrome which may follow the ingestion of some spoiled fish, characterized by urticara, headhache, gastrointestinal upset and rarely bronchospasm, shock, coronary ischemia and arrythmias. A sample of the consumed fish could be analysed, finding a very high level of hystamine concentration, conferming the diagnosis of sgombroid syndrome. A coronary angiography was performed and confermed the patient had a normal coronary tree, devoid of atherosclerotic lesions. Her anginal symptoms and ECG signs were probably due to functional ischemia determined by hystamine mediated vasoconstriction and hypotension. This not so rare but not well known syndrome is further discussed and addressed to the emergency physicians’ attention, because of its importance in the differential diagnoses of suspected food allergies

Evoked potential monitoring and temporary clipping in cerebral aneurysm surgery.

Temporary occlusion of the parent artery greatly facilitates the dissection of large cerebral aneurysms, while much reducing the risk of intraoperative rupture and avoiding the use of profound arterial hypotension. Intraoperative somatosensory evoked potential (SEP) monitoring was carried out in 25 aneurysm cases where temporary clipping was employed electively under moderate hypothermia. Occlusion times ranged from 6.3 to 52 minutes at 28.7 degrees C to 32.5 degrees C. Among 15 middle cerebral artery (MCA) occlusion cases the SEP was lost within 5 or 6 minutes in two cases undergoing early surgery and in one case with marked vasospasm and was lost within 9 minutes in one case with pre-existing infarction in the territory of the MCA. The SEP persisted throughout MCA occlusion periods of 6.3 to 52 minutes in 8 cases. Occlusion of parent arteries of unruptured aneurysms was well tolerated. At least 2 minutes of MCA occlusion after loss of the SEP were tolerated without neurological sequelae, while transient new deficits were seen when MCA occlusion was continued for 4 and for 4 + 11 minutes and an increased deficit was seen when occlusion was continued for 7 minutes after loss of the SEP. In each of the internal carotid artery (ICA) occlusion and bilateral anterior cerebral artery occlusion groups the SEP was lost in one case and was absent for about one minute before reperfusion was instituted. The ICA case had a transient deficit lasting about 4 hours; no other complications were seen in these two groups. Complications were not seen in any case where the SEP was not lost during the occlusion period. Factors affecting collateral perfusion and possible means of increasing tolerance to ischaemia in this situation are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension.

Profound arterial hypotension is a commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Profound arterial hypotension in dogs: brain electrical activity and organ integrity.

To determine whether non-invasive measurement of brain electrical activity can predict ischemic brain damage, we recorded the electroencephalogram (EEG) and somatosensory- (SEP) and auditory- (AEP) evoked potentials before, during, and after trimethaphan-induced profound arterial hypotension in dogs. The authors set out to compare the change in electrical activity with the degree of brain damage, as determined by microscopic examination. Dogs were anesthetized with halothane (1.4 vol % inspired), maintained horizontal (head at the level of the heart), and ventilated mechanically (FIO2 0.50); deviations from normal acid-base status were corrected. Twenty animals received a 1.5-mg/kg intravenous bolus of trimethaphan. Three animals were resistant to the drug. The remaining animals had profound hypotension [mean arterial blood pressure (MABP) at some steady level between 12 and 25 mmHg] for 1 h. Eight of these animals died during or soon after the hypotensive period as a consequence of cardiac arrest (three), intestinal bleeding (three) or unknown causes (two). In all survivors, EEG intensity and the amplitude of the SEP decreased during hypotension; both variables recovered with restoration of MABP. All nine animals surviving hypotension had no apparent neurologic or behavioral deficit nor any histologic evidence of ischemic brain cell injury. We were thus unable to find a MABP threshold for brain with minimal brain injury. Our findings suggest, under the conditions of our experiments, a great margin of tolerance for profound hypotension by the brain in this species. Other organ systems--the heart, gastrointestinal tract, and liver--proved to be more susceptible to ischemic damage. Eight of the nine surviving animals had elevations in serum alanine transaminase (SGPT), aspartate transaminase (SGOT), and alkaline phosphatase. Animals with the greatest increases in these enzymes showed centrilobular hepatocyte degeneration.

EVIDENCE OF PRESERVATION OF AEROBIC CEREBRAL METABOLISM DURING HALOTHANE-INDUCED HYPOTENSION

✓ The effect of halothane-induced profound systemic arterial hypotension on brain ischemia was evaluated by comparison with hypotension caused by oligemia and trimethaphan as well as nonhypotensive controls. Mean cerebral tissue lactate concentrations after halothane-induced hypotension at 5, 30, and 60 minutes were 4.34, 5.92, and 7.48 mM/kg. There was no significant difference between halothane and control animals during the experimental period. At 30 and 60 minutes, both oligemic and trimethaphan groups were higher than the control and halothane series. Definite protection from cerebral ischemia is provided by halothane during induced hypotension. Exact mechanisms of protection conveyed by halothane are unclear, but are probably not related to relative increased blood flow since cerebral vasodilation is maximal in these low blood-pressure ranges irrespective of etiology.

Hypotension in tetanus.

Three patients with severe tetanus had episodes of profound arterial hypotension lasting from minutes to hours. The blood pressure was recorded continuously for 13, 19, and six days respectively by an intra-arterial catheter, and other measurements included heart rate, central venous pressure, cardiac output, and blood gases.The hypotension was distinguished from that of "shock", for there was no clinical evidence of peripheral vasoconstriction and no tachycardia. It could not be attributed to disturbances of salt and water balance. During episodes of hypotension the blood pressure fell as low as 32/16 mm Hg, the heart rate fell from a mild tachycardia to normal values or a mild bradycardia, and the central venous pressure did not rise. The onset and the end of such episodes was often abrupt and the hypotension was often produced in response to a stimulus. In one patient extreme hypotension followed the aspiration of secretions from the trachea. These changes may represent another effect of tetanus on autonomic nervous activity, including impairment of baroreceptor reflexes.

VENOUS AIR EMBOLISM

Sudden profound arterial hypotension caused by massive venous air embolism occurred in two patients undergoing neurosurgical operations in the sitting position. In both cases intra-operative monitoring included the continuous display of intra-arterial blood-pressure which facilitated prompt diagnosis. The electrocardiograph was also continuously observed in both patients, but no abnormality was seen despite a profound fall in blood-pressure. Further entry of air was prevented and after resuscitation an uneventful recovery ensued. Intra-arterial blood-pressure should be continuously monitored in patients at risk from air embolism during surgery.

The nature and time course of the neuronal alterations resulting from oligaemia and hypoglycaemia in the brain of Macaca mulatta

(1) The time course of the neuronal alterations known as ‘ischaemic cell change’ has been studied after profound arterial hypotension or insulin-induced hypoglycaemia in the brains of rhesus monkeys fixed by perfusion at intervals of 15 min-4 h after the stress. (2) Arterial hypotension (a cerebral perfusion pressure less than 25 mm Hg for 4–36 min, produced by drugs, bleeding and head-up tilt) led to consistent neuronal alterations in the arterial boundary zones of the neocortex, and less frequent alterations in the hippocampus, basal ganglia and cerebellum. (3) Arterial glucose levels below 20 mg/100 ml (induced by insulin 800–1200 I.U., and sustained so that somatosensory-evoked potentials were abolished for 49–92 min) was followed by ischaemic neuronal alterations occurring diffusely in the neocortex and also in the hippocampus, caudate nucleus and putamen. (4) In the two situations the neuronal changes were identical both in their nature and time course. The earliest change was microvacuolation of the neuronal cytoplasm, visible after + 15 min and persisting up to + 150 min. This was followed by ischaemic cell change, recognizable after + 30–35 min and persisting up to + 4 h. Ischaemic cell change with incrustations appeared after + 90–150 min. (5) This sequence of changes occurred most rapidly in the smaller neocortical neurones, in which the time course was closely similar to that previously described in the rat brain.

Brain damage in the rhesus monkey resulting from profound arterial hypotension. I. Its nature, distribution and general physiological correlates

Profound arterial hypotension was induced in 15 rhesus monkeys under pentobarbital anaesthesia, by a ganglion-blocking agent (Arfonad), head-up tilt and arterial bleeding. After respiratory arrest mechanical ventilation ensured normal arterial oxygenation. The following variables were recorded during and after the period of hypotension: arterial and venous sinus blood pressure, intracranial pressure, oxygen saturation or tension and P co 2 and pH of arterial and cerebral venous blood samples, arterial and cerebral venous glucose concentrations, respiratory rate, body temperature, electrocardiogram, electrocorticogram and somatosensory cortical evoked responses. The pial blood vessels were observed and photographed through a cranial window. The animals were divided neuropathologically into: Group I (5 animals), normal brains. Group II (6 animals), ischaemic alterations in the arterial boundary zones of the cortices of cerebrum and cerebellum. In addition, lesions were seen in the basal ganglia (3 animals) and in the hippocampi (2 animals). Group III (4 animals), ischaemic alterations were diffuse in the cortex of cerebrum and cerebellum, and the hippocampi and variable in the basal ganglia. Brain damage occurred only when the cerebral perfusion pressure fell rapidly to below 25 mm Hg and was sustained at this level for at least 15 min. The time course of changes in the amplitude of the somatosensory cortical evoked response during hypotension clearly differentiated the 3 groups of animals. The survival time of the evoked response correlated inversely with the degree of brain damage; the duration of the period of reduced cerebral perfusion after the disappearance of the evoked response correlated directly with the degree of brain damage. The recovery of cerebral electrical activity and the return to consciousness was similar in animals of Groups I and II. Two animals in Group II showed motor disabilities. The animals in Group III failed to regain consciousness and showed a marked rise in intracranial pressure followed by a secondary loss of spontaneous respiration and cerebral electrical activity. At post mortem a downward herniation of the brain stem and inferior cerebellar vermis was seen. The lesions in the cerebral arterial boundary zones appear to result from a profound local reduction in cerebral blood flow which leads to a correspondingly localized metabolic disturbance, later recognisable as ‘ischaemic cell change’.

Brain damage in the rhesus monkey resulting from profound arterial hypotension. II. Changes in the spontaneous and evoked electrical activity of the neocortex

In 15 rhesus monkeys under pentobarbital anaesthesia changes in the spontaneous electrocortical activity and in somatosensory evoked potentials have been studied during and after a period of profound arterial hypotension (whose general physiological correlates and neuropathological consequences have been described in the preceding paper). The stages in the decline and recovery of the electrocorticogram are described. A significant phase of activation was not seen; a relative increase in slow activities was more frequent than an absolute increase; silence occurred after 4–32 min. Spindles were prominent in the 15–120 min required for recovery. No features correlated specifically with the occurrence of focal cortical (arterial boundary zone) lesions. Absence of recovery was seen with diffuse cortical lesions. The decline and recovery of different components of the somatosensory evoked response is described. Study, during hypotension, of the time course of changes in the amplitude of the primary surface-positive wave of the evoked response permits the differentiation of animals that will recover with no brain damage, those that will develop discrete cortical lesions and those that will develop diffuse cortical lesions. The extent of the lesions correlates with the severity of the metabolic deficit as indicated by the evoked potential changes. Recovery of the evoked potentials occurred in about one hour in non-brain-damaged monkeys and in those with relatively small boundary zone lesions but was abnormal in animals with severe neurological disabilities. Animals with diffuse cortical lesions did not regain consciousness and showed some transient recovery of evoked responses at a thalamic level but absence of recovery at the cortical level.

Effects of hypoxia on the monosynaptic reflex pathway in the cat spinal cord.

Effects of hypoxia on the monosynaptic reflex pathway in the cat spinal cord.R M Eccles, Y Loyning, and T OshimaR M Eccles, Y Loyning, and T OshimaPublished Online:01 Mar 1966https://doi.org/10.1152/jn.1966.29.2.315MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Download PDF FiguresReferencesRelatedInformation Cited ByCerebral perturbations during exercise in hypoxiaSamuel Verges, Thomas Rupp, Marc Jubeau, Bernard Wuyam, François Esteve, Patrick Levy, Stéphane Perrey, and Guillaume Y. Millet15 April 2012 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 302, No. 8Severe hypoxia affects exercise performance independently of afferent feedback and peripheral fatigueGuillaume Y. Millet, Makii Muthalib, Marc Jubeau, Paul B. Laursen, and Kazunori Nosaka15 April 2012 | Journal of Applied Physiology, Vol. 112, No. 8Different susceptibility of facilitatory and inhibitory spinal pathways to ischemia in the catNeuroscience Research, Vol. 47, No. 3Hypoxic Apnea, Epidural Anesthesia, and InfantsAnesthesiology, Vol. 89, No. 5Mechanisms of Motor Dysfunction After Transient MCA Occlusion: Persistent Transmission Failure in Cortical Synapses Is a Major DeterminantStroke, Vol. 29, No. 9Hypoxia Causes Apnea during Epidural Anesthesia in RabbitsAnesthesiology, Vol. 88, No. 3Changes in [Ca 2+ ] i and membrane currents during impaired mitochondrial metabolism in dissociated rat hippocampal neurons22 September 2004 | The Journal of Physiology, Vol. 507, No. 1Effect of magnesium on depression of the monosynaptic reflex induced by 2-chloroadenosine or hypoxia in the isolated spinal cord of neonatal ratsNeuroscience Letters, Vol. 101, No. 2Involvement of adenosine in synaptic depression induced by a brief period of hypoxia in isolated spinal cord of neonatal ratBrain Research, Vol. 462, No. 2Synapic depression and adenosineTrends in Pharmacological Sciences, Vol. 9, No. 10Different sensitivity to hypoxia in neuronal activities of lateral vestibular and spinal trigeminal nuclei.Stroke, Vol. 19, No. 3Extracellular potassium ion activity and electrophysiology in the hippocampal slice: paradoxical recovery of synaptic transmission during anoxiaBrain Research, Vol. 418, No. 2The H-reflex in the encephalopathy due to ammonia intoxicationExperimental Neurology, Vol. 96, No. 3Hyperexcitability following moderate hypoxia in hippocampal tissue slicesBrain Research, Vol. 337, No. 2Electrical activities of the frog spinal cord are resistant to perfusion with hypoxic mediumBrain Research, Vol. 274, No. 1Dependence of the viability of neurons in hippocampal slices on oxygen supplyBrain Research Bulletin, Vol. 8, No. 1A comparative analysis of short-latency somatosensory evoked potentials in man, monkey, cat, and ratExperimental Neurology, Vol. 72, No. 3Oxidative metabolism, extracellular potassium and sustained potential shifts in cat spinal cord in situBrain Research, Vol. 162, No. 1Modifications of presynaptic inhibition of various origins by local application of convulsant drugs on cat's spinal cordBrain Research, Vol. 71, No. 1Effects of hypoxia and hypercapnic hypoxia on the ultrastructure of central nervous synapsesExperimental Neurology, Vol. 40, No. 1Evidence for the anoxia sensitivity of the synaptic region at the outer plexiform layer in the fish retinaVision Research, Vol. 13, No. 5Muscle relaxation by drugs which stimulate sensory nerve endings—I. The effect of veratrum alkaloids, phenyldiguanide and 5-hydroxytryptamineNeuropharmacology, Vol. 12, No. 2A trigeminal monosynaptic reflex in reptiliaExperimental Neurology, Vol. 32, No. 2Activity pattern of visceral cortex neurons during asphyxiaExperimental Neurology, Vol. 32, No. 1Effect of hypoxia on protein metabolism in neuron- and neuroglia cell-enriched fractions from rabbit brainExperimental Neurology, Vol. 29, No. 1Effects of hemorrhagic hypotension and shock on the central nervous functionsJournal of Surgical Research, Vol. 10, No. 7Brain damage in the rhesus monkey resulting from profound arterial hypotension. II. Changes in the spontaneous and evoked electrical activity of the neocortexBrain Research, Vol. 13, No. 1Intracellular recording from cat spinal interneurons during acute asphyxiationBrain Research, Vol. 8, No. 1A trigeminal monosynaptic reflex in birdsExperimental Neurology, Vol. 18, No. 2 More from this issue > Volume 29Issue 2March 1966Pages 315-31 https://doi.org/10.1152/jn.1966.29.2.315PubMed5927464History Published online 1 March 1966 Published in print 1 March 1966 Metrics