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PubMed1988

Baroreceptor reflex modulation by vasopressin microinjected into the nucleus tractus solitarii of conscious rats.

To determine whether the central vasopressinergic system at the level of nucleus tractus solitarii (NTS) modulates the reflex control of heart rate, we employed a new method for microinjection into the brainstem of conscious, freely moving rats. Baroreceptor reflex function was assessed during pressure changes induced by intravenous administration of phenylephrine (0.25-8 micrograms/kg) and sodium nitroprusside (0.5-16 micrograms/kg) in rats microinjected, through a permanent cannula into the brainstem, with saline, arginine vasopressin (AVP), or an AVP blocker. Baseline levels of pressure and heart rate were not changed by either peptide pretreatment. Restricted injection of AVP (20 ng-0.2 microliter) into the NTS attenuated the reflex bradycardia during pressure increases, with an upward displacement of the baroreceptor reflex function line (p less than 0.01) without change in the sensitivity. Local blockade of endogenous AVP, d(CH2)5Tyr(Me)AVP (1 microgram-0.2 microliter), depressed baroreceptor reflex sensitivity with intense bradycardia to either small or large pressure increases. Baroreceptor reflex control of heart rate in response to decreases in pressure was preserved during pretreatment with AVP, whereas endogenous blockade of AVP increased baroreceptor reflex sensitivity. These effects were specific to the NTS, since in another four rats there were no effects when the injections were made 1 mm above, into the cerebellum. The changes in baroreceptor reflex control of heart rate in conscious, unrestrained rats caused by administration of AVP and its endogenous blockade provide evidence that central vasopressinergic synapses at the NTS are important physiological modulators of baroreceptor reflex function.

Animals↗
PubMed1988

Autoregulation of the systemic circulation in conscious rats.

Autoregulation of blood flow in various organ systems is a well-documented phenomenon. However, the net effect of these regional autoregulatory responses on the systemic circulation has not been studied in conscious rats despite the now extensive use of rats in cardiovascular research. The ability of the systemic circulation to autoregulate cardiac output has been proposed to play an important role in the development of increased vascular resistance in volume-dependent forms of hypertension. To better understand these events, we characterized responses to acute increases and decreases in blood volume in conscious areflexic rats that were chronically instrumented with arterial and venous catheters and an electromagnetic flow probe around the ascending aorta. Neurohumoral blockade was achieved with chlorisondamine (10 mg/kg), methscopolamine (0.5 mg/kg), captopril (1.0 mg/kg), and d(CH2)5Tyr(Me)arginine vasopressin (10 micrograms/kg). Mean arterial pressure was restored to normal levels with a constant i.v. norepinephrine infusion, which resulted in normal values of cardiac output, total peripheral resistance, and blood gases. Blood volume expansion (0.9 ml i.v. blood infusion for 6 minutes) increased cardiac output 9 +/- 1% and mean arterial pressure 30 +/- 3% and caused a 22 +/- 2% increase in total peripheral resistance (n = 7). Blood volume contraction (6-minute withdrawal of 0.9 ml of blood) decreased cardiac output 12 +/- 1% and mean arterial pressure 26 +/- 4%, which resulted in a 16 +/- 4% decrease in total peripheral resistance (n = 8). The slopes of the pressure-flow relationships during volume expansion were 0.24 and 0.41 during volume contraction, as compared with a nonautoregulating system (slope = 1) and a completely autoregulating system (slope = 0).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

The effects of coronary artery occlusion and reperfusion at 1 hour (1-hr group), 2 hours (2-hr group), and 3 hours (3-hr group) were compared with a permanently occluded group (P group) on measurements of overall left ventricular and regional endocardial function over a 4-week period. The studies were conducted in conscious dogs 1-2 weeks after recovery from instrumentation with solid state left ventricular pressure gauges, aortic, and left atrial catheters, hydraulic occluders, and Doppler flow transducers on the left anterior descending or left circumflex coronary arteries, and multiple pairs of ultrasonic transducers implanted in the endocardial third of the left ventricular free wall to measure endocardial segment shortening. During coronary artery occlusion, similar effects were observed in the four groups. At 1 hour after coronary artery occlusion, three classes of ischemia-induced dysfunction were observed; dyskinetic (systolic shortening completely lost and replaced by paradoxical bulging), severely hypokinetic (systolic shortening depressed by 65-95%), and moderately hypokinetic (systolic shortening depressed by 40-65%). Compared with the P group, significant (P less than 0.05) return of systolic shortening and velocity of shortening gradually occurred over the 4-week period following reperfusion in all classes of segments in the 1-hour group. In the 2-hour group, systolic shortening returned in the moderately and severely hypokinetic segments, but was slight and not significant in the dyskinetic segments. In the 3-hour group, significant systolic shortening returned only in the moderately hypokinetic segments. The effects of isoproterenol, 0.04 micrograms/kg per min, and exercise were compared on "salvaged" dyskinetic segments prior to and at 1, 2, 3, and 4 weeks after coronary artery occlusion and reperfusion. The responses to isoproterenol were significantly depressed at 1 week after reperfusion and gradually recovered over the 4-week period. At 3-4 weeks after reperfusion, severe exercise also increased shortening and velocity of shortening in "salvaged" segments. Thus, in the conscious dog, coronary artery reperfusion at 1 hour after coronary artery occlusion results in substantial return of endocardial function even in the most severely ischemic myocardium. The "salvaged" myocardium responds adequately to myocardial stress with increases in the extent and velocity of systolic shortening, as long as 3-4 weeks after reperfusion are allowed for recovery. However, after 3 hours of coronary artery occlusion, little salvage of regional myocardial function can be induced by acute reperfusion in this model.

Animals↗
PubMed1986

Hypothalamic beta 2-adrenoceptor control of renal sympathetic nerve activity and urinary sodium excretion in conscious, spontaneously hypertensive rats.

The contributions of beta 1-, B2-, and alpha 2-adrenoceptors in the posterior hypothalamus to the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from environmental stress (air jet) in conscious spontaneously hypertensive rats were examined. Air stress increased mean arterial pressure and renal sympathetic nerve activity (54% from 7.0 +/- 0.7 integrator resets/min), and decreased urinary sodium excretion (44% from 2.7 +/- 0.4 microEq/min per 100 g body weight). After bilateral injection of ICI 118,551 (beta 2-adrenoceptor antagonist) into the posterior hypothalamus of the same spontaneously hypertensive rats, air stress had no effect on renal sympathetic nerve activity (8% from 4.8 +/- 0.7 integrator resets/min) or urinary sodium excretion (2% from 5.2 +/- 0.8 microEq/min per 100 g body weight), but still increased mean arterial pressure. Bilateral injection of isoproterenolol (beta-adrenoceptor agonist) into the posterior hypothalamus enhanced the renal sympathetic nerve activity and urinary sodium excretion (but not mean arterial pressure) responses to air stress. Air stress had no effect on renal sympathetic nerve activity or urinary sodium excretion when ICI 118,551 was given into the posterior hypothalamus before isoproterenol. Atenolol (beta 1-adrenoceptor antagonist) had no effect on the renal responses to air stress when given alone or before isoproterenol. Similarly, ICI 118,551 administered into the lateral hypothalamus or lateral cerebral ventricle, or guanabenz (alpha 2-adrenoceptor agonist) given into the posterior hypothalamus, had no effects on the renal or mean arterial pressure responses to air stress. Thus, beta 2-adrenoceptors in the posterior hypothalamus mediate the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress in conscious spontaneous hypertensive rats.

Air↗
PubMed1987

Influence of heart rate on left ventricular performance in conscious dogs.

The effects of atrial pacing on the left ventricular end-systolic pressure-volume relation, a relatively load-insensitive index of left ventricular performance, were studied in 8 chronically instrumented, conscious dogs. Six of the dogs were studied while autonomically intact, and 2 were studied after autonomic blockade with 2 mg/kg i.v. propranolol and 0.2 mg/kg i.v. atropine. Left ventricular pressure was measured with a micromanometer and left ventricular volume was determined from 3 ultrasonic orthogonal dimensions. Pressure was varied by caval occlusions at control heart rate and after atrial pacing at 100, 120, 140, 160, 180, and 200 bpm. The end-systolic pressure-volume relation was linear in every case (r = 0.97 +/- 0.03, SD). In the autonomically intact dogs, Emax, the slope of the end-systolic pressure-volume relation, was directly and monotonically related to heart rate in every dog, increasing to 238 +/- 99% of control at peak pacing rate (p less than 0.05). V0, the zero pressure intercept of the relation was also directly related to heart rate in every dog and increased 8.6 +/- 5.5 ml from control to peak pacing rate (p less than 0.05). Autonomic blockade did not attenuate these effects. This rightward shift of the end-systolic pressure-volume relation results in a reduced stroke volume from any end-diastolic volume, modulating the hemodynamic benefits of enhanced contractility. T, the time constant of isovolumic pressure fall during ventricular relaxation, was determined from beats with matched end-systolic pressures. T was related to heart rate, falling by 20 +/- 10.3% over the range of rates studied in the autonomically intact dogs and by 23.1 +/- 6.2% in the autonomically blocked dogs. Thus, the ventricle relaxes more rapidly at higher heart rates. We conclude that the frequency of contraction is concluded as an important determinant of overall pump function throughout the cardiac cycle in conscious dogs.

Animals↗
PubMed1990

Importance of endogenous angiotensin II in the cardiovascular responses to sympathetic stimulation in conscious rabbits.

Pharmacological evidence indicates that angiotensin (Ang II) converting enzyme inhibitors attenuate cardiovascular responses to sympathetic stimulation. To investigate the physiological significance of this attenuation, the pressor and heart rate responses to bilateral carotid occlusion (BCO) were studied before and after administration of captopril and again during Ang II replacement in conscious, aortic nerve-sectioned rabbits with chronically implanted carotid occluders. In the control period, BCO produced increases (p less than 0.05) in mean arterial pressure (MAP) and heart rate (HR) of 37.3 +/- 3.0 mm Hg and 21.7 +/- 5.4 beats/min from baseline values of 79.1 +/- 2.5 mm Hg and 255.4 +/- 16.7 beats/min. Captopril (5 mg/kg i.v.) markedly reduced (p less than 0.05) both the pressor (10.2 +/- 2.6 mm Hg) and HR (5.0 +/- 4.0 beats/min) responses to BCO, in parallel with a decrease in plasma Ang II of 75%. Infusion of a subpressor dose of Ang II (5-25 ng/kg/min i.v.) increased plasma Ang II to precaptopril levels and fully restored (p less than 0.05) the pressor (33.0 +/- 5.7 mm Hg) and HR (19.8 +/- 7.7 beats/min) responses to BCO. In two additional series of experiments, the mechanism of the effects of captopril and Ang II were investigated. In the first series, cardiac baroreflex curves (pulse interval versus MAP) were generated by increasing or decreasing blood pressure with phenylephrine or nitroprusside (5-20 micrograms/kg/min i.v.). The slope of the linear region of the curve (2.9 msec/mm Hg) was not changed significantly by captopril treatment (3.1 msec/mm Hg) or Ang II replacement (3.2 msec/mm Hg), indicating that cardiac baroreflex sensitivity was not altered by blockade of the renin-angiotensin system. In the second series, the effect of captopril on the pressor response to exogenous norepinephrine (0.1-2.5 micrograms/kg/min i.v.) was tested. The response was reduced by less than 40%, indicating only a modest postsynaptic component to the action of captopril. These results provide physiological evidence for an important action of endogenous Ang II in facilitating the cardiovascular responses to sympathetic stimulation in conscious rabbits. This facilitation is not due to an action upon the baroreflex per se but results, at least in part, from a presynaptic action of Ang II.

Angiotensin II↗
PubMed1991

Relative roles of cardiac and arterial baroreceptors in vasopressin regulation during hemorrhage in conscious dogs.

To determine the relative roles of cardiac and sinoaortic baroreceptors in mediation of arginine vasopressin (AVP) release, hemorrhage was performed in five groups of conscious splenectomized dogs: 1) all nerves intact; 2) either chronic surgical or acute pharmacological (intrapericardial lidocaine) cardiac denervation (CD); 3) chronic sinoarotic denervation (SAD); 4) combined chronic sinoartic denervation plus either chronic or acute cardiac denervation (SAD + CD); and 5) all nerves intact, but with ganglionic blockade. Hemorrhage (0.5 ml/min/kg) reduced mean arterial pressure similarly in the intact and CD groups. Decreases in mean arterial pressure were augmented in SAD, SAD + CD, and ganglion-blocked groups compared with responses in intact and CD groups. There were no differences in responses of plasma AVP to hemorrhage in the intact and CD groups, but the AVP response was significantly blunted in the SAD + CD group as compared with SAD alone. When compared during the early stage of hemorrhage, at the same reduction in mean arterial pressure, the rise in AVP was greater in the ganglion-blocked group than in the SAD + CD group, but was less than in the intact group. With a protocol to reduce mean arterial pressure by 20 mm Hg over the same period (42 +/- 0.6 minutes) in four of the groups, the blood volume required to reduce mean arterial pressure by 20 mm Hg was similar in the intact (20 +/- 1 ml/kg) and CD (21 +/- 1 ml/kg) groups, but was less in the SAD (12 +/- 1 ml/kg) and SAD + CD (12 +/- 1 ml/kg) groups. Again, similar increases were observed in AVP between the intact (50 +/- 9 pg/ml) and CD (51 +/- 9 pg/ml) groups, whereas increases in AVP were diminished in the SAD (11 +/- 3 pg/ml) and SAD + CD (7 +/- 2 pg/ml) groups. In the presence of an AVP antagonist, decreases in mean arterial pressure and increases in total peripheral resistance with hemorrhage were affected similarly in both the intact and CD groups, whereas hemodynamic impairment by AVP blockade was less marked in the SAD and SAD + CD groups. These results indicate that cardiac receptors are not the major regulators of AVP release during progressive hemorrhage in conscious dogs. However, when the complicating influences of sinoaortic reflexes were eliminated, a modest role for cardiac receptors was uncovered.

Animals↗
PubMed1994

Role of nitric oxide in the regulation of oxygen consumption in conscious dogs.

The role of nitric oxide (NO) in the regulation of O2 consumption was studied in chronically instrumented conscious dogs. A specific NO synthesis inhibitor, nitro-L-arginine (NLA, 30 mg/kg i.v.), significantly increased mean arterial pressure from 100 +/- 4 to 134 +/- 5 mm Hg (mean +/- SEM) and total peripheral resistance by 157 +/- 16% and reduced cardiac output by 47 +/- 3% and heart rate by 34 +/- 6% after 120 minutes. Changes in arterial blood gases were not observed. There were significant changes in PO2 (-14 +/- 2 mm Hg), O2 saturation (-21 +/- 2%), the percentage of hemoglobin as oxyhemoglobin (-21 +/- 2%), and O2 content (-3.0 +/- 0.9 vol%) and a significant increase in percent reduced hemoglobin (21 +/- 1%) in mixed venous blood, associated with an increase in O2 extraction (5.1 +/- 0.2 vol%) (all P < .01). O2 consumption was increased from 124 +/- 6 to 155 +/- 9 mL/min (P < .05). Methoxamine, titrated to have hemodynamic effects similar to those of NLA (eg, mean arterial pressure increased from 97 +/- 4 to 131 +/- 5 mm Hg), had much smaller effects on venous blood gases, hemoglobin, and O2 extraction (2.3 +/- 0.7 vol%) and no significant effect on O2 consumption. NLA also caused an increase in O2 consumption of 37 +/- 8% (P < .01) in quietly resting conscious dogs that had undergone pretreatment with hexamethonium and atropine, but no significant change in O2 consumption in dogs anesthetized with barbiturate.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1998

Depressed heart rate variability and arterial baroreflex in conscious transgenic mice with overexpression of cardiac Gsalpha.

Recently, we developed a transgenic mouse with cardiac-specific Gsalpha overexpression (TG mouse), which exhibits enhanced postsynaptic beta-adrenergic receptor signaling, ultimately developing a cardiomyopathy. The goal of the present study was to determine whether cardiac Gsalpha overexpression alters autonomic cardiovascular control, which could shed light on the mechanism responsible for the later development of cardiomyopathy. Mean arterial pressure was increased (P<.05) in conscious, chronically instrumented TG mice (123+/-1 mm Hg) compared with age-matched wild-type (WT) control mice (103+/-1 mm Hg). Respiratory frequency was increased (P<.05) in TG mice (269+/-26/min) compared with WT mice (210+/-20/min). By use of telemetric techniques, baseline heart rate (HR) was elevated (P<.05) in conscious, untethered TG mice (696+/-13 bpm) compared with WT mice (568+/-28 bpm). Intrinsic HR, after propranolol and atropine or after ganglionic blockade with hexamethonium, was not different between TG and WT mice. Both the normal minute-to-minute and circadian variations of HR observed in WT mice were markedly blunted in TG mice. HR variability was assessed by the time-domain and frequency-domain methods. At baseline, time-domain analysis indices were reduced (P<.05) in TG mice compared with WT mice. Although the low frequency (LF) component was higher (P<.05) than the high frequency (HF) component in WT mice, the LF component was less (P<.05) than the HF component in TG mice. In addition, arterial baroreflex regulation of HR was markedly blunted in TG mice in response to both nitroglycerin-induced hypotension and phenylephrine-induced hypertension. The reduced LF/HF ratio in TG mice was surprising in view of enhanced beta-adrenergic signaling and may be due to reduced neural tone secondary to the elevated arterial pressure or alterations in arterial baroreflex control. Dobutamine infusion in WT mice also resulted in depressed HR variability. The combination of elevated baseline HR, arterial pressure, and respiratory frequency suggests that enhanced beta-adrenergic signaling in TG mice results in reduced HR variability, in terms of both minute-to-minute variability and the lack of circadian variations in HR. The lack of normal HR variability in general and the failure of HR to decline, even during sleep, may actually be critical mechanisms contributing to the ultimate development of cardiomyopathy in these animals.

Adrenergic beta-Agonists↗
PubMed2001

A(1) or A(3) adenosine receptors induce late preconditioning against infarction in conscious rabbits by different mechanisms.

We investigated whether activation of A(1) or A(3) adenosine receptors (ARs) induces late preconditioning (PC) against infarction in conscious rabbits using the selective AR agonists 2-chloro-N(6)-cyclopentyladenosine (CCPA) and N(6)-3-iodobenzyladenosine-5'-N-methylcarboxamide (IB-MECA). In vitro radioligand binding and cAMP assays demonstrated CCPA to be approximately 200- to 400-fold selective for the rabbit A(1)AR and IB-MECA to be approximately 20-fold selective for the rabbit A(3)AR. We observed that (1) pretreatment of rabbits 24 hours earlier with CCPA (100 microgram/kg IV bolus) or IB-MECA (100 or 300 microgram/kg) resulted in an approximately 35% to 40% reduction in the size of the infarct induced by 30 minutes of coronary artery occlusion and 72 hours of reperfusion compared with vehicle-treated rabbits, whereas pretreatment with the selective A(2A)AR agonist CGS 21680 (100 microgram/kg) had no effect; (2) the delayed cardioprotective effect of CCPA, but not that of IB-MECA, was completely blocked by coadministration of the highly selective A(1)AR antagonist N-0861; (3) inhibition of nitric oxide synthase (NOS) with N(omega)-nitro-L-arginine during the 30-minute occlusion abrogated the infarct-sparing action of CCPA but not that of IB-MECA; and (4) inhibition of ATP-sensitive potassium (K(ATP)) channels with sodium 5-hydroxydecanoate during the 30-minute occlusion blocked the cardioprotective effects of both CCPA and IB-MECA. Taken together, these results indicate that activation of either A(1)ARs or A(3)ARs (but not A(2A)ARs) elicits delayed protection against infarction in conscious rabbits and that both A(1)AR- and A(3)AR-induced cardioprotection involves opening of K(ATP) channels. However, A(1)AR-induced late PC uses an NOS-dependent pathway whereas A(3)AR-induced late PC is mediated by an NOS-independent pathway.

Adenine↗
PubMed2001

Nitroglycerin induces late preconditioning against myocardial infarction in conscious rabbits despite development of nitrate tolerance.

BACKGROUND: Recent studies suggest that the late phase of ischemic preconditioning (PC) can be mimicked by pretreatment with NO donors. The ability of clinically relevant NO donors to induce PC against infarction, however, has not been evaluated. Furthermore, it is unknown whether tolerance to the hemodynamic actions of nitrates also extends to their PC effects. METHODS AND RESULTS: Conscious rabbits underwent a 30-minute coronary occlusion and 3 days of reperfusion. A 60-minute intravenous (IV) infusion of nitroglycerin (NTG) ending 1 hour before occlusion reduced infarct size, indicating an early PC effect. When the time interval between NTG infusion and occlusion was extended to 24 or 72 hours, the infarct-sparing action of NTG became even more pronounced, indicating a robust late PC effect. Transdermal NTG patches elicited a late PC effect that was (1) equivalent to that induced by IV NTG, demonstrating the efficacy of transdermal NTG as an alternative form of NTG delivery for inducing late PC, and (2) similar in nitrate-tolerant and -nontolerant rabbits, demonstrating that tolerance does not extend to the PC effects of NTG. CONCLUSIONS: In conscious rabbits, administration of NTG via either the IV or the transdermal route elicits a robust protective effect against infarction that lasts for 72 hours. The magnitude of NTG-induced cardioprotection is equivalent to that observed during the late phase of ischemic PC and is not affected by the development of tolerance. These findings reveal a new action of nitrates and support novel applications of these drugs for protecting the ischemic myocardium in patients.

Administration, Cutaneous↗
PubMed2001

Central human cocaine- and amphetamine-regulated transcript peptide 55-102 increases arterial pressure in conscious rabbits.

We determined cardiovascular and neurohormonal responses to intracerebroventricular administration of human cocaine- and amphetamine-regulated transcript (CART) peptide 55-102 in conscious rabbits. Intracerebroventricular injection of CART 55-102 elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 1 nmol of CART 55-102 (+5.0+/-2.6 mm Hg and +72.5+/-20.8%) were obtained 40 and 60 minutes after injection, respectively. Plasma epinephrine and glucose concentrations significantly increased 30 and 60 minutes after intracerebroventricular injection of CART 55-102 (control versus 60 minutes for epinephrine, 77.0+/-62.4 versus 1067.5+/-329.3 pg/mL, P<0.01; for glucose, 6.25+/-0.33 versus 11.57+/-0.93 mmol/L, P<0.01). Plasma norepinephrine concentrations also significantly increased at 30 minutes. Plasma insulin, vasopressin, and cortisol concentrations increased at 60 minutes but did not attain significant values. However, pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular and neurohormonal responses. In contrast, intravenous injection of the same dosage of CART 55-102 (1 nmol) as that used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular human CART 55-102 acts in the central nervous system and activates sympathoadrenal outflow, which results in increases in arterial pressure and plasma glucose levels in conscious rabbits.

Animals↗
PubMed2002

Hypnosis modulates activity in brain structures involved in the regulation of consciousness.

The notion of consciousness is at the core of an ongoing debate on the existence and nature of hypnotic states. Previously, we have described changes in brain activity associated with hypnosis (Rainville, Hofbauer, Paus, Duncan, Bushnell, & Price, 1999). Here, we replicate and extend those findings using positron emission tomography (PET) in 10 normal volunteers. Immediately after each of 8 PET scans performed before (4 scans) and after (4 scans) the induction of hypnosis, subjects rated their perceived level of "mental relaxation" and "mental absorption," two of the key dimensions describing the experience of being hypnotized. Regression analyses between regional cerebral blood flow (rCBF) and self-ratings confirm the hypothesized involvement of the anterior cingulate cortex (ACC), the thalamus, and the ponto-mesencephalic brainstem in the production of hypnotic states. Hypnotic relaxation further involved an increase in occipital rCBF that is consistent with our previous interpretation that hypnotic states are characterized by a decrease in cortical arousal and a reduction in cross-modality suppression (disinhibition). In contrast, increases in mental absorption during hypnosis were associated with rCBF increases in a distributed network of cortical and subcortical structures previously described as the brain's attentional system. These findings are discussed in support of a state theory of hypnosis in which the basic changes in phenomenal experience produced by hypnotic induction reflect, at least in part, the modulation of activity within brain areas critically involved in the regulation of consciousness.

Analysis of Variance↗
PubMed1982

Early detection of oxygen-induced lung injury in conscious rabbits. Reduced in vivo activity of angiotensin converting enzyme and removal of 5-hydroxytryptamine.

Changes in lung endothelial metabolic function, determined in vitro, have been proposed as sensitive indexes of hyperoxic lung damage. However, it is unclear whether these changes are also seen in vivo. We studied the possibility, using conscious rabbits in which jugular and carotid catheters had previously been placed under halothane anesthesia. Approximately 24 h later, test animals were exposed to normobaric hyperoxia (96 +/- 2%), while a second group was maintained in room air. Multiple indicator dilution methods were used to study (1) metabolism of 3H-benzoyl-phe-ala-pro (BPAP), a synthetic substrate for angiotensin converting enzyme (ACE), and (2) removal of 14C-5-hydroxytryptamine (5-HT) during a single transpulmonary passage in conscious animals. Determinations were made serially during exposure (room air or hyperoxia) or until death occurred in the oxygen-treated animals. Lungs of air-exposed animals hydrolyzed 81 +/- 2% of injected BPAP (0.1 to 0.15 nmoles) during a single passage. Percent metabolism was unaltered during the next 72 h. However, in test animals, ACE activity, as reflected by BPAP metabolism, was significantly reduced after 16 h of exposure to oxygen (77 +/- 2%, p less than 0.01) and continued to decrease to a nadir of 66 +/- 3% at 40 h. Single-pass lung uptake of 14C-5-HT (77 +/- 2%) was unchanged throughout the 72-h period in air-exposed rabbits. In test animals, 14C-5-HT removal decreased to 65 +/- 4% (p less than 0.01) after 24 h of oxygen exposure; 5-HT removal remained depressed compared with the 0 h control determination for the oxygen group at all subsequent measurement intervals. Light and electron microscopy of lungs from oxygen-exposed rabbits demonstrating reduced 5-HT removal and ACE activity at 24 h revealed normal endothelial and type I cell morphologic features. We conclude that exposure to 100% oxygen produced significant reduction in pulmonary 5-HT removal and BPAP metabolism prior to the onset of morphologic damage.

Animals↗
PubMed1995

Evidence that the brain of the conscious dog is insulin sensitive.

The aim of this study was to determine whether a selective increase in the level of insulin in the blood perfusing the brain is a determinant of the counterregulatory response to hypoglycemia. Experiments were carried out on 15 conscious 18-h-fasted dogs. Insulin was infused (2 mU/kg per min) in separate, randomized studies into a peripheral vein (n = 7) or both carotid and vertebral arteries (n = 8). This resulted in equivalent systemic insulinemia (84 +/- 6 vs. 86 +/- 6 microU/ml) but differing insulin levels in the head (84 +/- 6 vs. 195 +/- 5 microU/ml, respectively). Glucose was infused during peripheral insulin infusion to maintain the glucose level (56 +/- 2 mg/dl) at a value similar to that seen during head insulin infusion (58 +/- 2 mg/dl). Despite equivalent peripheral insulin levels and similar hypoglycemia; steady state plasma epinephrine (792 +/- 198 vs. 2394 +/- 312 pg/ml), norepinephrine (404 +/- 33 vs. 778 +/- 93 pg/ml), cortisol (6.8 +/- 1.8 vs. 9.8 +/- 1.6 micrograms/dl) and pancreatic polypeptide (722 +/- 273 vs. 1061 +/- 255 pg/ml) levels were all increased to a greater extent during head insulin infusion (P < 0.05). Hepatic glucose production, measured with [3-3H]glucose, rose from 2.6 +/- 0.2 to 4.3 +/- 0.4 mg/kg per min (P < 0.01) in response to head insulin infusion but remained unchanged (2.6 +/- 0.5 mg/kg per min) during peripheral insulin infusion. Similarly, gluconeogenesis, lipolysis, and ketogenesis were increased twofold (P < 0.001) during head compared with peripheral insulin infusion. Cardiovascular parameters were also significantly higher (P < 0.05) during head compared with peripheral insulin infusion. We conclude that during hypoglycemia in the conscious dog (a) the brain is directly responsive to physiologic elevations of insulin and (b) the response includes a profound stimulation of the autonomic nervous system with accompanying metabolic and cardiovascular changes.

3-Hydroxybutyric Acid↗
PubMed1980

The consciousness disciplines and the behavioral sciences: questions of comparison and assessment.

In recent years a number of assessments of the non-Western consciousness disciplines have been undertaken by Western behavioral scientists. The author suggests that a variety of conceptual, methodological, experimential, and content inadequacies render the conclusions of these investigations of doubtful validity. He then describes the models of human nature postulated by these disciplines and the Western behavioral sciences, suggesting that comparing them results in a paradigm clash. The failure to recognize this clash seems to have resulted in inappropriate pathologizing interpretations. Attention is drawn to the relevance of recent findings in state-dependent learning, meditation studies, peak and transcendental experiences, transpersonal psychology, and quantum physics to an assessment of the consciousness disciplines, and suggestions for more adequate investigation are provided.

Behavioral Sciences↗
PubMed1997

The real unconscious: psychoanalysis as a theory of consciousness.

Inquiries into hallucinatory wish fulfillment and the unconscious converge and, by distinguishing the concept of the unconscious in psychoanalysis from that of cognitive psychology, serve to bring out what is most essential to the psychoanalytic conception. Freud's topographical model is used to stress that the psychoanalytic unconscious can be understood only in relation to theories of consciousness and wishing. Moreover, in contrast to the cognitive conception, psychoanalysis holds that the processing of thought in the human mind is inseparable from the activity of desire. This leads to further psychoanalytic reflections on the interrelation of conscious and unconscious, wishing and thinking, and, in consequence, on transference and the mechanism of unconscious fantasy.

Cognition↗
PubMed1997

What is consciousness?

In the past few years scientists and scholars in a variety of disciplines have been making concerted efforts to answer an ancient question, namely, How exactly do the physical processes in the brain cause consciousness? What is distinctive about the way in which modern scientists and scholars are approaching this question is that they are treating it as a scientific problem rather than a metaphysical one. This transition reflects the air of expectation in contemporary cognitive science to the effect that an empirical solution is imminent to a philosophical problem that previously was considered insoluble. Nevertheless, a recent authoritative review of the publications of such leading contemporary workers in the field as Francis Crick, Daniel Dennett, Gerald Edelman, Roger Penrose, and Israel Rosenfield has concluded that they have all failed to provide a satisfactory answer to the question (Searle 1995a). The present paper makes a psychoanalytic contribution to this interdisciplinary effort and provides an alternative answer to the question, based on Freud's conceptualization of the problem of consciousness. The paper takes a concrete example from Searle's review, reanalyses it within Freud's metapsychological frame of reference, and shows how this frame provides a radical solution to the problem. This implication of Freud's work has not hitherto been recognized and so has not received the attention it deserves.

Awareness↗