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PubMed1993

Influence of maternal insulin-dependent diabetes mellitus on neonatal morbidity.

OBJECTIVE: To compare the neonatal morbidity rates (corrected for gestational age at delivery and method of delivery) among infants of women with insulin-dependent diabetes mellitus and those of women without diabetes. DESIGN: Historical cohort analysis. SETTING: Tertiary care centre. PATIENTS: All liveborn infants of women with insulin-dependent diabetes mellitus (IDM group) born between Jan. 1, 1980, and Dec. 31, 1989, each matched for gestational age at delivery, method of delivery and year of birth with two newborns of women without diabetes (control group). MAIN OUTCOME MEASURES: Neonatal respiratory distress, jaundice, hypoglycemia, polycythemia, hypocalcemia, intraventricular hemorrhage, seizure and macrosomia. RESULTS: There were 230 infants in the IDM group and 460 in the control group. Compared with the control group the IDM group had significantly higher incidence rates of glucose infusion (odds ratio [OR] 5.38), birth weight above the 90th percentile (OR 4.15) and neonatal jaundice (OR 1.94). No significant difference was found in the incidence rate of respiratory distress, polycythemia or hypocalcemia. The maternal serum hemoglobin A (HbA) level was not significantly related to birth weight, and neither the serum HbA level nor the presence of macrosomia was predictive of neonatal morbidity. Nearly 25% of the infants in the IDM group were born before 37 weeks' gestation; 48.2% of these were delivered early because of maternal hypertension. CONCLUSIONS: Neonatal morbidity in infants of women with diabetes is determined more by gestational age at delivery than by the maternal diabetes. Within the limits obtained in this study the degree of control of the diabetes does not seem to affect neonatal morbidity.

Adult↗
PubMed1986

Influence of intracerebroventricularly infused anions on feeding response.

Chloride and bicarbonate solutions of potassium, calcium, sodium, and barium were infused into the third ventricle of the rats to observe the influence of anions on feeding response. Stainless steel cannulae were chronically implanted into the anteroventral part of the third ventricle of 54 rats, which were divided in 9 equal groups. While the control group was given 10 microliters of artificial cerebrospinal fluid intraventricularly, the remaining 8 groups received the equal quantity (10 microliters) of one of the hypertonic equimolar test solutions. Chloride solutions of potassium, calcium, and barium evoked significantly (p less than 0.05) higher feeding than the control group, while none of the bicarbonate solutions influenced feeding significantly. Chloride solutions of all the 4 cations elicited significantly (p less than 0.05) higher feeding than the corresponding bicarbonate solutions in 24 hr. It was observed that though the cations differed, there was no significant difference in the responses elicited by the different chloride solutions. Similarly, various bicarbonate solutions elicited similar responses. Osmolality and pH of the infusion solution have not influenced feeding significantly. It is concluded that the anionic, but not the cationic concentration of the fluid bathing juxtacerebroventricular sensors, predominantly influence the feeding response.

Animals↗
PubMed1989

Electrocardiographic and hemodynamic effects of intravenous cocaine in awake and anesthetized dogs.

Graded bolus and infusion doses of cocaine were given to 18 dogs, 6 under general anesthesia and 12 awake, to determine the range of hemodynamic and electrocardiographic effects. Blood pressure, electrocardiographic measurements, cocaine plasma levels, temperature, electrolytes, and arterial blood gases were measured before and after the initial bolus and/or infusion at 10 minutes and each 30 minutes up to a maximum of 180 minutes. At the end of the infusion, a single large intravenous terminal bolus of cocaine was given. The hemodynamic and electrocardiographic changes occurred by 10 minutes after the bolus and resolved by 30 minutes, independent of the infusion rate and dose. Only anesthetized dogs could tolerate the highest cocaine doses. Three ranges of bolus doses were given: the lowest range was the average initial bolus dose received by the awake group; the intermediate range was the average initial bolus dose received by the anesthetized group; and the highest range was the average terminal bolus dose. The heart rate changes were unpredictable and did not change significantly at any dose range. The blood pressure increased in the lowest dose range, remained unchanged at intermediate doses, and fell at the highest doses in four of six dogs. Electrocardiographic intervals increased as the dose range increased. Only at the highest doses did potentially lethal ventricular arrhythmia (ventricular tachycardia and an idioventricular escape rhythm) occur. Intravenous cocaine causes hemodynamic and electrocardiographic effects that are related to the dose and rate of administration. At high doses, hypotension, arrhythmia, and electrocardiographic changes consistent with infranodal and/or intraventricular conduction slowing can occur.

Anesthesia, General↗
PubMed1997

Reversible Schwann cell hyperplasia and sprouting of sensory and sympathetic neurites after intraventricular administration of nerve growth factor.

Substantial dysfunction and loss of cholinergic neurons occur in Alzheimer's disease (AD). Nerve growth factor (NGF) is a potent neurotrophic factor for cholinergic basal forebrain neurons, and the use of NGF to stimulate residual dysfunctional cells in AD is being considered. To define the effects of NGF on other cell populations in the brain, NGF was continuously infused into the lateral ventricle of rats for 7 weeks. At the end of treatment, Schwann cell hyperplasia and abundant sensory and sympathetic neurite sprouting were observed in the subpial region of the medulla oblongata and the spinal cord. Following withdrawal of NGF, the Schwann cell hyperplasia and sprouting of sensory and sympathetic neurites disappeared completely. These findings suggest that better temporal and spatial delivery systems for NGF must be explored to limit potential undesirable side effects while maintaining the survival and function of diseased basal forebrain cholinergic neurons.

Animals↗
PubMed1998

Effects of gastrointestinal prokinetic agents, TKS159 and cisapride, on the in situ canine heart assessed by cardiohemodynamic and electrophysiological monitoring.

Effects of a novel 5-HT4 receptor agonist TKS159 on the cardiovascular system were assessed in comparison with cisapride using an in vivo canine model. TKS159 in doses of 0.1, 1.0, and 10 mg/kg (n = 6) or cisapride in 1/10 doses of 0.01, 0.1, and 1.0 mg/kg (n = 6) was cumulatively infused over 10 min with a pause of 20 min. The doses of the drugs were determined according to the previous knowledge of their pharmacokinetics. Clinically effective plasma concentrations as a gastrointestinal prokinetic drug were obtained after the infusion of 0.1 mg/kg of the respective drugs. In TKS159-administered animals, no significant change was induced in each cardiovascular parameter by an infusion of 0.1 mg/kg. The blood pressure was decreased, and the effective refractory period and repolarization phase of the ventricle were prolonged after 1.0 mg/kg. The heart rate was decreased, and the atrioventricular, as well as intraventricular, conduction were suppressed after 10 mg/kg, while no significant changes were observed in the cardiac output and the ventricular contraction and the relative refractory period of the ventricle during the study. Meanwhile, in cisapride-administered animals, the repolarization phase and the effective refractory period were prolonged after 0.01 mg/kg. The heart rate and the blood pressure were decreased after 0.1 mg/kg. The cardiac output, the ventricular contraction, and the atrioventricular conduction were suppressed, the relative refractory period was prolonged, and early afterdepolarization was detected after 1.0 mg/kg, while no significant change was observed in the intraventricular conduction during the study. Thus, TKS159 may have a safer cardiovascular profile than cisapride.

Action Potentials↗
PubMed1996

Influence of corticotropin-releasing hormone on electrophysiological activity of locus coeruleus neurons.

These experiments examined the effects of corticotropin-releasing hormone (CRH) on single-unit electrophysiological activity of locus coeruleus (LC) neurons. As has been reported previously, infusion of CRH into the ventricular system of the brain (i.c.v.) of halothane-anesthetized adult male rats increased spontaneous discharge rate of LC neurons while producing no increase, and possibly a decrease, in sensory-evoked activity. However, when i.c.v. CRH was given to female rats or immature male rats, which had not been studied previously, LC activity was not altered. To attempt to understand this sex and age difference, potential mechanisms by which i.c.v. CRH elevates LC spontaneous activity in adult male rats were examined; in that i.c.v. CRH activates the pituitary-adrenal axis and autonomic nervous system, these response systems were manipulated. Adrenalectomy (with or without corticosterone replacement by pellet) did not affect the ability of i.c.v. CRH to increase LC spontaneous activity in adult male animals, but blockade of sympathetically-mediated autonomic responses, either by chlorisondamine or the beta adrenergic receptor blocker timolol, blocked this increase, indicating that afferent feedback from peripheral autonomic responses was critical for activating LC neurons following i.c.v. CRH. To determine whether CRH neurotransmission might play a role in this feedback pathway, the CRH antagonist alpha-helical CRH (alpha-hCRH) was microinjected into several brain regions including LC prior to i.c.v. CRH. alpha-hCRH microinjected into LC reduced the increase in LC activity caused by i.c.v. CRH; however, blockade of this increase was total when alpha-hCRH was microinjected into the lateral parabrachial nucleus ipsilateral to the LC recording site, suggesting that increased LC activity following i.c.v. CRH is mediated by CRH acting in the parabrachial region. During these studies, it was also observed that microinjection of alpha-hCRH into LC increased LC spontaneous discharge rate; consequently, CRH was microinjected into LC, and produced a dose-dependent decrease in LC spontaneous activity in both male and female rats, which could be blocked by microinjection of alpha-hCRH - these data indicated that the direct influence of CRH on LC neurons is to decrease their spontaneous activity. To reconcile this with the original report that CRH applied to LC neurons increases their activity, one possibility suggested is that the CRH microinjection procedure used in the present study stimulated inhibitory receptors on LC dendrites whereas the original study stimulated excitatory receptors on LC cell bodies. It is concluded that an inhibitory influence of CRH on LC activity is consistent with recent data indicating that decreased LC activity increases anxiety and stress-related responses, but that direct influences of CRH appear rather minor in determining LC neuronal activity in comparison to other inputs to LC such as are seen after i.c.v. CRH infusion.

Adrenalectomy↗
PubMed1985

Oxytocin improves male copulatory performance in rats.

The role of oxytocin in male copulatory performance was reexamined in rats. Adult male rats were trained seven times for copulatory behavior, at weekly intervals. Oxytocin, either intraperitoneally injected (200 ng/rat) or intracerebroventricularly infused (1 ng/rat in 4 microliter saline) 60 and 5 min, respectively, before the eighth test, significantly shortened both the ejaculation latency and the postejaculatory interval. The intracerebroventricular infusion of saline alone (4 microliter/rat) had no effect at all.

Animals↗
PubMedDate not supplied

Cerebellar norepinephrine infusions facilitate recovery after sensorimotor cortex injury.

This study reports the effects of norepinephrine infusions into cerebellum after unilateral sensorimotor cortex injury. The results demonstrate an immediate and permanent acceleration in motor recovery in awake rats infused with 150 micrograms norepinephrine into the cerebellum contralateral to a right sensorimotor cortex ablation. A vehicle infusion or infusion of norepinephrine into the ipsilateral cerebellum produced no beneficial effects on functional recovery.

Anesthesia↗
PubMed1980

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

1. Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. In a first series of experiments, short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2 . 7% NaCl. In the second series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3% NaCl. 2. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight. 3. Not only did the animals drink large volumes of 3% NaCl some rats drank daily volumes of water that exceeded their body weight. 3. Not only did the animals drink large volumes of 3% NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 months). 4. The response to continuous infusion of angiotensin II was dose-dependent. Both water and 3% NaCl intake increased over a dose range of 6 ng h-1 to 6000 ng h-1. The persistence of the sodium appetitite was also dose-dependent across the same range of doses. 5. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0 . 5 M-NH4Cl and only occasionally drank minimal amounts of 0 . 5 M-KCl during continuous infusion. 6. The large water turnover was not responsible for the Na appetite. Rats given access to 3% NaCl only during infusion of angiotensin copiously. Animals that were not infused but were given saccharine-flavoured water in order to increase their water intakes did not drink 3% NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotensin infusion did not drink the 3% NaCl but did drink some water. 7. Records of the drinking by rats infused with angiotensin show that firstly the onset of drinking after the start of angiotensin infusion varied from animal to animal, secondly, NaCl drinking was not temporally linked to water intake, although this was observed occasionally, and thirdly, most of the drinking occurred during the night although angiotensin was infused continuously throughtout the nychthemeron. 8. Therefore, increases in angiotensin levels, probably with other factors such as increased levels of aldosterone or ACTH, result in Na appetite. The hormonal changes may alter the animals' preception of salt making it more acceptable. By means that are not yet understood the increased accceptability of salt persists after the termination of angiotensin infusion.

Angiotensin II↗
PubMed2000

Blood interleukin-6 and tumor necrosis factor-alpha elevation after intracerebroventricular injection of Escherichia coli endotoxin in the rat is determined by two opposing factors: peripheral induction by LPS transferred from brain to blood and inhibition of peripheral response by a brain-mediated mechanism.

Following intracerebroventricular injection of LPS in rats, IL-6 and TNF-alpha appear in peripheral blood. To determine whether these changes are mediated by passage of the injected LPS from the brain to the blood, the time course of appearance in blood of bioactive LPS after intracerebroventricular injection was compared with the time course of appearance of IL-6 and of TNF-alpha in blood. Bioactive LPS was detected 30 min after intracerebroventricular injection, the first time interval tested. TNF-alpha appeared in peripheral blood at 30 min, IL-6 at 60 min and both cytokines as well as LPS achieved highest levels at 120 min. To determine pharmacokinetics of LPS transfer from brain to blood more precisely, radioiodinated LPS was injected intracerebroventricularly. (125)I-LPS was detected in blood as early as 5 min after intracerebroventricular injection, reached peak levels at about 2 h, and was transferred from brain to blood at a rate corresponding to bulk flow (% of brain content per min was 1.40 +/- 0.58 and 1.00 +/- 0.21% in series 1 and 2, respectively). 70.0% of total injected LPS had entered blood by 4 h. However, when administered intravenously (by a programmed pump) at the same rate that it enters the blood after intracerebroventricular injection LPS induced a much greater cytokine response than when given intracerebroventricularly. This paradoxical response was shown in further studies to be due to the simultaneous central inhibitory effect of LPS; coinjection of intracerebroventricular LPS markedly reduced the peripheral cytokine response to intravenous LPS infusion.

Animals↗
PubMed1984

Atropine prevents increases in brain blood flow during hypertension in newborn piglets.

Cerebral hyperperfusion associated with hypertension, may play an important role in the pathogenesis of intraventricular hemorrhage in preterm infants. To examine the effect of hypertension on changes in total and regional brain blood flow (BBF), we increased the mean arterial blood pressure (MABP) in nine awake newborn piglets by an infusion of 0.7 mg/kg of metaraminol bitartrate (Aramine) (group I) and studied cerebral circulatory changes. In order to prevent the Aramine-associated bradycardia, we pretreated nine other piglets with atropine, which produced a higher level of hypertension (group II). MABP and BBF were measured and cerebral vascular resistance (CVR) was calculated during baseline, the Aramine infusion, and twice at decreasing MABP following the discontinuation of the Aramine infusion. In group I, the significant increase in MABP from 68 +/- 3 to 100 +/- 3 mm Hg (mean +/- SEM) during the Aramine infusion resulted in a significant increase in BBF (98 +/- 9 to 118 +/- 11 ml X min-1 X 100 g-1). MABP decreased significantly (although remained significantly above baseline levels), when Aramine was discontinued; however, total BBF remained elevated. CVR increased during the Aramine infusion, but decreased significant (versus the Aramine-infused state) in the post-Aramine period. Regional BBF increased significantly to the cerebrum and cerebellar cortex, but remained unchanged to the other regions including the brain stem. In group II, the Aramine infusion resulted in a significantly greater increase in MABP, a sustained increase in vascular resistance, and no increase in total BBF. Thus, atropine prevents increased BBF during hypertension in the newborn piglet.

Animals↗
PubMed1990

Age-dependent baroreflex attenuation by centrally infused verapamil in rats.

Because oral administration of verapamil for 6 days reduces reflex tachycardia without affecting reflex bradycardia, we tested chronotropic baroreflexes in conscious rats aged 5 or 15 months before and after verapamil was infused intracerebroventricularly for 6 days to determine whether a central action contributes to the reflex attenuation. Baroreflex responses consisted of reflex bradycardia elicited during pressor responses to methoxamine and reflex tachycardia during depressor responses to sodium nitroprusside. As we have shown previously, all reflex heart rate responses were initially smaller in 15-month-old than in 5-month old rats. Osmotic minipumps filled with saline or verapamil (100 micrograms/kg/day) were connected to cannulas in a lateral ventricle or femoral vein and, after 6 days, baroreflexes were recorded again. Control infusions of either saline intracerebroventricularly or verapamil intravenously were ineffective. In contrast, intracerebroventricular infusions of verapamil attenuated reflex heart rate responses to methoxamine or sodium nitroprusside differently in the two age groups: both reflex tachycardia and bradycardia were attenuated in 5-month-old rats; however, in 15-month-old rats only reflex bradycardia was reduced, whereas reflex tachycardia was unaffected. The selective reduction of reflex tachycardia in 5-month-old, but not in 15-month-old, rats suggests that intracerebroventricularly infused verapamil affects central baroreflex regulation differently depending on age.

Age Factors↗
PubMed1988

On the 7-oxo-PgI2 induced lasting protection against ouabain arrhythmias in anesthetized guinea pigs.

In our earlier experiments prolonged administration of the stable PgI2 analogue: 7-oxo-PgI2 ephedrine salt to dogs afforded a long-lasting protection against coronary occlusion induced ischemia as well as against postocclusion and reperfusion arrhythmias. In the present experiments we wanted to clear, whether this prolonged protective action is present in other types of arrhythmia, which are not due to ischemia. The ouabain-arrhythmia seemed to be suitable for elucidation of this question. Therefore guinea pigs were pretreated with 50 micrograms/kg i.p. 7-oxo-PgI2 and 24, 48, 72 and 96 hrs after treatment anesthetized with 35 mg/kg sodium pentobarbitone. To prevent ouabain bradycardia, 0.4 mg/kg atropine was administered i.p. Ouabain was applied by intermittent infusion technique i.e. an initial infusion for 5 minutes of a total dose of 60 micrograms/kg into the right jugular vein was followed after a 25 minutes interval by infusions of 30 micrograms/kg for 2.5 minutes every 10 minutes until cardiac arrest. The ouabain induced rhythm disturbances appeared in the following order: Anomalies in T wave morphology, ventricular or nodal extrasystoles, atrio-ventricular and intraventricular conduction disturbances, ventricular tachycardia, ventricular fibrillation and finally cardiac arrest. If 50 micrograms/kg i.p. 7-oxo-PgI2 was given to ouabain-intoxicated animals at the appearance of the first extrasystole a transient aggravation of this arrhythmia developed. In 7-oxo-PgI2 pretreated animals the total amount of ouabain necessary to induced rhythm disturbances was markedly elevated, the appearance of the various arrhythmias significantly delayed. Maximal protective effects were seen 48 hrs after the administration of 50 micrograms/kg 7-oxo-PgI2.

Animals↗
PubMedDate not supplied

Glucose-insulin infusion for the early treatment of non-oliguric hyperkalemia in extremely-low-birth-weight infants.

In order to investigate the status of non-oliguric hyperkalemia and to evaluate glucose-insulin infusion treatment among extremely-low-birth-weight (ELBW) infants, 161 infants weighting less than 1000 gm at birth were enrolled for this study. They were divided into two groups: a hyperkalemic group and a non-hyperkalemic group. Hyperkalemia was defined here as a serum potassium level of greater than 6 mEq/L in a non-hemolyzed arterial blood sample. A glucose-insulin infusion was administered to the patients when hyperkalemia was detected in them during the first few days after birth. The infusion was discontinued when the serum potassium levels had been less than 6 mEq/L and stabilized for 6 hours. The incidence of non-oliguric hyperkalemia among ELBW infants in this study was 58% (93/161). The mean gestational age of neonates was 25.7 +/- 1.8 weeks (hyperkalemic) and 26.6 +/- 1.7 weeks (non-hyperkalemic). The mean rate of increases in serum potassium levels was 0.32 +/- 0.29 mEq/L/hr (hyperkalemic) and 0.13 +/- 0.12 mEq/L/hr (non-hyperkalemic). The incidence of severe intraventricular hemorrhage (IVH) was 19% (18/93) (hyperkalemic) and 4.4% (3/68) (non-hyperkalemic). The incidence of cardiac arrhythmia was 12% (11/93) (hyperkalemic) and 0% (non-hyperkalemic) respectively. Neonates with fewer weeks of gestation at birth and faster increases in serum potassium levels were associated with a more prominent tendency toward hyperkalemia. Hyperkalemia markedly increases the risk of severe IVH and arrhythmia for ELBW infants. A higher glucose infusion rate should be maintained to prevent hypoglycemia following insulin treatment.

Case-Control Studies↗
PubMed1982

Chronic intraventricular administration of lysergic acid diethylamide (LSD) affects the sensitivity of cortical cells to monocular deprivation.

In kittens, but not in adult cats, depriving one eye of pattern vision by suturing the lids shut (monocular deprivation or MD) for one week reduces the proportion of binocular units in the visual cortex. A sensitivity of cortical units in adult cats to MD can be produced by infusing exogenous monoamines into the visual cortex. Since LSD interacts with monoamines, we have examined the effects of chronic administration of LSD on the sensitivity to MD for cortical cells in adult cats. Cats were assigned randomly to one of four conditions: MD/LSD, MD/No-LSD, No-MD/LSD, No-MD/No-LSD. An osmotic minipump delivered either LSD or the vehicle solution alone during a one-week period of MD. The animals showed no obvious anomalies during the administration of the drug. After one week the response properties of single units in area 17 of the visual cortex were studied without knowledge of the contents of the individual minipumps. With the exception of ocular dominance, the response properties of units recorded in all animals did not differ from normal. In the control animals (MD/No-LSD, No-MD/LSD, No-MD/No-LSD) the average proportion of binocular cells was 78%; similar to that observed for normal adult cats. However, in the experimental animals, which received LSD during the period of MD, only 52% of the cells were binocular. Our results suggest that chronic intraventricular administration of LSD affects either directly or indirectly the sensitivity of cortical neurons to MD.

Animals↗
PubMed1990

Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats.

We previously reported that neostigmine injected into the third cerebral ventricle stimulated adrenal secretion of epinephrine, secretion of glucagon from the pancreas, and direct neural innervation of the liver, resulting in hepatic venous plasma hyperglycemia in anesthetized fed rats. However, receptor type of these 3 mechanisms is not known. Therefore, we examined the effects of intraventricularly injected cholinergic or adrenergic antagonists on neostigmine-induced catecholamines in intact rats, glucagon secretion which is mediated by direct neural innervation of pancreas in bilateral adrenalectomized (ADX) rats, and hepatic venous hyperglycemia which is mediated by direct neural innervation of liver in ADX rats receiving constant infusion of somatostatin from femoral vein. Atropine injected into the third cerebral ventricle suppressed epinephrine secretion and dose-dependently inhibited hepatic venous hyperglycemia induced by neostigmine in intact rats. The neostigmine-induced glucagon secretion which occurs in ADX rats was suppressed by atropine. Atropine also prevented the neostigmine-induced hyperglycemia in ADX rats receiving constant somatostatin infusion through femoral vein (ADX-Somato rats). On the other hand, phentolamine, propranolol and hexamethonium showed no significant inhibitory effect on neostigmine-induced hyperglycemia, epinephrine and glucagon secretion in intact rats, glucagon secretion in ADX rats, or hyperglycemia in ADX-Somato rats. These results suggest that neostigmine-induced epinephrine and glucagon secretion and increased hepatic glucose output stimulated by direct neural innervation to liver is mediated by central muscarinic receptor in fed rats.

Adrenergic Fibers↗
PubMed1993

Effect of intracarotid and intraventricular morphine on regional cerebral blood flow and metabolism in pentobarbital-anesthetized dogs.

Potent opiate analgesics, administered either epidurally, intrathecally, or intravenously, are a common adjunct to pain control in the perioperative period. Little is known, however, of the effects of opiate agonists on cerebral blood flow (CBF) and metabolism. Current studies are complicated by the hypotensive effects of these compounds and their route of administration. To circumvent these difficulties we studied the effects of intraventricular and intracarotid morphine sulfate, in doses that do not affect arterial blood pressure, on regional CBF and total cerebral oxygen consumption (CMRO2) in pentobarbital-anesthetized dogs. Five dogs received 0.04 mg/kg morphine via intracarotid injection. Five additional dogs received 0.2 mg/kg morphine via ventricular cisternal infusion over 5 min, and five control dogs received mock cerebrospinal fluid at the same infusion rate. CBF was measured using the radiolabeled microsphere technique. Intracarotid morphine decreased neurohypophyseal blood flow to 58% of control, but it did not alter blood flow to any other brain region, except caudate nucleus, or cause a change in CMRO2. Infusion of mock cerebrospinal fluid in the cerebral ventricles did not alter CBF or CMRO2. Ventricular-cisternal perfusion of morphine caused a transient increase in CBF (24 +/- 2 to 37 +/- 6 mL min-1 100 kg-1) but had no effect on spinal cord blood flow or CMRO2. Neurohypophyseal blood flow, however, decreased to 40% of control levels (480 +/- 76 to 176 +/- 42 mL min-1 100 kg-1) after 2 min and gradually returned to control levels at 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗