Orbital cortical influences on cardiovascular dynamics and myocardial structure in conscious monkeys

1977 ◽  
Vol 46 (5) ◽  
pp. 638-647 ◽  
Author(s):  
Richard E. Hall ◽  
Robert B. Livingston ◽  
Colin M. Bloor

✓ The posterior orbital cortex of the frontal lobes in conscious monkeys was stimulated electrically to study the influence of this structure on cardiovascular hemodynamics and cardiac morphology. Stimulating electrodes, cardiac output flow probes, and arterial blood pressure transducers were chronically implanted by aseptic procedures into eight Macaca fascicularis monkeys. Cardiovascular changes induced by stimulating the orbital cortex included both biphasic and unidirectional alterations in cardiac output, blood pressure, heart rate, stroke volume, and total systemic resistance. Electrode position and the rate (Hz) of applied stimulation were the primary determinants of the direction and magnitude of the response. All animals stimulated demonstrated acute, discrete interventricular septal myocytolysis, characteristic of early ischemic lesions. Since the orbital cortex is a part of the limbic system, changes induced by its stimulation suggest a pathophysiological mechanism whereby emotional expression may effect dynamic shifts in cardiovascular functions and may thus induce permanent and manifest myocardial lesions.

1986 ◽  
Vol 64 (5) ◽  
pp. 780-786 ◽  
Author(s):  
Robert J. Hariri ◽  
Elizabeth L. Supra ◽  
John Paul Roberts ◽  
Michael H. Lavyne

✓ Transient global cerebral ischemia (TGI) was induced in awake rats using the “four-vessel” occlusion model of Pulsinelli and Brierley. Blood pressure, arterial blood gases, cerebral blood flow, and cardiac output were measured during the acute (up to 2 hours) and chronic (2 to 72 hours) postischemic time periods. Coincident with the onset of TGI, cardiac output and caudate blood flow were depressed. The former returned to baseline within 30 minutes after the conclusion of TGI, and the latter progressed to hyperemia at 12 hours (81.8 ± 4.9 vs 68.6 ± 3.9 ml/min/100 gm tissue (mean ± standard error of the mean)) and oligemia at 72 hours (45.5 ± 4.8 ml/min/100 gm tissue) post-TGI in the untreated control rats. Arterial blood gases and blood pressure were unchanged. Naloxone (1 mg/kg) given at the time of TGI or as late as 60 minutes post-TGI and every 2 hours thereafter for 24 hours or bilateral cervical vagotomy prevented the depression in cardiac output and blocked the hyperemic-oligemic cerebral blood flow pattern that was predictive of stroke in this rat model. Changes in cardiac output after TGI in this model appear to be mediated by parasympathetic pathways to the heart from the brain stem. Opiate receptor blockade probably blocks endogenous opioid peptide stimulation of these brain-stem circulatory centers, which results in inhibition of parasympathetic activity and improvement in cardiac output. The usefulness of naloxone in the treatment of experimental stroke may be a function of its ability to improve cerebral perfusion in pressure-passive cerebrovascular territories. Variations in cardiac output during experimental stroke may explain the dissimilar responses to naloxone treatment reported by other investigators of experimental stroke.


1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.


1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.


1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.


2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.


2001 ◽  
Vol 204 (22) ◽  
pp. 3963-3971 ◽  
Author(s):  
S. F. Perry ◽  
J. E. McKendry

SUMMARYFish breathing hypercarbic water encounter externally elevated PCO2 and proton levels ([H+]) and experience an associated internal respiratory acidosis, an elevation of blood PCO2 and [H+]. The objective of the present study was to assess the potential relative contributions of CO2versus H+ in promoting the cardiorespiratory responses of dogfish (Squalus acanthias) and Atlantic salmon (Salmo salar) to hypercarbia and to evaluate the relative contributions of externally versus internally oriented receptors in dogfish.In dogfish, the preferential stimulation of externally oriented branchial chemoreceptors using bolus injections (50 ml kg–1) of CO2-enriched (4 % CO2) sea water into the buccal cavity caused marked cardiorespiratory responses including bradycardia (–4.1±0.9 min–1), a reduction in cardiac output (–3.2±0.6 ml min–1 kg–1), an increase in systemic vascular resistance (+0.3±0.2 mmHg ml min–1 kg–1), arterial hypotension (–1.6±0.2 mmHg) and an increase in breathing amplitude (+0.3±0.09 mmHg) (means ± s.e.m., N=9–11). Similar injections of CO2-free sea water acidified to the corresponding pH of the hypercarbic water (pH 6.3) did not significantly affect any of the measured cardiorespiratory variables (when compared with control injections). To preferentially stimulate putative internal CO2/H+ chemoreceptors, hypercarbic saline (4 % CO2) was injected (2 ml kg–1) into the caudal vein. Apart from an increase in arterial blood pressure caused by volume loading, internally injected CO2 was without effect on any measured variable.In salmon, injection of hypercarbic water into the buccal cavity caused a bradycardia (–13.9±3.8 min–1), a decrease in cardiac output (–5.3±1.2 ml min–1 kg–1), an increase in systemic resistance (0.33±0.08 mmHg ml min–1 kg–1) and increases in breathing frequency (9.7±2.2 min–1) and amplitude (1.2±0.2 mmHg) (means ± s.e.m., N=8–12). Apart from a small increase in breathing amplitude (0.4±0.1 mmHg), these cardiorespiratory responses were not observed after injection of acidified water.These results demonstrate that, in dogfish and salmon, the external chemoreceptors linked to the initiation of cardiorespiratory responses during hypercarbia are predominantly stimulated by the increase in water PCO2 rather than by the accompanying decrease in water pH. Furthermore, in dogfish, the cardiorespiratory responses to hypercarbia are probably exclusively derived from the stimulation of external CO2 chemoreceptors, with no apparent contribution from internally oriented receptors.


1991 ◽  
Vol 261 (3) ◽  
pp. R677-R685 ◽  
Author(s):  
B. L. Brizzee ◽  
R. D. Russ ◽  
B. R. Walker

Experiments were performed to examine the potential role of circulating arginine vasopressin (AVP) on baroreflex sensitivity during hypotensive and nonhypotensive hemorrhage in the conscious rat. Animals were chronically instrumented for measurement of cardiac output, blood pressure, and heart rate (HR). Three potential stimuli for release of AVP were utilized: 1) rapid 20% arterial hemorrhage that resulted in hypotension, 2) nonhypovolemic hypotension induced by intravenous infusion of nitroprusside, and 3) nonhypotensive hemorrhage (rapid 10% arterial blood withdrawal). Hypotensive hemorrhage was associated with significant reductions in blood pressure, cardiac output, HR, and calculated total peripheral resistance, an increase in baroreflex (BRR) bradycardia in response to pressor infusions of phenylephrine, and a moderate elevation in circulating AVP. Prior intravenous administration of a specific V1-vasopressinergic antagonist augmented the hypotensive response to hemorrhage; however, neither V1- nor V2-blockade affected hemorrhage-induced augmentation of the BRR. Inducement of hypotension by infusion of nitroprusside did not alter subsequent BRR sensitivity. Finally, nonhypotensive hemorrhage was associated with an increase in resting HR and augmented BRR sensitivity. However, in contrast to hypotensive hemorrhage, either V1- or V2-antagonism attenuated the increase in BRR sensitivity seen with 10% hemorrhage. These data suggest that, although AVP may play a role in blood pressure maintenance via its direct vasoconstrictor actions during hypotensive hemorrhage, the observed augmentation of BRR sensitivity associated with severe blood loss is not attributable to a vasopressinergic mechanism activated by circulating AVP. However, blood-borne AVP may contribute to BRR sensitivity alterations in response to mild blood loss.


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