Biomedical subjects

R C Koehler

Publications and source records attributed to R C Koehler.

At least 109 records · Page 6Linked to original sources

PubMed1991

Improved blood flow during prolonged cardiopulmonary resuscitation with 30% duty cycle in infant pigs.

BACKGROUND: Sustained compression is recommended to maximize myocardial and cerebral blood flow during cardiopulmonary resuscitation (CPR) in adults and children. We compared myocardial and cerebral perfusion during CPR in three groups of 2-week-old anesthetized swine using compression rates and duty cycles (duration of compression/total cycle time) of 100 per minute, 60%; 100 per minute, 30%; and 150 per minute, 30%. METHODS AND RESULTS: Ventricular fibrillation was induced and CPR was begun immediately with a sternal pneumatic compressor. Epinephrine was continuously infused during CPR. Microsphere-determined blood flow and arterial and sagittal sinus blood gas measurements were made before cardiac arrest was induced and after 5, 10, 20, 35, and 50 minutes of CPR. At 5 minutes of CPR, ventricular and cerebral blood flows were greater than 25 ml.min-1 x 100 g-1 and were not significantly different between groups. When CPR was prolonged, however, myocardial and cerebral blood flows were significantly higher with the 30% duty cycle than with the 60% duty cycle. By 35 minutes, all myocardial regions had less than 5 ml.min-1 x 100 g-1 flow with the 60% duty cycle. In contrast, CPR with the 30% duty cycle at either compression rate provided more than 25 ml.min-1 x 100 g-1 to all ventricular regions for 50 minutes. By 20 minutes, most brain regions received 50% less flow with the 60% duty cycle compared with animals undergoing CPR with the 30% duty cycle (p less than 0.05). Cerebral oxygen uptake was better preserved with the 30% duty cycle. Chest deformation from loss of recoil was greater with the 60% duty cycle compared with the 30% duty cycle. CONCLUSIONS: We conclude that the shorter duty cycle provides markedly superior myocardial and cerebral perfusion during 50 minutes of CPR in this infant swine model. These data do not support recommendations for prolonged compression at rates of 100 per minute during CPR in infants and children.

Animals↗

PubMed1991

Effect of adrenergic drugs on cerebral blood flow, metabolism, and evoked potentials after delayed cardiopulmonary resuscitation in dogs.

BACKGROUND AND PURPOSE: Epinephrine administration during cardiopulmonary resuscitation increases cerebral blood flow by increasing arterial pressure. We tested whether potential beta-adrenergic effects of epinephrine directly influence cerebral blood flow and oxygen consumption independently of raising perfusion pressure. METHODS: Four groups of seven anesthetized dogs were subjected to 8 minutes of fibrillatory arrest followed by 6 minutes of chest compression, ventricular defibrillation, and 4 hours of spontaneous circulation. Cerebral perfusion pressure was increased to approximately equivalent ranges during resuscitation by either 1) epinephrine infusion, 2) epinephrine infusion after pretreatment with the lipophilic beta-adrenergic antagonist pindolol, 3) infusion of the alpha-adrenergic agonist phenylephrine, or 4) descending aortic balloon inflation without pressor agents. RESULTS: We found no difference in cerebral blood flow, oxygen extraction, or oxygen consumption during chest compression among groups. After ventricular defibrillation, depressed levels of cerebral blood flow, cerebral oxygen consumption, and somatosensory evoked potential amplitude were not different among groups. CONCLUSIONS: We detected no evidence that after 8 minutes of complete ischemia, epinephrine administration during resuscitation substantially influences cerebral blood flow or cerebral oxygen consumption independent of its action of raising arterial pressure or or that epinephrine has a negative impact on immediate metabolic or electrophysiological recovery attributable to its beta-adrenergic activity.

Animals↗

PubMed1991

Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum.

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.

Adenosine Triphosphate↗

PubMed1991

Blood-brain barrier disruption after cardiopulmonary resuscitation in immature swine.

We investigated blood-brain barrier permeability in 2-3-week-old anesthetized pigs during and after cardiopulmonary resuscitation. We assessed permeability by tissue uptake of radiolabeled aminoisobutyric acid, after correcting for plasma counts in tissue with radiolabeled inulin. Among 14 regions examined, the transfer coefficient of aminoisobutyric acid in nonischemic control animals ranged from 0.0018 +/- 0.0001 ml/g/min in diencephalon to 0.0049 +/- 0.0003 ml/g/min in cervical spinal cord. After 8 minutes of cardiac arrest followed by either 10 or 40 minutes of continuous sternal compression, there was no increase in the transfer coefficient. Likewise, during the immediate period after ventricular defibrillation, there was no increase in transfer coefficient despite the brief, transient hypertension. However, after 8 minutes of arrest, 6 minutes of cardiopulmonary resuscitation, and 4 hours of spontaneous circulation, the transfer coefficient was significantly increased by 59-107% in 10 of 11 regions rostral to the pons. Plasma volume in tissue measured by inulin was not elevated, suggesting that the increased transfer coefficient was not due to increased surface area. Thus, after an 8-minute period of complete ischemia, the blood-brain barrier remains intact during and immediately after resuscitation despite large vascular pressure fluctuations. However, in contrast to previous work on adult dogs, immature pigs are prone to a delayed increase in permeability, thereby allowing circulating substances greater access to the brain.

Aminoisobutyric Acids↗

PubMed1991

Conjugated superoxide dismutase reduces extent of caudate injury after transient focal ischemia in cats.

We tested the efficacy of preischemic and postischemic systemic treatment with 30,000 units polyethylene glycol-conjugated superoxide dismutase in a reperfusion model of focal cerebral ischemia. Forty-one anesthetized cats underwent 2 hours' occlusion of the left middle cerebral artery and both common carotid arteries followed by 4 hours of reperfusion. Cats were blindly assigned to one of three groups: treatment with vehicle (10% polyethylene glycol in saline, n = 17), pretreatment with drug 3 hours before ischemia (n = 12), and posttreatment with drug at the time of reperfusion (n = 12). Size of the ischemic injury was calculated from 2,3,5-triphenyltetrazolium chloride staining. Injury in the caudate nucleus was significantly reduced with pretreatment (28 +/- 6% of ipsilateral caudate volume, mean +/- SEM) compared with the vehicle (56 +/- 8%). Posttreatment did not significantly ameliorate caudate injury (46 +/- 10%). Between the first and second hours of ischemia ipsilateral caudate blood flow determined using microspheres increased significantly from 11 +/- 4 to 16 +/- 5 ml/min/100 g with pretreatment, but blood flow remained constant throughout ischemia with vehicle (8 +/- 2 ml/min/100 g) and posttreatment (10 +/- 3 ml/min/100 g). The size of cortical injury (vehicle, 17 +/- 5%; pretreatment, 11 +/- 3%; posttreatment, 17 +/- 5% of hemispheric volume) did not differ significantly among groups. Somatosensory evoked potential recovery did not differ among groups. We conclude that pretreatment with conjugated superoxide dismutase can ameliorate the extent of injury in an end-artery region, such as the caudate nucleus, in a reperfusion model of focal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Glutamine synthetase inhibition prevents cerebral oedema during hyperammonemia.

The relationship between cerebral oedema and cerebral glutamine accumulation was investigated during acute hyperammonemia in anesthetized rats. Six hours of ammonium acetate infusion resulted in an increase in cortical glutamine concentration and a decrease in specific gravity. Pretreatment with methionine sulfoximine inhibited glutamine synthetase, prevented the increase in glutamine during hyperammonemia, and prevented the decrease in specific gravity. We conclude that the increase in brain water content is linked to the glutamine accumulation derived from the detoxification of ammonia by glutamine synthetase.

Acetates↗

PubMed1990

Blood-brain barrier disruption following CPR in piglets.

We studied blood-brain barrier (BBB) integrity in immature piglets during the following cardiopulmonary resuscitation (CPR). As in our previous work in the dog, there was no disruption during CPR after eight minutes of cardiac arrest, or immediately following resuscitation using a small molecule, alpha-aminoisobutyric acid. However, unlike the dog, where the BBB remained intact, we found delayed disruption of the BBB four hours after resuscitation. Young animals may be more prone to a delayed increase in BBB permeability after cardiac arrest and CPR.

Aminoisobutyric Acids↗

PubMed1990

Cerebrovascular and metabolic responses to hypoxia during hypoglycemia in dogs.

The effects of insulin-induced hypoglycemia on the response of cerebral blood flow (CBF-microspheres), electroencephalogram (EEG), and cerebral uptake/production of oxygen (CMRO2), glucose (CMRglu), lactate, pyruvate, beta-hydroxybutyrate, and acetoacetate to isocapnic hypoxic hypoxia were studied in pentobarbital-anesthetized, mechanically ventilated dogs. Hypoglycemia [1.3 +/- 0.2 mumol/ml, (+/-SE); n = 9] did not produce an isoelectric EEG and did not affect base-line CBF or CMRO2. When arterial O2 content was reduced from 17.4 +/- 0.6 to 7.5 +/- 0.5 and 5.1 +/- 0.2 vol% during hypoglycemia, CBF increased from 25 +/- 3 to 54 +/- 6 and 84 +/- 8 ml.100 g-1.min-1, respectively. This response was not different from that during normoglycemia (3.5 +/- 0.3 mumol/ml; n = 12). During normoglycemia, hypoxia increased CMRglu from 17.0 +/- 1.2 to 32.2 +/- 4.7 and 49.9 +/- 6.6 mumol.100 g-1.min-1, respectively. Hypoglycemia did not affect CMRglu during normoxia, but the hypoxia-induced increase in CMRglu was abolished. CMRO2 during hypoxia was unaffected by hypoglycemia. We conclude that levels of hypoglycemia that do not produce an isoelectric EEG may impair the normal increase in CMRglu during hypoxia but do not alter the global CBF response to hypoxia.

Animals↗

PubMed1990

Hypoglycemia and cerebral autoregulation in anesthetized dogs.

We examined the effects of moderate hypoglycemia with near-normal cerebral glucose consumption on cerebral autoregulation during graded hemorrhagic hypotension in anesthetized dogs. Four groups of animals (n = 8 each) were studied: normoglycemia, insulin-induced hypoglycemia (1.1 mM), normoglycemia plus alpha- and beta-adrenergic blockade [propranolol (1 mg/kg loading dose + 1 mg.kg-1.h-1 infusion) plus phentolamine (2 mg/kg loading dose + 2 mg/min infusion)], and hypoglycemia plus alpha- and beta-adrenergic blockade. As cerebral perfusion pressure was reduced to 40-50 mmHg, cerebral blood flow and O2 consumption increased in the hypoglycemic group. These increases were not observed after adrenergic blockade or in the normoglycemic groups. The perfusion pressure at which cerebrovascular resistance was minimal was higher during hypoglycemia (40 mmHg) and hypoglycemia plus blockade (50 mmHg) than in either of the normoglycemic groups (30 mmHg). This study demonstrates that hypoglycemia increases the lower limit of cerebral autoregulation during hypotension. Furthermore, adrenergic mechanisms acting during combined hypoglycemia and hemorrhagic hypotension increase cerebral blood flow and O2 consumption and attenuate the hypoglycemia-induced increase in the lower limit of autoregulation.

Anesthesia↗

PubMed1990

Arterial pH modulation of regional cerebral blood flow during hyperammonemia in dogs.

Acute hyperammonemia at normal arterial pH causes selective increases in midbrain blood flow in dogs. Unexpectedly, further increases occur with hypocapnia. We investigated whether metabolic acidemia and alkalemia modulate the distribution of ammonium across the blood-brain barrier and if, in turn, midbrain blood flow is effectively modulated. In dogs anesthetized with pentobarbital sodium, hyperammonemia (approximately 940 microM) was produced by a 210-min infusion of ammonium acetate. Concurrent infusion of NaHCO3 increased arterial pH to 7.53 +/- 0.02 (SE), whereas HCl infusion decreased pH to 7.11 +/- 0.01. Normocapnia was maintained. Cerebrospinal fluid [HCO3-] increased 5 mM with alkalemia (one-half of the increase in blood) and was unchanged with acidemia. Thus cerebrospinal fluid [H+]/blood [H+] was greater with alkalemia than acidemia. The corresponding ratio for ammonium was likewise greater with alkalemia (0.70 +/- 0.06) than acidemia (0.44 +/- 0.08). Microsphere-determined blood flow to midbrain more than doubled in the alkalemic group but was unchanged in the acidemic group. No other region along the neuraxis or in cerebrum showed increased blood flow in either hyperammonemic group. Alkalemia without hyperammonemia did not increase midbrain blood flow. Thus metabolic acidemia-alkalemia significantly alters ammonium partitioning into cerebrospinal fluid, and this alteration is sufficiently great to exert a specific physiological effect manifested by changes in midbrain blood flow.

Ammonia↗

PubMed1990

Age-related effects of compression rate and duration in cardiopulmonary resuscitation.

The effects of various compression rate and duration combinations on chest geometry and cerebral perfusion pressure during cardiopulmonary resuscitation (CPR) were studied in immature swine. Pentobarbital-anesthetized 2- and 8-wk-old piglets received CPR after ventricular fibrillation. At compression rates of 40, 60, 80, 100, 120, and 150/min, duty cycle (compression duration/total cycle time) was increased from 10 to 80% by 10% increments. Mean aortic and sagittal sinus pressures, pulsatile displacement, and deformity of the anterior chest wall were measured. Increasing duty cycle increased cerebral perfusion pressure until chest relaxation time was compromised. Inadequate chest recoil, development of static chest deformation, and limitation of pulsatile chest wall movement occurred in both age groups when relaxation time was very short (150-200 ms in 2-wk-old piglets, 250-300 ms in 8-wk-old piglets). These changes in chest geometry correlated with deterioration of cerebral perfusion pressure only in 8-wk-old piglets. In the younger group, perfusion pressures plateaued but did not deteriorate. These data emphasize the importance of duty cycle in generating cerebral perfusion pressure and indicate that younger animals can tolerate high compression rates except at extremely long duty cycles.

Aging↗

PubMed1990

Consistency of cerebral blood flow and evoked potential alterations with reversible focal ischemia in cats.

To enhance the consistency of the ischemic insult caused by reversible transorbital middle cerebral artery occlusion, we investigated the variability of somatosensory evoked potential amplitudes and regional cerebral blood flow in 26 anesthetized cats using four procedures to induce transient ischemia. These procedures included 60 minutes of left middle cerebral artery occlusion with or without left common carotid artery occlusion and 120 minutes of left middle cerebral artery occlusion with or without bilateral common carotid artery occlusion. Blood flow in the left middle cerebral artery territory was markedly and consistently reduced to less than 20 ml/min/100 g with simultaneous occlusion of the left middle cerebral artery and both common carotid arteries. The standard deviation of blood flow with this procedure (5.4) was less than that with the other three procedures (13-25). The amplitudes of ipsilateral somatosensory evoked potentials were decreased to approximately 20% of control during ischemia with all four procedures. During reperfusion, amplitudes recovered more slowly, to half of control, after both procedures involving 120 minutes of ischemia. After 120 minutes of reperfusion, the range of amplitudes was smallest in the group exposed to middle cerebral artery occlusion with bilateral common carotid artery occlusion. The degree of recovery of the somatosensory evoked potentials correlated with residual blood flow in both the ipsilateral middle cerebral artery territory and in the white matter during ischemia. We conclude that the most consistent model of focal ischemia and reperfusion in cats in which there is partial recovery of somatosensory evoked potentials is occlusion of one middle cerebral artery and both common carotid arteries for 120 minutes.

Animals↗

PubMed1990

Blood-brain barrier integrity during cardiopulmonary resuscitation in dogs.

Blood-brain barrier integrity during cardiopulmonary resuscitation may be important because of the potential effects of adrenergic agonists administered during arrest on cerebral metabolism and the cerebral vasculature. As an index of blood-brain barrier permeability to small molecules, we measured the brain uptake of [14C]alpha-aminoisobutyric acid during a 10-minute period in 25 anesthetized dogs. To correct for the amount of carbon-14 label in the plasma space, we administered [3H] inulin 2 minutes before death. The mean transfer coefficient in 14 brain regions of five control dogs ranged from 0.002 to 0.007 ml/g/min. After 8 (n = 15) or 15 (n = 5) minutes of cardiac arrest, external chest compression was instituted to maintain aortic blood pressure above 60 mm Hg. The transfer coefficient was not elevated during chest compression (n = 10), immediately following defibrillation (n = 5), or 4 hours after resuscitation (n = 5); in some brain regions the transfer coefficient decreased. However, the decrease in the transfer coefficient was proportional to the decrease in the cerebral plasma volume as measured by the ratio of the [3H]inulin concentration in the tissue to that in the plasma. Thus, it is unlikely that a decrease in capillary surface area masked an increase in blood-brain barrier permeability. Therefore, we found no evidence of blood-brain barrier disruption during or after cardiopulmonary resuscitation in dogs. Despite the large phasic increases in sagittal sinus pressure associated with external chest compression, concurrent increases in cerebrospinal fluid pressure apparently protect the microcirculation from increased transmural pressure.

Aminoisobutyric Acids↗

PubMed1989

A compartmental model for oxygen transport in brain microcirculation.

A compartmental model is formulated for oxygen transport in the cerebrovascular bed of the brain. The model considers the arteriolar, capillary and venular vessels. The vascular bed is represented as a series of compartments on the basis of blood vessel diameter. The formulation takes into account such parameters as hematocrit, vascular diameter, blood viscosity, blood flow, metabolic rate, the nonlinear oxygen dissociation curve, arterial PO2, P50 (oxygen tension at 50% hemoglobin saturation with O2) and carbon monoxide concentration. The countercurrent diffusional exchange between paired arterioles and venules is incorporated into the model. The model predicts significant longitudinal PO2 gradients in the precapillary vessels. However, gradients of hemoglobin saturation with oxygen remain fairly small. The longitudinal PO2 gradients in the postcapillary vessels are found to be very small. The effect of the following variables on tissue PO2 is studied: blood flow, PO2 in the arterial blood, hematocrit, P50, concentration of carbon monoxide, metabolic rate, arterial diameter, and the number of perfused capillaries. The qualitative features of PO2 distribution in the vascular network are not altered with moderate variation of these parameters. Finally, the various types of hypoxia, namely hypoxic, anemic and carbon monoxide hypoxia, are discussed in light of the above sensitivity analysis.

Animals↗

PubMed1989

Interaction of fentanyl and pentobarbital on peripheral and cerebral hemodynamics in newborn lambs.

The effects of 3.0 mg.kg-1 fentanyl on cerebral and peripheral hemodynamics alone and when combined with subanesthetic doses of pentobarbital (4.0 mg.kg-1), were studied in 11 unanesthetized, newborn lambs, in whom catheters had been previously inserted. After a control period, drugs were administered at 20-min intervals by intravenous bolus injection. Group 1 animals (n = 5) received fentanyl, pentobarbital, and naloxone (0.01 mg.kg-1), whereas Group 2 animals (n = 6) had the order of fentanyl and pentobarbital reversed. All animals responded to pain (withdrawal to tail clamping) and appeared conscious (eyes open, alert to sound) when either fentanyl or barbiturate was given alone. The combination of drugs, however, produced complete unresponsiveness. All of these effects were reversed by naloxone. Cardiac output did not change after either fentanyl or pentobarbital was administered individually but decreased significantly (29% in Group 1, 21% in Group 2) after administration of the combination of both. Mean arterial pressure and heart rate were unchanged. Cerebral blood flow, oxygen (O2) transport, and O2 consumption did not change after either administration of fentanyl or pentobarbital alone but decreased significantly after both (22%, 30%, 19%, respectively, in Group 1 and 35%, 40%, 38%, respectively, in Group 2). The decrease in cerebral O2 transport nearly paralleled the decrease in cerebral O2 consumption such that the ratio, the fractional O2 extraction, increased slightly. Fentanyl decreased kidney blood flow alone (24%) and in combination with pentobarbital (25%), although pentobarbital did so only when combined with fentanyl.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Cerebral blood flow and evoked potentials during Cushing response in sheep.

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

Animals↗

PubMed1989

Hemodilution causes size-dependent constriction of pial arterioles in the cat.

Cerebral blood flow (CBF) rises as hematocrit (Hct) falls. We previously attributed this rise in CBF to two independent factors of equal importance, decreased arterial O2 content and decreased blood viscosity. We hypothesized that decreased arterial O2 content would dilate cerebral arterioles and that the magnitude of the vasodilation would depend on the magnitude of the passive fall in vascular resistance attributable to decreased viscosity. The present study was designed to test the hypothesis that anemia is accompanied by cerebral vasodilation. Using a closed cranial window, we measured the diameters of 42 pial arterioles (35-305 microns) in 7 cats as serial isovolemic hemodilution lowered Hct by 44% from 31 +/- 4 to 17 +/- 3%. Hemodilution increased CBF (microsphere technique) but did not change mean arterial blood pressure or arterial blood gases. Anticipated vasodilation did not occur; instead, pial arterioles constricted as Hct fell. Maximum vasoconstriction was observed when Hct reached 65-70% of the initial value. Vasoconstriction lessened as Hct was lowered further, but arteriolar diameters at the lowest Hcts remained less than base-line levels. Constriction was greater in small (less than 100 microns) than in large (greater than or equal to 100 microns) arterioles. The initial constriction of pial arterioles may represent myogenic vasoconstriction in response to flow-induced vasodilation of more proximal portions of the cerebrovascular bed and/or to washout of an endogenous vasodilator. Arteriolar relaxation with more profound hemodilution may reflect superimposed metabolic vasodilation.

Animals↗

PubMed1989

Chemodenervation does not alter cerebrovascular response to hypoxic hypoxia.

We tested the hypothesis that sinoaortic chemodenervation would alter the increase in cerebral blood flow (CBF) during isocapnic hypoxic hypoxia in 1- to 7-day-old lambs. Lambs were anesthetized with pentobarbital and studied during moderate (arterial O2 content [CaO2] = 10 vol/100 ml) and severe (CaO2 = 6 vol/100 ml) hypoxic hypoxia. Regional brain blood flows were measured with the radioactive microsphere technique. Cerebral oxygen consumption (CMRO2) was calculated as the product of forebrain blood flow and the difference in oxygen contents between arterial and sagittal sinus blood. Lambs were then subjected to either sham surgery (n = 6) or to carotid chemodenervation and cervical vagotomy (n = 6). Chemodenervation was verified by abolition of the transient increase in blood pressure after intravenous injection of sodium cyanide in intact subjects. Neither sham surgery nor chemodenervation had an effect on CMRO2 or CBF during hypoxic hypoxia. These data thus do not support the hypothesis that arterial chemoreceptors play any substantial role in the regulation of cerebral vascular tone during hypoxic hypoxia in the 1- to 7-day-old anesthetized lamb.

Animals↗