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PubMed1975

Hyperglycaemia produced by drugs with analgesic properties introduced into the cerebral ventricles of cats.

1 The effects on blood glucose of four substances with analgesic properties (apomorphine, pethidine, codeine and etorphine) and of prostaglandin E(1) were examined in unanaesthetized cats. They were applied by the intraventricular route being either injected into a lateral ventricle or infused into the fourth ventricle through implanted Collison cannulae.2 Apomorphine gave rise to pronounced hyperglycaemia in a dose of 0.75 mg which produced scarcely any hyperglycaemia on intravenous injection. It was more effective on infusion into the fourth ventricle than on injection into a lateral ventricle and was approximately half as potent as morphine in provoking hyperglycaemia.3 Codeine produced no hyperglycaemia in doses of 0.75 and 1.5 mg.4 Pethidine had a weak hyperglycaemic action in doses of 0.75 and 1.5 mg, but the effect was not regularly obtained. Potency of the drug was at most only a third to a sixth that of morphine.5 Etorphine produced strong hyperglycaemia on infusion into the fourth ventricle in a dose of 10 mug. Unlike apomorphine or morphine it was more potent on injection into a lateral ventricle when it produced a strong hyperglycaemic response in doses of 5 or 1 mug, which were subthreshold on infusion into the fourth ventricle. However, this response may have been brought about indirectly as a result of severe asphyxia and of convulsions associated with the injections. On infusion into the fourth ventricle, etorphine was about 75 times as potent as morphine in producing hyperglycaemia.6 Prostaglandin E(1) had no hyperglycaemic action when infused into the fourth ventricle in a dose of 400 ng.

Analgesics↗

PubMed2006

Remote myocardium gene expression after 30 and 120 min of ischaemia in the rat.

The aim of the present study was to investigate how early the onset of ischaemia-induced changes in gene expression is in remote myocardium, and whether these changes would be different for left and right ventricles. Wistar rats (n=27) were randomly assigned to left coronary artery (LCA) ligation for 30 or 120 min and sham groups. Evans Blue infusion revealed antero-apical left ventricle (LV) and left intraventricular (IV) septal ischaemia (35.5+/-0.6% of LV mass). LCA ligation induced transient LV systolic dysfunction and sustained biventricular slowing of relaxation. Regarding mRNA levels, type B natriuretic peptide (BNP) was upregulated in the LV at 30 (+370+/-191%) and 120 min (+221+/-112%), whilst in the right ventricle (RV) this was only significant at 120 min (+128+/-39%). Hipoxia-inducible factor 1alpha and interleukin 6 overexpression positively correlated with BNP. Inducible NO synthase upregulation was present in both ventricles at 120 min (LV, +327+/-195%; RV, +311+/-122%), but only in the RV at 30 min (+256+/-88%). Insulin-like growth factor 1 increased in both ventricles at 30 (RV, +59+/-18%; LV, +567+/-192%) and 120 min (RV, +69+/-33%; LV, +120+/-24%). Prepro-endothelin-1 was upregulated in the RV at 120 min (+77+/-25%). Ca2+-handling proteins were selectively changed in the LV at 120 min (sarcoplasmic reticulum Ca2+ ATPase, 53+/-7%; phospholamban, +31+/-4%; Na+-Ca2+ exchanger, 31+/-6%), while Na+-H+ exchanger was altered only in the RV (-79+/-5%, 30 min; +155+/-70%, 120 min). Tumour necrosis factor-alpha and angiotensin converting enzyme were not significantly altered. A very rapid modulation of remote myocardium gene expression takes place during myocardial ischaemia, involving not only the LV but also the RV. These changes are different in the two ventricles and in the same direction as those observed in heart failure.

Animals↗

PubMed1989

Comparison of intracerebroventricular and intracarotid infusions of PGE2 in conscious sheep.

Conscious sheep chronically prepared with nonocclusive indwelling vascular and cerebroventricular catheters were used to compare hemodynamic, hematologic, hormonal, and behavioral responses of intracarotid (ic) prostaglandin E2 (PGE2) to intracerebroventricular (ivt) PGE2. PGE2 had less potent hemodynamic effects when infused ivt than when infused ic. Intracarotid PGE2, 100 ng.kg-1.min-1, increased arterial pressure and heart rate 31 mmHg and 26 beats/min, respectively (P less than 0.01), whereas ivt PGE2, 300 ng.kg-1.min-1, did not alter heart rate and increased arterial pressure 9 mmHg (P less than 0.01). Both ic and ivt PGE2 increased packed cell volume 3% (P less than 0.01). Neither ic nor ivt PGE2 caused changes in plasma concentrations of epinephrine or norepinephrine. Despite ivt PGE2S less potent hemodynamic effects, ivt administration of PGE2 decreased plasma osmolality 2 mosmol/kg (P less than 0.05) and sodium concentration 2 meq/l (P less than 0.01) and increased plasma vasopressin concentration 2.5-fold (P less than 0.05). Intracerebroventricular PGE2 also caused some physical and behavioral changes that were not observed during ic PGE2 administration or during ivt infusion of vehicle. These changes included pupillary constriction, vocalization, and coughing. We conclude that PGE2 given ivt may not reach the same sites in the brain as does ic PGE2 or that ivt PGE2 may reach the same sites in different concentrations.

Animals↗

PubMed1998

Systemic alpha-MSH suppresses LPS fever via central melanocortin receptors independently of its suppression of corticosterone and IL-6 release.

Systemically administered alpha-melanocyte-stimulating hormone (alpha-MSH) inhibits endotoxin (lipopolysaccharide; LPS)- or interleukin (IL)-1-induced fever and adrenocortical activation, but the sites of these actions and the mechanisms involved are unknown. The aims of this study were, first, to determine whether melanocortin receptors (MCR) located within the central nervous system mediate the suppressive effects of peripherally administered alpha-MSH on LPS-induced fever and activation of the pituitary-adrenal axis and, second, to determine whether systemic alpha-MSH suppresses the LPS-induced rise in plasma IL-6 levels, potentially contributing to its antipyretic effect. Male rats received Escherichia coli LPS (25 microg/kg ip). Core body temperatures (Tb) were determined hourly by radiotelemetry (0-8 h), and blood was withdrawn via venous catheters for plasma hormone immunoassays (0-2 h) and IL-6 bioassay (0-8 h). alpha-MSH (100 microg/kg ip) completely prevented the onset of LPS-induced fever during the first 3-4 h after LPS and suppressed fever throughout the next 4 h but did not affect Tb in afebrile rats treated with intraperitoneal saline rather than LPS. Intraperitoneal alpha-MSH also suppressed the LPS-induced rise in plasma IL-6, ACTH, and corticosterone (CS) levels. Intracerebroventricular injection of SHU-9119, a potent melanocortin-4 receptor (MC4-R)/MC3-R antagonist, completely blocked the antipyretic effect of intraperitoneal alpha-MSH during the first 4 h after LPS but had no effect on alpha-MSH-induced suppression of LPS-stimulated plasma IL-6 and CS levels. Taken together, the results indicate that the antipyretic effect of peripherally administered alpha-MSH during the early phase of fever is mediated by MCR within the brain. In contrast, the inhibition of LPS-induced increases in plasma CS and IL-6 levels by intraperitoneal alpha-MSH appears to be mediated by a different mechanism(s), and these effects do not contribute to its antipyretic action.

Adrenocorticotropic Hormone↗

PubMed1988

Histaminergic regulation of prolactin secretion: involvement of tuberoinfundibular dopaminergic neurons.

It has been shown that histamine (HA) stimulates prolactin (PRL) secretion via H2 receptors following intra-cerebroventricular infusion and via H1 receptors following systemic (intra-arterial) infusion. Since the effect of HA appears to be exerted at a suprapituitary level, we investigated the involvement of the tuberoinfundibular dopaminergic (TIDA) system in HA-induced PRL secretion in urethane-anesthetized male rats. HA infused intracerebroventricularly (30 micrograms) or intra-arterially (420 micrograms) decreased the dopamine (DA) concentration in pituitary portal blood by 30 and 23%, respectively. Blockade of DA receptors by pimozide did not prevent the stimulation of PRL secretion induced by intracerebroventricular infusion of HA or the H2 receptor agonist dimaprit. Furthermore, during DA receptor blockade intracerebroventricular infusion of the H1 receptor agonist 2-thiazolylethylamine inhibited PRL secretion. In contrast, pimozide prevented the stimulation of PRL secretion induced by intra-arterial infusion of HA and the H1 receptor agonist 2-thiazolylethylamine. In fact, under these conditions intra-arterial infusion of HA or the H2-receptor agonist dimaprit inhibited PRL secretion. During treatment with alpha-methyl-p-tyrosine, which reduced the hypothalamic DA content by 50%, HA infused intracerebroventricularly stimulated PRL secretion, while HA infused intra-arterially inhibited the secretion, which is in accordance with the results obtained during pimozide treatment. Cholinergic blockade by atropine did not prevent the HA-induced PRL release, excluding the possibility that the observed effect of pimozide is due to its anticholinergic property. We suggest that intracerebroventricular infusion of HA by activation of H2 receptors may stimulate PRL secretion partly via inhibition of the TIDA system and partly via other mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Urotensin II acts centrally to increase epinephrine and ACTH release and cause potent inotropic and chronotropic actions.

Urotensin II is a small peptide whose receptor was recently identified in mammals as the orphan G protein-coupled receptor-14. The reported cardiovascular responses to systemic urotensin II administration are variable, and there is little detailed information on its central cardiovascular actions. We examined the cardiovascular and humoral actions of intracerebroventricular urotensin II (0.02 and 0.2 nmol/kg and vehicle) and intravenous urotensin II (2, 20, and 40 nmol/kg and vehicle) in conscious ewes previously surgically implanted with flow probes and intracerebroventricular guide tubes. Two hours after intracerebroventricular infusion of urotensin II (0.2 nmol/kg over 1 hour; n=5), heart rate (+56+/-13 beats per minute [bpm]), dF/dt (an index of cardiac contractility; +533+/-128 L x min(-1) x s(-1)), and cardiac output (+3.4+/-0.4 L/min) increased significantly compared with vehicle, as did renal, mesenteric, and iliac blood flows and conductances. Plasma epinephrine, adrenocorticotropic hormone, and glucose levels also increased dramatically (+753+/-166 pg/mL, +14.3+/-3.5 pmol/L, and +7.0+/-1.4 mmol/L, respectively). All of these variables remained elevated for up to 4 hours after infusion. In contrast, 1 hour after intravenous urotensin II (40 nmol/kg bolus; n=6), a sustained tachycardia (+25+/-8 bpm) ensued, but cardiac output, cardiac contractility, total peripheral conductance, and plasma glucose levels did not change significantly. In summary, this is the first study to show that urotensin II acts centrally to stimulate sympathoadrenal and pituitary-adrenal pathways, resulting in increased adrenocorticotropic hormone and epinephrine release and potent chronotropic and inotropic actions. In contrast, tachycardia was the only major response to intravenous urotensin II. These findings suggest that urotensin II is a novel stimulator of central pathways that mediate responses to alerting stimuli or stress.

Adrenocorticotropic Hormone↗

PubMed1989

Possible mechanisms involved in growth hormone secretion induced by galanin in the rat.

The mechanisms by which central or systemic administration of galanin stimulates GH secretion were investigated in either conscious or urethane-anesthetized male rats. Intracerebroventricular injection of synthetic porcine galanin, a 29-amino acid gut-brain peptide (0.12, 0.6, and 3 nmol/rat), resulted in a dose-related increase in plasma GH. The plasma GH level was increased by an N-terminal galanin fragment [galanin-(1-19)], but not by C-terminal fragments [galanin-(2-29) and -(21-29)]. Intravenous injection or infusion of galanin (0.6 and 3 nmol/100 g BW) also raised plasma GH. The plasma GH increase induced by galanin was inhibited by pretreatment with rabbit antiserum specific for rat GRF. Pretreatment with yohimbine or phenoxybenzamine, alpha-adrenergic blockers, or picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, blunted the plasma GH increase induced by intracerebroventricular injection of galanin. On the other hand, the plasma GH increase induced by iv injection of galanin was suppressed by picrotoxin, but not by phenoxybenzamine. These findings suggest that 1) both central and systemic administration of galanin stimulate GH secretion in the rat; 2) the N-terminal structure of galanin is required to stimulate GH secretion; 3) the stimulating effect of galanin is mediated, at least in part, by hypothalamic GRF; and 4) central alpha-adrenergic and GABAergic mechanisms may be involved in GH release induced by central administration of galanin, whereas systemic injection of galanin stimulates GH release predominantly through GABAergic mechanisms in the rat.

Adrenergic alpha-Antagonists↗

PubMed1989

[The effects of PGE2, 2-DG and L-arginine on hypothalamic GHRH and SRIF releases in conscious rats, with respect to GH secretion].

The effects of prostaglandin E2 (PGE2), 2-deoxy-D-glucose (2-DG) and L-arginine on hypothalamic GHRH and SRIF release with respect to GH secretion were studied in conscious male rats. Intracerebroventricular (icv) injection of 5 micrograms PGE2 and intravenous (iv) infusion of 1 g/kgBW L-arginine caused an increase in plasma GH levels, but icv (36 micrograms) or iv (400 mg/kgBW) injection of 2-DG suppressed spontaneous GH surge in conscious rats. The concentration of hypothalamic GHRH was decreased in all three groups of the animals, but the concentration of hypothalamic SRIF was decreased only in 2-DG-treated animals. In the perifusion system using rat hypothalamus, PGE2 (0.28 microM, 2.8 microM), 2-DG (22 mM) and L-arginine (3 mM) stimulated GHRH release from rat hypothalamus. 2-DG also stimulated SRIF release more predominantly than GHRH release. Passive immunization with anti-GHRH serum inhibited the GH secretion induced by icv injection of 5 micrograms PGE2 and by iv infusion of 1 g/kgBW L-arginine in conscious rats. In contrast, GH secretion induced by iv injection of 50 micrograms/kgBW PGE2 was not affected by the pretreatment with the antiserum. These results suggest that the central effect of PGE2 and peripheral effect of L-arginine to stimulate GH secretion are mediated by hypothalamic GHRH release, and that the inhibitory effect of 2-DG on GH secretion is predominantly mediated by hypothalamic SRIF release rather than GHRH release in rats.

Animals↗

PubMed1985

Oxytocin and sexual behaviour in the male rat and rabbit.

In male New Zealand white rabbits, it was shown that oxytocin but not vasopressin concentrations in plasma were markedly raised after ejaculation. In male Wistar rats, oxytocin infused into the internal carotid artery reduced the number of intromissions made before ejaculation but had no other significant effect. Infusion of oxytocin into the third ventricle increased the latencies to the first mount and intromission and lengthened post-ejaculatory refractory periods. It is suggested that oxytocin released into the periphery during coitus, while not essentially involved in ejaculation, may exert effects on the genital periphery. Behavioural effects of centrally administered oxytocin suggest that it may play a role in the neural mechanisms underlying post-ejaculatory refractoriness.

Animals↗

PubMed2000

Inhibitory effect of central calcitonin-gene related peptide (CGRP) on pancreatic secretion in conscious rats.

The inhibitory effect of central administration of calcitonin-gene related peptide (CGRP) on pancreatic secretion stimulated by bile-pancreatic juice diversion was determined in conscious rats. Rats were prepared with separate cannulae for draining bile and pancreatic juice and with a duodenal cannula and an extrajugular vein cannula. In addition, another cannula was stereotactically implanted into the left lateral cerebral ventricle. Rats were placed in restraint cages and experiments were conducted 4 d after the operation without anesthesia. An injection of CGRP (1 nmol/10 microl) into the left lateral cerebral ventricle (i.c.v.) inhibited pancreatic secretion as well as cholecystokinin (CCK) release induced by bile-pancreatic juice diversion. Intravenous infusion of alpha- and beta-adrenergic receptor antagonist, phentolamine and propranolol did not reverse the inhibition of pancreatic secretion. Intravenous infusion of CGRP did not affect pancreatic secretion or plasma CCK concentrations. The inhibitory action of central CGRP (i. c.v.) on pancreatic secretion and CCK release stimulated by bile-pancreatic juice diversion is partially mediated by an alpha-adrenergic mechanism, although its precise mechanism has not been elucidated.

Adrenergic alpha-Antagonists↗

PubMed2000

Systemic coadministration of chloramphenicol with intravenous but not intracerebroventricular morphine markedly increases morphine antinociception and delays development of antinociceptive tolerance in rats.

Chloramphenicol, an in vitro inhibitor of the glucuronidation of morphine to its putative antianalgesic metabolite, morphine-3-glucuronide (M3G), was coadministered with morphine in adult male Sprague-Dawley rats to determine whether it inhibited the in vivo metabolism of morphine to M3G, thereby enhancing morphine antinociception and/or delaying the development of antinociceptive tolerance. Parenteral chloramphenicol was given acutely (3-h studies) or chronically (48-h studies). Morphine was administered by the i.v. or i.c.v. route. Control rats received chloramphenicol and/or vehicle. Antinociception was quantified using the hotplate latency test. Coadministration of chloramphenicol with i.v. but not i.cv. morphine increased the extent and duration of morphine antinociception by approximately 5.5-fold relative to rats that received i.v. morphine alone. Thus, the mechanism through which chloramphenicol enhances i.v. morphine antinociception in the rat does not directly involve supraspinal opioid receptors. Acutely, parenteral coadministration of chloramphenicol and morphine resulted in an approximately 75% increase in the mean area under the serum morphine concentration-time curve but for chronic dosing there was no significant change in this curve, indicating that factors other than morphine concentrations contribute significantly to antinociception. Antinociceptive tolerance to morphine developed more slowly in rats coadministered chloramphenicol, consistent with our proposal that in vivo inhibition of M3G formation would result in increased antinociception and delayed development of tolerance. However, our data also indicate that chloramphenicol inhibited the biliary secretion of M3G. Whether chloramphenicol altered the passage of M3G and morphine across the blood-brain barrier remains to be investigated.

Analgesics, Opioid↗

PubMed2004

Melatonin precursor; L-tryptophan protects the pancreas from development of acute pancreatitis through the central site of action.

Melatonin, produced from L-tryptophan, protects the pancreas against acute damage by improving the antioxidative status of tissue. Melatonin receptors have been detected in the brain, but the contribution of these receptors to the pancreatic protection is unknown. The aim of our study was to compare the effects of melatonin precursor; L-tryptophan given intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) on the course of acute pancreatitis. Acute pancreatitis was induced by subcutaneous infusion of caerulein (5 microg/kg-h x 5 h). L-tryptophan was given i.p. (2.5, 25 or 250 mg/kg) or administered into right cerebral ventricle (0.02, 0.2 or 2.0 mg/rat) 30 min prior to the start of caerulein infusion. Plasma amylase, lipase and TNF alpha activities were measured to determine the severity of caerulein-induced pancreatitis (CIP). The lipid peroxidation products: malonylodialdehyde and 4-hydroksynonenal (MDA + 4-HNE) and activity of superoxide dismutase (SOD) were measured in the pancreas of intact or CIP rats with or without L-tryptophan pretreatment. Melatonin blood level was measured by RIA. CIP was confirmed by histological examination and manifested as an edema and rises of plasma levels of amylase, lipase and TNF alpha (by 550%, 1000% and 600%). MDA + 4-HNE was increased by 600%, whereas SOD activity was reduced by 75% in the pancreas of CIP rats. All manifestations of CIP were significantly reduced by pretreatment of the rats with L-tryptophan given i.c.v. at doses of 0.2 or 2.0 mg/rat, or by peripheral administration of this amino acid used at dose of 250 mg/kg i.p. In control rats plasma level of melatonin averaged about 40 +/- 2 pg/ml and was not significantly affected by CIP, by central application of L-tryptophan (0.02, 0.2 or 2.0 mg/rat) or by peripheral administration of this melatonin precursor used at doses of 2.5 or 25 mg/kg i.p. Plasma melatonin level was markedly increased by pretreatment of the rats with L-tryptophan given i.p. at dose of 250 mg/kg. We conclude that central administration of melatonin precursor; L-tryptophan, as well as peripheral application of high dose of this melatonin precursor prevented the pancreatic damage produced by CIP. The favorable effect of peripherally administered L-tryptophan could be related to the rise of melatonin plasma level and to pancreatoprotective action of this indoleamine. The beneficial effect of centrally administered L-tryptophan could be mediated through activation of central receptors for locally produced melatonin.

Acute Disease↗

PubMed1987

Oxygenation of cardioplegic solutions. Potential for the calcium paradox.

Oxygenation of crystalloid cardioplegic solutions is beneficial, yet bicarbonate-containing solutions equilibrated with 100% oxygen become highly alkaline as carbon dioxide is released. In the isolated perfused rat heart fitted with an intraventricular balloon, we recently observed a sustained contraction related to infusion of cardioplegic solution. In the same model, to record these contractions, we studied myocardial preservation by multidose bicarbonate-containing cardioplegic solutions in which first the calcium content and then the pH was varied. An acalcemic cardioplegic solution (Group 1) and the same solution with calcium provided by adding calcium chloride (Group 2) or blood (Group 3) were equilibrated with 100% oxygen. Ionized calcium concentrations were 0, 0.10 +/- 0.06, and 0.11 +/- 0.07 mmol/L and pH values were 8.74 +/- 0.07, 8.54 +/- 0.08, and 8.40 +/- 0.07, all highly alkaline. Hearts were arrested for 2 hours at 8 degrees +/- 2.5 degrees C and reperfused for 1 hour at 37 degrees C. At end-arrest, myocardial adenosine triphosphate was depleted in all three groups, significantly in Groups 2 and 3. In Group 1 the calcium paradox developed upon reperfusion, with contracture (left ventricular end-diastolic pressure = 60 +/- 7 mm Hg), creatine kinase release up to 620 +/- 134 U/L, a profound further decrease in adenosine triphosphate to 1.9 +/- 1.7 nmol/mg dry weight, and either greatly impaired or no functional recovery (17% +/- 10% of prearrest developed pressure). Three hearts in this group released creatine kinase during arrest and did not resume beating during reperfusion. In Groups 2 and 3, the calcium paradox did not occur; functional recovery was 61% +/- 4% and 71% +/- 9% at 5 minutes of reperfusion. In two additional groups (4 and 5), the pH of the acalcemic cardioplegic solution was decreased by equilibration with 2% and 5% carbon dioxide in oxygen to 7.53 +/- 0.03 and 7.11 +/- 0.02. Contractions during arrest were smaller than in Groups 1, 2, and 3; adenosine triphosphate was maintained during arrest; functional recovery was 101% +/- 3% and 96% +/- 4% at 5 minutes of reperfusion. We conclude that acalcemic solutions with carbon dioxide are superior to highly alkaline calcium-containing solutions. If oxygenation of cardioplegic solutions, of proved value, causes severe alkalinity, then calcium paradox may result even with hypothermia. This hazard is prevented by adding calcium or blood to the solution or carbon dioxide to the oxygen used for equilibration.

Adenine Nucleotides↗

PubMed1998

Roles of brain angiotensin II and C-type natriuretic peptide in deoxycorticosterone acetate-salt hypertension in rats.

OBJECTIVE: To investigate the roles of brain angiotensin II and C-type natriuretic peptide (CNP) in the hypertensive mechanism of deoxycorticosterone acetate (DOCA)-salt hypertension. METHODS: We injected 50 microg/kg CV-11 974, an angiotensin II type-1 receptors antagonist, 30 nmol/kg CNP-22, or the vehicle (artificial cerebrospinal fluid) into the cerebral ventricle or intravenously 5 min before the intracerebroventricular infusion of 1.5 mol/I NaCl solution for 30 min into either male normotensive Wistar rats or DOCA-salt hypertensive rats anesthetized with urethane, and their arterial pressures and heart rates were continuously recorded. Blood (2 ml) was collected at the end of the infusion for the measurement of plasma concentration of arginine vasopressin. We infused 10 or 50 microg/kg per day CV-11 974, 10 or 50 nmol/kg per day CNP-22, or the vehicle (1 microl/h) into the cerebral ventricles of DOCA-salt hypertensive rats for 7 days by using osmotic minipumps, and measured their systolic arterial pressures, pulse rates, and urinary excretions of vasopressin. RESULTS: Intracerebroventricular pre-administrations of CV-11 974 and of CNP-22 inhibited increases in mean arterial pressure, heart rate, and plasma vasopressin concentration induced by intracerebroventricular infusion of 1.5 mol/l NaCl into normotensive rats; increases in hemodynamics and plasma level of vasopressin induced by intracerebroventricular infusion of 1.5 mol/l NaCl were suppressed by intracerebroventricular pre-injections of CV-11 974, but not of CNP-22, into DOCA-salt hypertensive rats. Continuous intracerebroventricular infusions of 50 microg/kg per day CV-11 974 attenuated hypertension in DOCA-salt treated rats, accompanied by a reduction in urinary excretion of vasopressin. Continuous intracerebroventricular infusions of 50 nmol/kg per day CNP-22, however, affected neither hypertension nor urinary excretion of vasopressin in DOCA-salt hypertensive rats. CONCLUSION: Brain angiotensin II could play a role in the pressor mechanism of DOCA-salt hypertension by increasing release of vasopressin via type 1 receptors. That brain CNP has an inhibitory effect on release of vasopressin in acute experiments indicates that the impairment of this inhibitory effect of brain CNP on secretion of vasopressin could be involved in the pathogenesis of DOCA-salt hypertension in rats.

Angiotensin II↗

PubMed1984

Cerebral blood flow and experimental intraventricular hemorrhage.

We evaluated the effects of acute hypovolemic hypotension followed by rapid, corrective blood infusion upon sequential regional cerebral blood flows (rCBF) in nine anesthetized 24-48-h-old beagle pups using the radioactive microsphere technique. After 5 min of hemorrhagic hypotension, during which time systemic arterial blood pressures were reduced 35-45%, cerebral blood flow to all regions increased by 31-42% over steady-state values. After blood reinfusion, rCBF increased by 39-88% over control values. Highest blood flows during hypovolemia were in the medulla and pons; slightly lower values were in the cerebellum, midbrain, cortex, and thalamus; and the lowest flows were in the white matter. These flows paralleled the hierarchy of flows to these regions in the steady state. Increases in blood flow during hemorrhagic hypotension were statistically significant when compared with the control values in the medulla (P less than 0.01), pons (P less than 0.01), midbrain (P less than 0.01), cerebellum (P less than 0.01), and cortex (P less than 0.01). One minute after reinfusion of the withdrawn blood volume, blood flows further increased by substantial margins in the medulla and pons; by moderate degree in the thalamus, midbrain, and cerebellum; and mildly in the cortex and white matter. Reinfusion state flow increases were significant when compared with control values in the medulla (P less than 0.01), pons (P less than 0.01), midbrain (P less than 0.01), cerebellum (P less than 0.01), cortex (P less than 0.05), and white matter (P less than 0.01). After flow values were corrected to compensate for variations in PCO2, the increases remained significant during both hypovolemia and reperfusion for medullary, thalamic, cortical, and white matter flows. Three of the nine puppies had macroscopic intraventricular hemorrhages at autopsy.

Animals↗

PubMed1984

[Antidotal treatment of acebutolol poisoning].

In rats, the intravenous infusion with acebutolol lead to a dose dependent decrease of arterial blood pressure, heart rate, cardiac output and total peripheral resistance, to sinus bradycardia, widening of the QRS complex, 1st and 2nd degree AV-block and intraventricular conductance disturbances. Nine possible antidotes were administered i.v. to rats which had been infused with 2 mg/kg X min acebutolol for 60 min. Isoprenaline proved the best antidote against acebutolol antagonizing the bradycardia by 88% and the hypotension completely. The activities of orciprenaline and prenalterol were lower than those of isoprenaline. Dopamine, epinephrine and norepinephrine antagonized acebutolol-induced hypotension, but did not influence considerably the bradycardia. Glucagon, on the other hand, antagonized the acebutolol-induced bradycardia by 47% but exerted only a small activity on the hypotension. Aminophyllin and calcium were nearly ineffective as antidotes against acebutolol. Isoprenaline and dopamine infused simultaneously restored heart rate, arterial blood pressure and cardiac output of acebutol-poisoned rats. The survival time of rats infused with 4 mg/kg X min acebutolol was doubled by the additional infusion of 0.2 mg/kg X min isoprenaline. The antagonistic activity of a treatment with isoprenaline and dopamine against the cardiovascular toxicity of acebutolol was confirmed in rabbits.

Acebutolol↗

PubMed1983

Effect of resuscitative fluids upon physical properties of blood perfusing the brain.

Acute physiologic changes induced by the infusion of resuscitative fluids may be harmful, resulting in the clinical sequelae of pulmonary and intraventricular hemorrhage. Using a chronically catheterized lamb model, changes in plasma sodium concentration, osmolality, hematocrit, glucose, colloid osmotic pressure, and arterial pressure were quantified in blood directly perfusing the brain, following distal infusions of fluids commonly used during neonatal resuscitation: molar and .5M NaHCO3, D10W and D25W, and whole blood. Distal infusion of hypertonic solutions resulted in acute alterations in electrolyte and osmotic equilibrium in the common carotid artery. All infused solutions caused a brief elevation in mean blood pressure; whole blood transfusion resulted in a sustained increase in blood pressure.

Animals↗

PubMedDate not supplied

Alternate routes of administration.

The less common methods of medication administration that used to be used only in the hospital are also now used in alternate settings. Understanding the treatment modalities, care requirements, and complications of these alternate routes of administration is important for nurses who participate in the care of patients receiving infusions. Several alternate routes of administration are discussed, with emphasis on the more commonly used methods: intra-arterial, intraspinal, intraventricular, intraperitoneal, intraosseous, and several other routes.

Drug Administration Routes↗