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PubMed1998

Myocardial protection by pressure- and volume-controlled continuous hypothermic coronary perfusion in combination with Esmolol and nitroglycerine for correction of congenital heart defects in pediatric risk patients.

OBJECTIVE: This study assesses the technical applicability and the clinical value of the continuous coronary perfusion with oxygenated blood as a method for myocardial protection used for congenital heart surgery in pediatric risk patients. METHODS: Thirty non-consecutive pediatric risk patients aged from 1 month to 16 years (mean 3.9 years; 11/30 patients aged <6 months) underwent open heart procedures on the beating heart for simple and complex cardiac malformations using a self designed perfusion system with pressure- and volume-controlled continuous hypothermic coronary perfusion (PVC-CONTHY-CAP) in combination with ultra-short beta1-receptor blockade (Esmolol) and nitroglycerine for myocardial protection. The following procedures were done: VSD patch closure (n = 6), repair of total a-v canal with 'double patch' (n = 4), total repair of tetralogy of Fallot (n = 7), correction of truncus arteriosus communis type IV (n = 1), mitral valve reconstruction (n = 4), total cavo-pulmonary connection (n = 4), and Rastelli procedure (n = 4). RESULTS: The mean cardio-pulmonary bypass time was 131.5 min (range: 44-245 min), the mean coronary perfusion time: 90.1 min (range: 13-202 min). The weaning off extracorporeal circulation was uneventful in all patients, in 21 patients with low-dose and in nine patients with moderate catecholamine support: the mean weaning time was 25 min (range: 7 58 min). The post-operative mean peak creatine kinase (CK-MB) value was 58 U/l, (range: 14-202 U/l). The mean ICU stay in the cardiac surgery unit was 2.9 days, (range: 1-10 days). The mean post-operative mechanical ventilatory support was 2 days (range: 6 h-9 days). Six patients developed thrombocytopenia with values <40 tsd/microl, four patients renal dysfunction, two patients ascites, five patients heart rhythm disturbances, one patient neurological deficits. In three patients (VSD closure: n = 2; age: 1 and 2 months; total a-v-canal: n = 1; age: 3 months) re-do procedures for significant intraventricular shunt had to be done, in one patient implantation of a permanent pacemaker system was necessary. One patient died due to multiple organ failure after uneventful surgery (total cavo-pulmonary connection for single ventricle). CONCLUSIONS: PVC-CONTHY-CAP can be successfully used for repair of simple and complex congenital cardiac malformations. However, in children less than 3 months of age, the transatrial repair of intraventricular defects is technically much more demanding and challenging than under conventional cardioplegic arrest and is possibly accompanied by an increased incidence of residual or recurring intraventricular shunts.

Adolescent↗

PubMed2003

Myocardial perfusion and adrenergic innervation in patients with RBBB and LAfB: the effect of altering the activation sequence with right ventricular apical pacing.

The aim of this study was to investigate myocardial perfusion and adrenergic innervation in patients with intraventricular conduction disturbances and to detect any changes caused by alteration of the ventricular activation sequence as a result of right ventricular apical pacing. We studied 15 patients with right bundle branch block (RBBB) and left anterior fascicular block (LAFB), while 15 healthy individuals served as controls. All patients underwent planar and single-photon emission computed tomography (SPECT) myocardial imaging after intravenous infusion of 5mCi 123I-metaiodobenzylguanidine (123I-MIBG) and a SPECT thallium201 myocardial perfusion study before and 3 months after pacemaker implantation. The heart to mediastinum ratio was calculated during the 123I-MIBG study in order to assess the global cardiac sympathetic activity and was significantly smaller in patients than in controls (P < 0.001). Patients with RBBB and LAFB revealed regional adrenergic innervation defects, mostly in the inferior and posterior walls. After a medium-term pacing period, a redistribution of 123I-MIBG uptake was detected, with aggravation of adrenergic innervation defects in the apical and posterior walls and amelioration in septal and anterior walls. Five patients showed perfusion defects that remained unchanged after pacing. Two others displayed mild myocardial perfusion defects that did not exist before pacing. In conclusion, patients with RBBB and LAFB reveal global and regional disturbances of myocardial adrenergic innervation, which shows redistribution as a result of the altered propagation of the ventricular electrical activation. To a smaller degree these patients reveal myocardial perfusion disturbances in which pacing has a limited medium-term effect.

Aged↗

PubMed1983

Angiotensin II and bradykinin: interactions between two centrally active peptides.

Two neuropeptides, bradykinin (BK) and angiotensin II (ANG II), produce an increase in blood pressure when injected into the brain ventricles. This study is an example of central peptide-peptide interaction and was carried out to determine if BK and ANG II share a common mechanism in the brain to control blood pressure and drinking in rats. Prior injection of saralasin [10 micrograms intraventricularly (ivt)] was found to enhance the pressor response to ivt BK (5 micrograms) by 44%. The same dose of saralasin attenuated the pressor response to ivt ANG II (200 ng) by 55%. 50 ng ANG II and 5 micrograms BK given together ivt did not significantly alter blood pressure or urine conductance compared to 50 ng ANG II alone. Drinking to ivt infusions of ANG II (14 ng/min) was significantly attenuated when combined with BK (0.7 micrograms or 2.8 micrograms/min). Pretreatment with 10 micrograms indomethacin ivt diminished the pressor response to 5 micrograms ivt BK. Prostaglandin E2 (1.4 micrograms/min), but not prostaglandin A2, inhibited drinking to 14 ng/min ivt infusions of ANG II. The results suggest that ANG II and BK share an interrelationship with respect to their central actions: ANG II inhibits the BK pressor response and BK acts to inhibit drinking induced by ANG II. Prostaglandins of the E series may mediate these central actions of bradykinins.

Angiotensin II↗

PubMed1986

Elevated CSF osmolality inhibits thermoregulatory heat loss responses.

The effect of intracerebroventricular (icv) infusions of hypertonic NaCl or sucrose on thermoregulatory responses to heat was studied in conscious rabbits to test the idea that brain osmoreceptors are involved in the inhibition of evaporative heat loss and elevation of body temperature in dehydrated mammals at high ambient temperature (Ta). In rabbits hydrated ad lib and resting at a Ta of 33 degrees C, icv infusion (3.4 microliter/min) of hypertonic (1,500 mosm) NaCl or sucrose in artificial cerebrospinal fluid (ACSF) produced a significant reduction in respiratory frequency (f) and in ear skin temperature (Te) and a rise in brain temperature (preoptic area, Tpoa). icv infusion of ACSF alone or ACSF + NaCl at 500 and at 750 mosm had no effect on f or on Te or Tpoa. Infusion of NaCl + ACSF at 1,000 mosm reduced f but did not affect Te or Tpoa. In hydrated rabbits, icv infusion of 1,500 mosm NaCl abolished the rise in f and in Te elicited by POA heating at Ta of 25 degrees C. In dehydrated rabbits at 33 degrees C, f was below hydrated levels and icv infusion of water (6.8 microliter/min) produced a reversible elevation in f. These findings suggest that brain osmoreceptors can influence thermoregulation in hot environments.

Animals↗

PubMed1984

The cardiovascular effects of neuropeptide Y (NPY).

NPY (1ng-10/micrograms) had no effect on mean arterial pressure (MAP) or heart rate (HR) when administered into the lateral brain ventricle or cisterna magna of conscious, chronically instrumented normotensive, male Wistar rats. However upon intravenous injection (0.1-5/micrograms) it produced a dose related pressor response accompanied by bradycardia. This pressor effect was not influenced by prazosin infusion (100 micrograms/kg/min). These results suggest that NPY has no direct role in central cardiovascular regulation, but peripherally is a very potent vasoconstrictor peptide.

Animals↗

PubMed1990

Is adenosine 5'-triphosphate derangement or free-radical-mediated injury the major cause of ventricular dysfunction during reperfusion? Role of adenine nucleoside transport in myocardial reperfusion injury.

The aim of this study was to determine the dual role of ATP as an energy substrate and as a major source of oxygen-derived free-radical-mediated reperfusion injury by using adenine nucleoside blocker, p-nitrobenzylthioinosine (NBMPR), and adenosine deaminase inhibitor, erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA). In a randomized study, 16 dogs were instrumented with minor-axis LTZ-piezoelectric crystals and intraventricular pressure transducers to monitor, off bypass, left ventricular performance by using a sensitive and load-independent index of contractility (slope of the stroke work-end-diastolic length relation). Hearts were subjected to 60 minutes of normothermic global ischemia and 120 minutes of reperfusion. Normal saline without (Group 1, n = 8) or with (Group 2, n = 8) NBMPR and EHNA was infused in three boluses into the cardiopulmonary bypass reservoir before ischemia and reperfusion. Transmural serial biopsies were obtained before and during ischemia and reperfusion and analyzed for myocardial adenine nucleotide pool intermediates by using high-performance liquid chromatography. In the control group, three hearts developed ischemic contracture and another three hearts exhibited cardiogenic shock during reperfusion. In the EHNA/NBMPR-treated group, left ventricular performance recovered within 30 minutes of reperfusion (p less than 0.05 vs. control). Myocardial ATP was depleted to 20% of normal in both groups by the end of ischemia (p less than 0.05). Intramyocardial adenosine in the EHNA/NBMPR-treated group was 12-fold greater (15.09 +/- 1.6 nmol/mg protein) than the control group at the end of the ischemic period (p less than 0.05). Inosine was about fourfold higher in the control group (19.07 +/- 1.50 nmol/mg protein) compared with the drug-treated group (p less than 0.05). During reperfusion, myocardial ATP levels increased to approximately 50% of normal in the EHNA/NBMPR group while remaining depressed (20% of normal) in the control group. Thus, despite the dramatic loss of myocardial ATP during ischemia, complete recovery of ventricular performance and significant repletion of ATP during reperfusion were observed when adenosine transport and deamination were modulated during ischemia and reperfusion. These results suggest that 1) the myocardium may have more ATP than is needed for basic cardiac functions and 2) washout of ATP diffusible catabolites is detrimental to ventricular performance during reperfusion. Specific blockade of nucleoside transport resulted in complete functional recovery despite low but critical ATP levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenine↗

PubMed1979

[Electrophysiologic effects of dobutamine on cardiac conduction system (author's transl)].

The electrophysiologic effects of dobutamine (D) (3 and/or 6microgram/kg/min), a new beta1 stimulator, was studied in 12 patients with different disturbances of rhythm (sinus-node dysfunction, AV-block, sinus-bradycardia, paroxysmal tachycardia) utilizing His-bundle electrography and right atrial pacing. During infusion of D sinus-rate (HR) increased significantly from 61 to 71/min. Not only in cases with enhanced sinus-node-recovery-time (SKEZ) both, the absolutely (p less than 0.05) and the corrected SKEZ(-18%,-26%) were reduced by D otherwise the calculated sino-atrial-conduction time (SACTc) was shortened only in single cases. No effect could be registered in intraventricular (HV) conduction time, whereas the AV-nodal conduction time (AH) was significantly (p less than 0.05) reduced, more effect was seen at increasing stimulation of heart rate. The intraatrial conduction time (Ah-t) was shortened not significantly. In connection with reduced AH-interval the maximum of conduction frequency of the AV-node was significantly enhanced (10%, 13%). D shortened the refractory-period (RP) of atrium and AV-node, the effect was significant (p less than 0.05) only in the functional-RP of the atrium and relative RP of the AV-node.

Adult↗

PubMed1981

Effects of lidocaine on regional intraventricular conduction in patients with coronary artery disease.

Studies of isolated heart muscle and canine models of myocardial ischemia have demonstrated that lidocaine slows conduction in abnormal but not in normal tissues. To determine lidocaine's effects on intraventricular conduction (IVENT) in patients with coronary artery disease (CAD), we studied this agent in seven patients following left anterior descending coronary artery (LAD) bypass surgery. Epicardial electrodes were placed on the right atrium, left ventricle (LV) in the distribution of the LAD, and on the right ventricle (RV). On postoperative day 7, lidocaine was administered as 100 mg bolus followed by 4 mg/minute infusion for 2 hours. At constant atrially paced rate, bipolar electrograms were recorded from the LV and RV for the 2 hours of infusion and for 2 hours after discontinuation of infusion. Conduction intervals were measured from the earliest onset of QRS in three simultaneously recorded surface ECG leads to the major deflection of the electrogram from each ventricle. At peak effect, with mean lidocaine level of 2.7 +/- 0.5 mg/ml, lidocaine slowed LV conduction by a mean of 6 +/- 1 msec (14 +/- 2%) (p less than 0.001) and in the RV by 1 +/- 0.3 msec (4 +/- 1%) (p less than 0.01), QRS duration changed 1 +/- 1 msec) 1 +/- 1%) (NS). The values returned to baseline within 2 hours after discontinuation of lidocaine infusion. The difference in lidocaine's effect between the diseased LV and the normal RV was significant (p less than 0.001).

Adult↗

PubMed1990

Effects of propofol on cerebral hemodynamics and metabolism in patients with brain trauma.

The authors determined the effect of propofol on cerebral blood flow, intracranial pressure, and cerebral arteriovenous oxygen content difference in severely brain-injured patients during orthopedic treatment of fractures of the extremities. The Glasgow Coma Scale score was 6 or 7 at the time of the study. Data were collected in the operating room before and during (5 and 15 min) administration of propofol (2 mg/kg iv bolus immediately followed by a 150 micrograms.kg-1.min-1 infusion) before surgical stimulation. Propofol was infused during 41.4 +/- 7.3 min. After operation, the last set of measurements was made 15 min after propofol was stopped. The study was performed on 10 adults (age range, 15-40 yr) whose lungs were mechanically ventilated (air/O2) and who were sedated (phenoperidine, 1 mg/h), and was conducted using a radial artery cannula; a 7.5-Fr, thermodilution, flow-directed, pulmonary artery catheter; an intraventricular catheter; and a catheter in the jugular venous bulb. The 133xenon intra-internal carotid artery injection technique was used to determine regional cerebral blood flow (rCBF). Anesthetic blood concentration of propofol (3-5 micrograms/ml) was associated with decreases in cerebral perfusion pressure (CPP; from 82 +/- 14 to 59 +/- 7 mmHg; P less than 0.001), rCBF (from 35 +/- 6 to 26 +/- 5 ml.100 g-1.min-1; P less than 0.001), and intracranial pressure (ICP; from 11.3 +/- 2.6 to 9.2 +/- 2.5 mmHg; P less than 0.001). Cerebrovascular resistance and cerebral arteriovenous oxygen content difference were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Prostaglandins affect the central nervous system to produce hyperglycemia in rats.

The influence of prostaglandins (PG) on central nervous system regulation of blood sugar homeostasis was studied in rats. Substances were injected into the third cerebral ventricle of anesthetized rats while rectal temperature and hepatic venous plasma glucose concentration were recorded. Stereotaxic microinjection of PGD2, E1, E2, and F2 alpha produced hyperglycemia and hyperthermia. The relative order of potency in hyperglycemia, PGF2 alpha greater than D2 greater than E1 greater than E2, was not consistent with that of hyperthermia, PGE2 greater than F2 alpha greater than E1 greater than D2, which suggests that hyperglycemia was a primary, not secondary, response to hyperthermia. Injection of PGF2 alpha caused a dose dependent (5-200 micrograms) increase in the hepatic venous plasma glucose level. Neither the injection of PGF2 alpha (50 micrograms) into the cortex nor into the systemic vein caused hyperglycemia. The injection of PGF2 alpha into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norephinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through the femoral vein completely prevented the increase of glucagon after administration of PGF2 alpha, although the increase of plasma glucose level was still observed. PGF2 alpha-induced hyperglycemia did not occur in adrenodemedullated rats. Intravenous injection of naloxone or propranolol did not affect the hyperglycemia, but phentolamine significantly prevented the hyperglycemic effect of PGF2 alpha. These results suggest that intraventricular PGF2 alpha affects the central nervous system to produce hyperglycemia by increasing epinephrine secretion from the adrenal medulla.

Alprostadil↗

PubMed1999

The use of alteplase in a newborn receiving extracorporeal membrane oxygenation.

OBJECTIVE: To present a case of the use of alteplase for the successful resolution of an upper extremity occlusion in a newborn receiving extracorporeal membrane oxygenation (ECMO). CASE SUMMARY: A two-day-old full-term Hispanic girl receiving ECMO support developed a left upper extremity occlusion distal to the brachial artery. Alteplase therapy was initiated with a bolus dose of 0.48 mg/kg followed by a continuous infusion of 0.27 mg/kg/h for three hours. A repeat Doppler ultrasound revealed little improvement, resulting in continuation of alteplase therapy at an infusion rate of 0.27 mg/kg/h for an additional three hours. At the completion of the infusion, perfusion was greatly improved with palpable radial pulse present. While remaining on ECMO support, a brain ultrasound approximately 13 hours after alteplase therapy revealed a grade I right caudate head hemorrhage with normal ventricles. ECMO support was discontinued during the next 24 hours, with a repeat brain ultrasound three days later indicating no acute hemorrhage, normal ventricles, and almost complete resolution of the intraventricular hemorrhage. The neonate was discharged 19 days after discontinuing ECMO support. DISCUSSION: Patients receiving ECMO support are at risk of hematologic complications, including thrombi formation. Moreover, limited information is available regarding the most appropriate thrombolytic therapy for patients receiving ECMO support. Alteplase is an attractive thrombolytic agent given its antigenicity, clot specificity, and pharmacokinetic profile. However, both ECMO support and thrombolytic therapy are risk factors for the development of intraventricular hemorrhage, which our patient developed. Therefore, close monitoring of patients receiving ECMO support and alteplase therapy is essential given the potential for hematologic adverse effects. CONCLUSIONS: Alteplase is an effective thrombolytic agent in neonates receiving ECMO support. Additional experience with alteplase is necessary to determine the optimal dose and duration of therapy in this patient population.

Arm↗

PubMed1986

Sustained postischemic cardiodepression following magnesium-diltiazem cardioplegia.

Magnesium-diltiazem cardioplegia was evaluated in the intact, perfused rat heart to determine whether the joint administration of these agents would adversely affect myocardial contractile and high-energy phosphate recovery following intermittent, normothermic global ischemic arrest. Sequential metabolic and functional analyses were performed on isolated perfused rat hearts during each phase of the experimental protocol: control (10 min), normoxic cardioplegia (10 min), intermittent global ischemic arrest (two 15-min periods separated by 2 min infusion of the normoxic cardioplegic perfusate), and normoxic postischemic control reperfusion (60 min). Four different cardioplegic solutions were evaluated: 30 mM KCl, 30 mM KCl with 2 mg diltiazem/liter, 20 mM MgCl2, and 20 mM MgCl2 with 2 mg diltiazem/liter. Myocardial phosphatic metabolite levels and intracellular pH were analyzed nondestructively in the intact hearts by phosphorus-31 NMR spectroscopy. Corresponding measurements of peak left intraventricular pressure, rate of peak pressure development (dP/dt), and contraction frequency were performed at the midpoint during each 5-min interval of 31P NMR signal averaging. Magnesium plus diltiazem-treated hearts were distinguished from all other groups by a marked delay in postischemic functional recovery consisting of a prolonged depression in contractility (34% of control, P less than 0.01) that persisted throughout the first 50 min of postischemic reperfusion. Diltiazem in combination with magnesium cardioplegia was detrimental to postischemic functional recovery, despite a rapid restoration of high-energy phosphate stores. The apparent adverse interactive effects of excess magnesium and diltiazem suggest that elective ischemic arrest with magnesium cardioplegia in combination with diltiazem may be contraindicated clinically. The mechanistic basis and drug specificity of this response require further clarification. The present findings appear to exclude ATP and PCr production, and structural causes as the basis for the observed aberrant functional recovery from global ischemia of magnesium plus diltiazem-arrested hearts.

Adenosine Triphosphate↗

PubMed1980

Intracerebroventricular osmosensitivity in the Pekin Duck. Properties and functions in salt and water balance.

Pekin ducks were implanted with devices allowing intracerebroventricular (i.c.v.) microinfusions at rates of 0.1--0.4 mul/min during 15 min in the conscious animals. When hydrated by intragastric infusion of 1 ml/min tap water, i.c.v. infusion of hypertonic NaCl solutions reduced urine flow and increased osmolality, presumably due to increased ADH release. Osmotically equivalent Li+ salts (Cl-, Br-, So24-) caused a slightly prolonged antidiuresis, while Ca2+ and Mg2+ salts caused a more protracted antidiuresis. Urea solution osmotically equivalent to 4.8% NaCl had no effect on diuresis, while osmotically equivalent mannitol solution slightly enhanced diuresis. Angiotensin II (0.5--2.5 pmol in 15 min) and Carbachol (3.0 pmol in 15 min) infused in 0.9% saline caused antidiuresis. The results suggest that the central control of ADH release in birds is similarly organized as in mammals, with receptive elements reacting to ionic rather than osmotic changes and with Na+ as the naturally involved cation. In ducks with their salt glands activated by i.v. infusion of 800 mosmol NaCl/kg H2O at 0.2 ml/min, salt gland secretion was not augmented by i.c.v. microinfusion of hypertonic NaCl but inhibited by i.c.v. infusion of osmotically equivalent mannitol solution. The supraorbital salt glands, when activated appear to be little stimulated further by a rise but may be inhibited by a fall of i.c.v. Na+ concentration.

Angiotensin II↗

PubMed2002

Role of the haem oxygenase-carbon monoxide pathway in insulin-induced hypothermia: evidence for carbon monoxide involvement.

A reduction of body temperature (T(b)) is a phenomenon concomitant with hypoglycaemia in mammals. Haem oxygenase (HO) catalyses the metabolism of haem to biliverdin, free iron and carbon monoxide (CO). Recently, the HO pathway has been shown to play an important role in thermoregulation. The present study was designed to test the hypothesis that the HO pathway plays a role in insulin-induced hypothermia and that CO, rather than free iron or biliverdin, is the HO product involved in this response. Body temperature (T(b)) of Wistar rats was measured by biotelemetry. Infusion of insulin (0.2 U/kg per h, i.v.) caused a significant drop in T(b). Intracerebroventricular (i.c.v.) administration of zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG, a HO inhibitor, 200 nmol) combined with saline infusion had no effect on T(b) but increased insulin-induced hypothermia significantly. The i.c.v administration of neither the iron chelator deferoxamine (250 microg) nor biliverdin (152 nmol) altered the hypothermic response to insulin, whereas CO-saturated saline significantly reduced insulin-induced hypothermia. These data indicate that the HO pathway prevents excessive drops in T(b) in insulin-induced hypothermia. Because biliverdin and iron had no effect, while CO significantly reduced the hypothermic response elicited by insulin infusion, these data imply that CO is the HO product involved in the thermoregulatory effect of insulin-induced hypothermia.

Animals↗

PubMed1984

Rat brain angiotensin II receptors: effects of intracerebroventricular angiotensin II infusion.

Angiotensin II (Ang II) was infused into a lateral cerebral ventricle of male Sprague-Dawley rats and its effects on blood pressure, water balance and specific [125I]Ang II binding to brain and adrenal tissues were studied. The infusion was maintained at a rate of 500 ng/microliter/h for 6 days using subcutaneously implanted osmotic minipumps. A control group was infused intracerebroventricularly (i.c.v.) with 0.9% saline at a rate of 1 microliter/h for 6 days. Angiotensin II treated rats showed a four-fold increase in water intake and urine volume and a moderate increase in blood pressure; these effects were not observed in rats given saline i.c.v. There was no significant difference in [125I]Ang II binding site density or binding affinity in either the hypothalamus-thalamus-septum-midbrain (HTSM) or the brainstem between Ang II-treated and saline-treated groups. In addition, [125I]Ang II binding sites in the adrenals were also unaffected by i.c.v. infusion of Ang II. The results suggest that brain Ang II receptors are unresponsive to increased Ang II levels in cerebrospinal fluid.

Adrenal Glands↗

PubMed1993

Corticotropin-releasing factor enhances noradrenaline release in the rat hypothalamus assessed by intracerebral microdialysis.

Corticotropin-releasing factor (CRF) at a dose of 3 micrograms administered intracerebroventricularly (i.c.v.) elicited increases in noradrenaline (NA) release, which was assessed by intracerebral microdialysis in the anterior hypothalamus of conscious rats. These increases persisted until 140 min after infusion of CRF. These results indicate that CRF enhances NA release in the hypothalamus, an effect which may underlie the 'stress-like' properties of CRF.

Animals↗

PubMed1980

Impaired drinking to angiotensin II after subdiaphragmatic vagotomy in rats.

Rats received total bilateral subdiaphragmatic vagotomy and, one month later, were fitted with chronic intravenous or intracerebroventricular cannulas. The vagotomized rats showed much reduced drinking compared with controls during intravenous infusion of angiotensin II. Their drinking to intracerebroventricularly administered angiotensin II was, however, less affected. The possible role of the vagus nerve in the mediation of angiotensin and other types of drinking is discussed.

Angiotensin II↗

PubMed2000

Effect of a neuroactive steroid infused into the cerebral ventricles of fetal sheep in utero using small infusion volumes.

Placental progesterone metabolites may influence fetal behaviour during late gestation. We have investigated the effect of the neuroactive metabolite, pregnanolone, on the sleep/awake behaviour of fetal sheep. These studies can only be effectively performed in unanesthetized animals with chronically implanted leads and catheters. The relatively large internal volumes of these catheters raises problems for cerebroventriclear infusions. Therefore, we developed a device with negligible deadspace ( approximately 10 microl) consisting of a ventricular cannula attached to a small cap which allowed the instillation of microl volumes of neuroactive steroids into a cerebral ventricle of fetal sheep in utero. Two catheters attached to the cap allow it to be filled in a push-pull configuration. The smaller internal diameter of the ventricular cannular prevents the solution entering the ventricle until the outflow catheter is occluded and solution is forced through the probe. Using this device, the infusion of 5beta-pregnane-3alpha-ol-20-one (pregnanolone, 1 mg), in 35% hydroxypropyl-beta-cyclodextrin, resulted in a marked suppression of fetal behaviour parameters indicative of arousal, while vehicle alone did not affect these parameters. We conclude that neuroactive steroids can be infused into the cerebroventricular system of chronically catheterised fetal sheep in small volumes and that pregnanolone may act directly to influence fetal behaviour.

Animals↗