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PubMed1999

Desensitization of catecholamine release. The novel catecholamine release-inhibitory peptide catestatin (chromogranin a344-364) acts at the receptor to prevent nicotinic cholinergic tolerance.

Nicotinic cholinergic receptors undergo desensitization upon repeated or prolonged exposure to agonist. We investigated the effects of a novel chromogranin A catecholamine release-inhibitory fragment, catestatin (chromogranin A344-364), on agonist-induced desensitization of catecholamine release from pheochromocytoma cells. In a dose-dependent fashion, the nicotinic antagonist catestatin blocked agonist desensitization of both catecholamine release (IC50 approximately 0.24 microM) and 22Na+ uptake (IC50 approximately 0.31 microM), the initial step in nicotinic cationic signal transduction; both secretion inhibition and blockade of desensitization were noncompetitive with agonist. Desensitizing effects of the nicotinic agonists nicotine and epibatidine were blocked. This antagonist action was specific to desensitization by nicotinic agonists, since catestatin did not block desensitization of catecholamine release induced by agents which bypass the nicotinic receptor. Hill plots with slopes near unity suggested noncooperativity for catestatin effects on both nicotinic responses (secretory antagonism and blockade of desensitization). Human, bovine, and rat catestatins (as well as substance P) had similar potencies. IC50 values for secretion inhibition and blockade of desensitization paralleled each other (r = 0.76, n = 10 antagonists, p = 0.01) for several noncompetitive nicotinic antagonists. Peptide nicotinic antagonists (catestatins, substance P) were far more potent inhibitors of both secretion (p = 0.019) and desensitization (p = 0.005) than nonpeptide antagonists (trimethaphan, hexamethonium, procaine, phencyclidine, cocaine, or clonidine), and the peptides displayed enhanced selectivity to block desensitization versus secretion (p = 0.003). We conclude that catestatin is a highly potent, dose-dependent, noncompetitive, noncooperative, specific inhibitor of nicotinic desensitization, an effect which may have implications for control of catecholamine release.

Animals↗
PubMed1984

Autoregulation of cortical blood flow and oxygen tension in the rabbit.

The relationship between cerebral blood flow autoregulation and oxygen tension of cerebral tissue is not fully known. We have examined the autoregulation of local cortical blood flow (CoBF) and cortical oxygen tension (bPO2) in the rabbit. CoBF was measured continuously by using the heated thermocouple technique and bPo2 was monitored by the polarographic method. Intravenous injection of phenylephrine hydrochloride or trimethaphan camsylate was used to test for autoregulation by increasing or decreasing perfusion pressure. The mean values of CoBF and bPO2 were 36 +/- 5 ml/100g/min and 32 +/- 12 mmHg respectively at 90 mmHg mean arterial blood pressure (MABP). The changes in both CoBF and bPO2 with changing perfusion pressure were often relatively small at near baseline blood pressure and became more pronounced with large increases or decreases in MAPB. On returning from high MABP to baseline blood pressure, a hysteresis effect on CoBF was observed in 20 out of 22 cases. The autoregulation of CoBF was maintained in the range between 80 and 100 mmHg MABP. On the other hand, bPO2 was maintained constant in the range between 75 and 110 mmHg. This range is significantly wider than that of CoBF. We conclude that autoregulation of CoBF limits changes in local CoBF to maintain constant oxygen tension in brain tissue.

Animals↗
PubMed1975

Effects of morphine-nitrous oxide anesthesia on cerebral autoregulation.

The effects of morphine-nitrous oxide anesthesia on cerebral autoregulation were studied in healthy male volunteers. Anesthesia was morphine, 2 mg/kg, and 70 per cent nitrous oxide in oxygen. Ventilation was controlled and carbon dioxide added to keep Paco-2 constant at 40 torr. Cerebral blood flow was measured first at the subject's normal mean arterial blood pressure, than at 60 torr and at 120 torr in a randomly assigned balanced order. Last, in five subjects cerebral blood flow was measured again at normal mean pressure. Blood pressure alteration was accomplished using phenylephrine or trimethaphan. Cerebral blood flow was 38.9 plus or minus 6.4 (SEM) ml/100 g/min at normal mean pressure, 49.5 plus or minus 10.7 ml/100 g/min at 60 torr. These values are not different a P IS LESS THAN 0.05. The data were analyzed for the possible effect of time on cerebral blood flow, and no change could be domonstrated. It is concluded that with Paco-2 constant at 40 torr morphine-nitrous oxide anesthesia does not significantly affect cerebral autoregulation in normal man.

Anesthesia, Inhalation↗
PubMed1979

Intracranial pressure in the cat during nitroglycerin-induced hypotension.

Intracranial pressure measurements were made during nitroglycerin-induced hypotension in the cat anesthetized with halothane. A total of 48 individual observations were made in eight animals. The administration of sufficient nitroglycerin to decrease mean arterial pressure from a control value of 87 +/- 7 torr by 12 +/- 4 torr resulted in an increase in mean intracranial pressure from a control value of 7 +/- 2 torr to 12 +/- 2 torr. Larger decreases in mean blood pressure were associated with larger increases in intracranial pressure. The increase in intracranial pressure was similar to that previously reported for nitroprusside, and greater as well as more reproducible than that reported for trimethaphan. Thus, nitroglycerin may produce significant increases in intracranial pressure, and this may be a limiting factor in its clinical use.

Anesthesia, Inhalation↗
PubMed1985

Cardiovascular responses to hemodilution and controlled hypotension in the dog.

Cardiovascular responses to acute hemodilution and controlled hypotension were studied in mongrel dogs anesthetized with halothane and paralyzed with pancuronium. Regional blood flows were determined by microsphere injections. Hemodilution to an hematocrit of 23% was produced by removal of whole blood and simultaneous infusion of Ringer's lactate solution. Subsequently, hypotension to a mean arterial pressure of 55 mmHg was produced for 90 min by intravenous infusion of trimethaphan. The hypotension resulted entirely from a 55% decrease in total peripheral resistance. Thirty minutes after initiation of controlled hypotension, there were significant increases in blood flow to the brain, liver, skeletal muscles, and diaphragm. However, at 30 min, calculated oxygen delivery had decreased to brain (-16%), renal cortex (-51%), heart (-45%), and retina (-44%). By 90 min, retinal, adrenal, and renal cortical blood flows were decreased significantly relative to control, and cerebral blood flows had returned to control levels. Absence of changes in acid-base status during the period of hemodilution and hypotension may indicate that whole body oxygen delivery was maintained at adequate levels. However, major decreases in calculated oxygen delivery after 90 min to critical tissue beds such as renal cortex (-67%) and retina (-78%) indicate that extension of the procedure past 30 min may involve risks that are not warranted by the benefits.

Animals↗
PubMed1986

Electrical correlates of brain injury resulting from severe hypotension and hemodilution in monkeys.

The effects of hypotension, hemodilution, and their combination on the relationship between concurrent brain electrical activity and resulting brain injury were studied in anesthetized monkeys. The authors compared changes in the electroencephalogram and somatosensory and auditory evoked potentials with eventual neuropathologic outcome. Our goals were: 1) to define the margin of safety for the monkey brain during hemodilution and hypotension under several simulated clinical conditions; and 2) to determine whether noninvasive measurements of brain electrical activity can predict ischemic brain cell damage. Forty-one monkeys were anesthetized with halothane (0.8 vol % inspired) and ventilated mechanically. Arterial hypotension was induced with trimethaphan (25 +/- 8 mmHg mean arterial blood pressure [MABP] for 30 min). Hemodilution was induced by replacing blood with lactated Ringer's solution (14 +/- 2% hematocrit for 1 h). Combined hemodilution and hypotension consisted of 30 min of hemodilution alone followed by superimposing hypotension for 30 min (16 +/- 3% hematocrit and 29 +/- 5 mmHg MABP). Ten monkeys died following severe hypotension alone or combined hemodilution and hypertension as a consequence of cardiac arrest or undetermined (possibly neurologic) causes. No histologic evidence of ischemic brain cell injury was found in surviving monkeys subjected to hemodilution or hypotension alone. Neuropathologic alterations in the cerebral cortex, cerebellum, hippocampus and globus pallidus as well as neurologic and behavioral deficits were found in seven of 16 surviving monkeys subjected to both hemodilution and hypotension. These findings resulted from combinations of hematocrit less than 20% and MABP below 40 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The effect of nimodipine on post-ischemic cerebral glucose utilization and blood flow in the rat.

The authors hypothesized that pretreatment with the calcium entry blocker nimodipine would preserve cerebral glucose utilization and maintain favorable brain blood flow after cerebral ischemia. Three groups of pentobarbital anesthetized rats were studied: control (group 1), ischemia (group 2), and ischemia plus nimodipine pretreatment, 1 mg X kg-1 ip, 1 h prior to ischemia (group 3). Forebrain ischemia was induced with bilateral carotid clamping, administration of trimethaphan, and blood withdrawal to obtain a mean arterial pressure of 50 mmHg. The carotid clamps were released and blood re-infusion was begun 9 min after the onset of an isoelectric EEG signal. Ten minutes later, determination of regional cerebral glucose utilization (rCGU) was begun by injecting 3H-2-deoxyglucose in saline. After 60 min of reperfusion, regional cerebral blood flow (rCBF) was determined by the indicator fractionation method, using 14C-iodoantipyrine. The brain was divided into hemisphere, diencephalon, cerebellum, and brainstem. Tissue radioactivities were determined by standard techniques. Compared to group 1, hemispheric rCGU (mean +/- SEM, mumoles X 100 g-1) was significantly (P less than 0.05) reduced in groups 2 and 3 (40 +/- 3 vs. 27 +/- 2 and 22 +/- 2). Hemispheric rCGU was not significantly different in groups 2 and 3. Group 2 exhibited significantly (P less than 0.05) reduced rCBF (mean +/- SEM, ml X 100 g-1 X min-1) in the hemispheres compared to control (85 +/- 6 vs. 135 +/- 17). However, nimodipine pretreatment prevented this post-ischemic hypoperfusion in group 3 (133 +/- 18).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The interaction of sodium nitroprusside, hypotension, and isoflurane in determining cerebral vasculature effects.

Eighteen mongrel dogs were anesthetized with isoflurane and prepared for determining cerebral blood flow (CBF, sagittal sinus outflow), cerebral metabolic rate (CMRO2), and ICP. Dogs were divided into three groups of six each. Group 1 dogs were maintained on 1 MAC isoflurane and, following control measurements (step 1), sodium nitroprusside (SNP) was infused to decrease mean arterial pressure (MAP) to 60 mmHg (step 2). After 20 min SNP was discontinued and a second control period of 20 min followed (step 3). Thereafter, SNP was repeated for 20 min as in step 2, but MAP was maintained by inflating a balloon in the descending aorta (step 4). SNP was again discontinued followed by a final 20 min control period (step 5). During SNP with hypotension (step 2) there was a significant 21% decrease in CBF and no change in ICP. During SNP with normotension (step 4) both CBF and ICP increased (16 and 39%, respectively). In group 2 dogs isoflurane was discontinued and a spinal anesthetic was administered. Thereafter, these dogs were studied as in group 1. The only significant change in these dogs was a 35% increase in ICP during SNP with normotension. Group 3 dogs were studied identically to group 2, but hypotension was induced with trimethaphan (TMP). There were no significant changes in these dogs. The authors conclude that SNP, in the absence of isoflurane, dilates capacitance vessels because ICP increased without a concomitant increase in CBF at normotension. In the presence of isoflurane, SNP dilates both capacitance and resistance vessels because ICP and CBF increased concomitantly at normotension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Postischemic brain oxygenation with barbiturate therapy in rats.

We measured rat brain cortex PO2 (PtO2) with gold microelectrodes (tip diameter 5--10 micron) for up to 2 hours after 16 min of transient global brain ischemia with and without thiopental 90 mg/kg infused iv over 60 min beginning at 5 min postischemia. Seventeen rats were immobilized and mechanically ventilated on 1% halothane in oxygen with continuous monitoring of PtO2, ECG, end-expiratory CO2, rectal temperature, and arterial blood pressure. Global ischemia was induced by trimethaphan hypotension to an MAP of about 50 torr and a neck tourniquet inflated to 1500 torr. Postischemia, nine control rats (11 PtO2 measurements) were untreated and eight rats (8 PtO2 measurements) received thiopental 90 mg/kg. Preischemia, PtO2 values in both groups ranged from less than 5--70 torr with values of greatest frequency between 10 and 15 torr. Postischemia, PtO2 in control rats peaked at 45 +/- 8 (SEM) torr at 20 min. In thiopental treated rats, peak PtO2 was 24 +/- 6 torr at 10 min postischemia. Relative frequency histograms of PtO2 revealed that PtO2 in thiopental treated rats was lower (p less than 0.05) between 15 and 30 min postischemia. The magnitude of the decrease in PtO2 between 105 and 120 min postischemia appeared to correlate directly with the absolute preischemic value (i.e., the higher the preischemic PtO2, the greater the decrease in PtO2 postischemia). These results suggest that thiopental administered in large doses in early postischemia does not improve brain oxygenation secondary to a reduction in brain oxygen consumption. The relevance of the correlation between the magnitude of the fall in PtO2 postischemia and the magnitude of the preischemic value is discussed.

Animals↗
PubMed1988

Impaired baroreflex changes in muscle sympathetic nerve activity in adolescents who have a family history of essential hypertension.

To evaluate the baroreflex changes and basal sympathetic vasomotor tone among three groups of adolescent normotensives or borderline hypertensives with and normotensives without a family history of hypertension, we continuously recorded muscle sympathetic nerve activity, arterial pressure and heart interval. Baroreflex slopes were calculated either by plotting the heart interval against the preceding peak systolic arterial pressure, or by relating the percentage changes in muscle sympathetic nerve activity to the mean changes in systolic arterial pressure produced by intravenous phenylephrine. The baroreflex slopes for the heart interval were significantly smaller in borderline hypertensive offspring (14 +/- 2 ms/mmHg) than in control normotensives (23 +/- 2 ms/mmHg) or normotensive offspring (19 +/- 3 ms/mmHg), whereas those for muscle sympathetic nerve activity were significantly smaller both in normotensive offspring (-8.3 +/- 1.0%/mmHg) and borderline hypertensive offspring (-7.9 +/- 0.5%/mmHg) than in control normotensives (-16.3 +/- 1.4%/mmHg). Baseline muscle sympathetic nerve activity was higher in borderline hypertensive offspring (20.1 +/- 3.0 bursts/min) than in control normotensives (10.1 +/- 1.2 bursts/min) or normotensive offspring (12.8 +/- 1.4 bursts/min), and also the depressor responses to trimethaphan were significantly enhanced in borderline hypertensive offspring [-19.2 +/- 2 versus 14 +/- 1 (normotensive offspring) or 12 +/- 2 (control normotensives)]. These results indicate that baroreflex inhibition of muscle sympathetic nerve activity was reduced in adolescents with a family history of hypertension even when they were normotensive. This reduced reflex sympatho-inhibition could lead to the development of hypertension by increasing sympathetic vasomotor tone.

Adult↗
PubMed2003

The sympathetic nervous system in hypertension: assessment by blood pressure variability and ganglionic blockade.

OBJECTIVE: To determine if the contribution of the sympathetic nervous system to blood pressure could be evidenced by low-frequency oscillations of systolic blood pressure (LF(SBP)), reflecting vascular sympathetic modulation, or by the decrease in blood pressure after autonomic blockade. DESIGN: We studied multiple system atrophy (MSA) patients, in whom supine hypertension is maintained by residual sympathetic tone ('positive controls'); pure autonomic failure (PAF) patients, in whom supine hypertension is largely independent of sympathetic tone ('negative controls'); essential hypertensive patients (HTN) and normotensive subjects (NTN). RESULTS: Supine systolic blood pressure (SBP) was 204 +/- 8, 185 +/- 6, 177 +/- 9 and 130 +/- 4 mmHg in MSA, PAF, HTN and NTN, respectively. LF(SBP) was higher in MSA and HTN (5.7 +/- 1.5 and 5.8 +/- 1.4 mmHg(2) compared to NTN and PAF (3.3 +/- 0.5 and 1.1 +/- 0.5 mmHg(2). Trimethaphan 2-4 mg/min induced complete autonomic blockade and lowered SBP below 125 mmHg in all NTN and all but one MSA (to 111 +/- 3 and 97 +/- 9 mmHg). SBP remained elevated in PAF (164 +/- 7 mmHg). Responses in HTN were variable; SBP decreased below 125 mmHg in three and remained elevated in four patients. The decrease in LF(SBP) correlated with the reduction in SBP, with a steeper slope in MSA and HTN compared to NTN (29.0 +/- 5.5, 8.4 +/- 1.6 and 3.6 +/- 1.2 mmHg/mmH (2), respectively). CONCLUSION: Ganglionic blockade, alone or coupled to LF(SBP), discriminated between human models of sympathetic-dependent (MSA) and independent (PAF) hypertension. This approach may aid in assessing the contribution of the sympathetic nervous system in essential hypertension, in which sympathetic dependence is variably expressed.

Aged↗
PubMed1990

Effect of nimodipine on cerebral blood flow in human volunteers.

The present study was undertaken to examine the effect of a clinically relevant dose of nimodipine (30 micrograms/kg/h) on the autoregulation of CBF in 12 young healthy volunteers. Mean arterial blood pressure (MABP) was measured intraarterially (i.a.), and changes in cerebral blood flow (CBF) were estimated by the arteriovenous-oxygen [(a-v)O2]-difference method. The lower limit (LL) of CBF autoregulation was calculated by a computerized program and tested for different factors for correction of the PaCO2-induced changes in CBF. MABP was increased by norepinephrine (NE) and decreased by ganglion blockade (trimethaphane camphosulfonas) in combination with lower body negative pressure. The MABP manipulations were performed 1 h after infusion of nimodipine. MABP was reduced by 13 mm Hg (8-15 mm Hg), and CBF was increased by 8% (3-12%) during nimodipine infusion. Autoregulation was preserved in 11 of the 12 volunteers. A CO2-correction factor of 1% CBF/0.1 kPa was used. The LL was 75 mm Hg (71-80 mm Hg) [SE 3 mm Hg (2-4 mm Hg)] and not significantly different from a previous control group of healthy volunteers. No side effects were observed. The present study shows a maintained autoregulation of CBF during nimodipine infusion; however, this could be obtained only by reducing the correction for changes in carbon dioxide to 1%/0.1 kPa from 3%/0.1 kPa, which was used in a similar study in healthy volunteers.

Adult↗
PubMed1992

Endothelium-dependent and -independent vasodilation and reactive hyperemia in healthy smokers.

Although cigarette smoking elicits a transient increase in peripheral vascular resistance in humans, the basal blood pressure (BP) is usually slightly lower in smokers. We hypothesized that this may be due to a compensatory increase in sensitivity in smokers to endogenous vasodilators. To test this, we studied endothelium-dependent and -independent vasodilator responses, and reactive hyperemia (RH) in the forearm of 25 healthy subjects [11 smokers (S) and 14 nonsmokers (NS)]. Endothelium-dependent vasodilation was induced by infusion into a brachial artery of stepwise increasing dosages of acetylcholine (ACh, 10-60 micrograms/kg/min) and endothelium-independent vasodilation by a similar infusion of nitroprusside (N, 1-6 micrograms/kg/min). RH was induced by release of a 5-min upper arm arterial occlusion. Forearm blood flow (FBF) was recorded by plethysmography. Endothelium-dependent vasodilation was more pronounced in S than in NS (p < 0.01), the maximal FBF during infusion of ACh being 20 +/- 6 and 14 +/- 4 ml/100 ml/min, respectively. Endothelium-independent vasodilation was also larger in S than in NS (p < 0.001), the maximal FBF during infusion of N being 14 +/- 3 and 12 +/- 2 ml/100 ml/min, respectively. ACh-induced vasodilator responses in S and NS were completely blocked by atropine. They were not decreased by trimethaphan, a nicotinic receptor inhibitor. RH was slightly more pronounced in S than in NS (p < 0.02), the postocclusive FBF 15 s after release of the occlusion being 25 +/- 4 and 21 +/- 3 ml/100 ml/min, respectively We propose that cigarette smoking increases the sensitivity of the vascular smooth muscle to vasodilator stimuli.

Acetylcholine↗
PubMed1999

"Skin-CNS-bladder" reflex pathway for micturition after spinal cord injury and its underlying mechanisms.

PURPOSE: A "skin-CNS-bladder" reflex pathway for inducing micturition after spinal cord injury has been established in cat. This reflex pathway which is basically a somatic reflex arc with a modified efferent limb that passes somatic motor impulses to the bladder, has been designed to allow spinal cord injured patients to initiate voiding by scratching the skin. MATERIALS AND METHODS: The skin-CNS-bladder reflex was established in the cat by intradural microanastomosis of the left L7 ventral root (VR) to the S1 VR while leaving the L7 dorsal root (DR) intact to conduct cutaneous afferent signals that can trigger the new micturition reflex arc. After allowing 11 weeks for axonal regeneration, urodynamic, pharmacological and electrophysiological studies were conducted in pentobarbital or chloralose anesthetized animals. RESULTS: A detrusor contraction was initiated at short latency by scratching the skin or by percutaneous electrical stimulation in the L7 dermatome. Maximal bladder pressures during this stimulation were similar to those activated by bladder distension in control animals. Electrophysiological recording revealed that single stimuli (0.3 to 3 mA, 0.02 to 0.2 msec duration) to the left L7 spinal nerve in which the efferent axons had degenerated evoked action potentials (0.5 to 1 mV) in the left S1 spinal nerve distal to the anastomosis. In addition, increases in bladder pressure were elicited by trains of the stimuli (5 to 20 Hz, 5 seconds) applied to the L7 spinal nerve. Urodynamic studies including external sphincter EMG recording demonstrated that the new reflex pathway could initiate voiding without detrusor-external urethral sphincter dyssynergia. Atropine (0.05 mg./kg., i.v.) or trimethaphan (5 mg./kg., i.v.), a ganglionic blocking agent, depressed the bladder contractions elicited by skin stimulation. The skin-CNS-bladder reflex could also be elicited after transecting the spinal cord at the L2-L3 or L7-S1 levels. CONCLUSION: The cross-wired somato-autonomic bladder reflex is effective in initiating bladder contractions and coordinated voiding in cats with an intact neuraxis and can also induce bladder contractions after acute transection of the lumbar spinal cord. The new pathway is mediated by cholinergic transmission involving both nicotinic and muscarinic receptors. It is concluded that somatic motor axons can innervate bladder parasympathetic ganglion cells and thereby transfer somatic reflex activity to the bladder smooth muscle.

Anastomosis, Surgical↗
PubMed1991

Hemodynamic response with passive neck flexion in brain death.

Twelve brain-dead patients admitted to the Department of Traumatology, Osaka University Hospital, from July 1988 to August 1989 were studied. A hemodynamic response elicited by passive neck flexion was observed in 10 of the 12 patients. After passive neck flexion, blood pressure began to rise, and the heart rate increased slightly. Blood pressure peaked about 2 minutes after the initiation of neck flexion and then decreased gradually to the baseline level within a few minutes. These responses were suppressed completely by administration of the ganglion blocker trimethaphan camsilate, which suggests that the efferent pathway of the response is mediated by the sympathetic nervous system.

Adolescent↗
PubMed1978

Posterior spinal fusion with Harrington instrumentation using "balanced" anesthesia.

In our experience nitrous oxide-oxygen-morphine-curare anesthesia has proved preferable because of the need for swifly awakening patients after instrumentation to ascertain neurologic status. Adjunctively, doxapram has been used to awaken patients in a predictably short time span. To prevent massive blood loss, hypotension has been attained by pentolinium, trimethaphan camsylate, and sodium nitroprusside.

Anesthesia↗
PubMed1990

Succinylcholine-induced increases in CSF pressure are not affected by PaCO2 or mean arterial pressure in dogs.

The effects of PaCO2 and mean arterial pressure (MAP) on succinylcholine-induced changes in cerebrospinal fluid (CSF) pressure were examined in 31 dogs anesthetized with halothane (0.7% end-expired) and nitrous oxide (66% inspired) in oxygen. Group 1 (n = 9) received succinylcholine (1.5 mg/kg i.v.) without control of PaCO2 or MAP. Group 2 (n = 12) received succinylcholine with CO2 maintained at control, and no regulation of MAP. Group 3 (n = 10) received succinylcholine without regulation of PaCO2 and maintenance of MAP at control values with trimethaphan. Succinylcholine produced an increase in CSF pressure of 1.7 +/- 1.7-3.9 +/- 3.6 cm H2O (mean +/- SD). There were no differences in CSF pressure increase between groups. The increase in CSF pressure was compared to the variation in the uncontrolled physiological parameter (i.e., CSF pressure was compared to PaCO2 and MAP in group 1, MAP in group 2, and PaCO2 in group 3). The CSF pressure increase over time did not strictly parallel changes in PaCO2 and/or MAP, and the magnitude of increase of CSF pressure did not correlate significantly with PaCO2 and/or MAP. It is concluded that, in anesthetized dogs, succinylcholine produces relatively small increases in CSF pressure whether or not PaCO2 or MAP is controlled. These results do not support the hypothesis that a succinylcholine-induced increase in CSF pressure is due chiefly to an increase in PaCO2 and/or MAP and can be abolished by preventing those changes.

Journal Article↗
PubMed1991

Effects of ethanol on spinal cord blood flow in the rat.

This study examines the effects of low and high concentrations of ethanol on spinal cord blood flow (SCBF) in the rat. SCBF was measured in the following blood pressure ranges: (a) <60 mm Hg, (b) 60-90 mm Hg, (c) 90-120 mm Hg, (d) 120-150 mm Hg, and (e) >150 mm Hg. Rats were anesthetized with 1.4% isoflurane in air and randomly assigned to the following treatment groups: group 1 (n = 12), intraperitoneal (i.p.) saline injection; group 2 (n = 10), 1 g/kg of ethanol i.p.; and group 3 (n = 14), 4 g/kg of ethanol i.p. Blood pressure was increased by intravenous phenylephrine infusion or lowered by a combination of intravenous trimethaphan and blood withdrawal. The SCBF was measured in cervical, thoracic, and lumbar segments using radioactive microspheres. The plasma ethanol concentration was 0 mg/ml for group 1, 0.64 +/- 0.06 mg/ml (mean +/- SEM) in group 2, and 4.18 +/- 0.11 mg/ml in group 3. In control rats, the cervical SCBF was higher than the thoracic or lumbar SCBF, evaluated over the entire blood pressure range (analysis of variance, p <0.05). This difference in regional SCBF was abolished by ethanol. Ethanol produced a significant decrease in cervical and lumbar SCBF (p <0.05) but not thoracic SCBF (p = 0.07). This decrease in SCBF was most pronounced at high blood pressures. These results suggest that ethanol produces vasoconstriction in the spinal cord that is countered by autoregulatory vasodilation at low blood pressures.

Journal Article↗