Circulatory and Respiratory Changes during Unilateral and Bilateral Cranial Nerve IX and X Block in Two Asthmatics

1971 ◽  
Vol 40 (2) ◽  
pp. 117-125 ◽  
Author(s):  
John H. Eisele ◽  
Sushil K. Jain
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vital Capacity ◽  
Ventilatory Response ◽  
Cranial Nerves ◽  
Systemic Blood Pressure ◽  
Hypoxic Ventilatory Response ◽  
Circulatory Effects ◽  
Obstructive Airways Disease ◽  
Pulmonary Arterial

1. The respiratory and circulatory effects of bilateral block of the IXth and Xth cranial nerves (IX and X) with local anaesthetic were studied in two subjects with obstructive airways disease (asthma). 2. In one subject bilateral block of IX and X decreased alveolar ventilation as evidenced by a rise in Pa,co2 and a fall in Pa,o2. There was no apparent ventilatory change in the other subject. The lung volumes (ERV and FRC) were unaffected by the block; however, the forced vital capacity and 1 s forced expired volume were slightly improved in both subjects. 3. During bilateral IX and X block neither subject showed a ventilatory response after 3 min of breathing 8·7% O2 in 91·3% N2. In one subject during a left-sided IX and X block, there was a normal hypoxic-ventilatory increase, whereas during a right-sided IX and X block the hypoxic-ventilatory response was slightly less than normal. 4. Unilateral IX and X block in both subjects produced tachycardia and hypertension which was approximately one half the increased heart rate and blood pressure that followed bilateral IX and X blockade. 5. Unlike the control responses, breathing 8·7% O2 in 91·3% N2 during bilateral IX and X block produced no change in heart rate and there was a continuous fall in the systemic blood pressure. The pulmonary arterial pressure, however, increased in response to hypoxia in the same manner as before the block.

scholarly journals PROGNOSTIC VALUE OF HEART RATE AND SYSTEMIC BLOOD PRESSURE IN PULMONARY ARTERIAL HYPERTENSION

2010 ◽  
Vol 55 (10) ◽  
pp. A154.E1443
Author(s):  
Malcolm M. Bersohn ◽  
Shelley Shapiro ◽  
Michelle P. Turner ◽  
Glenna Traiger ◽  
Adaani E. Frost
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Prognostic Value ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pulmonary Arterial

scholarly journals Changes in Respiratory Rate, Blood Pressure and Heart Rate Variability in Rabbits during Orthostasis

2006 ◽  
Vol 75 (1) ◽  
pp. 3-12 ◽  
Author(s):  
J. Mokrý ◽  
T. Remeňová ◽  
K. Javorka
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Respiratory Rate ◽  
Supine Position ◽  
Spectral Power ◽  
Systemic Blood Pressure ◽  
Microcomputer System ◽  
Systemic Blood ◽  
Frequency Bands

The purpose of the study was to evaluate the changes of respiratory rate, systemic blood pressure and heart rate variability parameters (HRV) during orthostasis in anaesthetized rabbits. Furthermore, these changes were influenced by affecting the renin-angiotensin-aldosterone (RAA) system and autonomic nervous system (ANS) to study the mechanisms participating in activity of spectral frequency bands of HRV in rabbits. Ten adult rabbits (Chinchilla) were anaesthetized by ketamine and flunitrazepam. The systemic blood pressure, tidal volume and respiratory rate were measured. HRV was evaluated by microcomputer system VariaPulse TF3E. The R-R intervals were derived from the electrocardiogram signal from subcutaneous needle electrodes. The evaluation of HRV in very low (VLF; 0.01-0.05 Hz), low (LF; 0.05-0.15 Hz) and high frequency bands (HF; 0.15-2.0 Hz) was made and parameters of frequency and time analysis were calculated. The measurements were made in horizontal (supine) position, in orthostasis (the angle of 60 °) and again in supine position before and after enalapril (0.5 mg/kg b.w.), metipranolol (0.2 mg/kg b.w.), and after subsequent bilateral cervical vagotomy. The orthostasis in anaesthetized rabbits is accompanied by depression of respiratory rate reversed only by vagotomy. Furthermore, decrease of systemic blood pressure, unchanged heart rate and increased characteristics of heart rate variability were found, with predominant increase of spectral power in LF and VLF bands. This elevation can be eliminated only by complete blockade of ANS. Although the participation of ANS or RAA system in modification of individual HRV frequency bands is not as specific as in humans, we confirmed the participation of RAA system in determination of the VLF band.

Neural mechanism underlying basilar arterial constriction by intracisternal L-NNA in anesthetized dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H103-H107 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
T. Okamura
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebral Arteries ◽  
Neural Mechanism ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Anesthetized Dogs ◽  
Arterial Constriction ◽  
Synthase Inhibitor

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.

Respiratory and cardiovascular responses to increased and decreased carotid sinus pressure in sleeping dogs

1995 ◽  
Vol 78 (5) ◽  
pp. 1688-1698 ◽  
Author(s):  
K. W. Saupe ◽  
C. A. Smith ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Eye Movement ◽  
Carotid Sinus ◽  
Minute Ventilation ◽  
Control Level ◽  
Cardiovascular Responses ◽  
Systemic Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

The purpose of this study was to determine the effects of changing blood pressure in the carotid sinus (Pcs) on ventilatory output during wakefulness and non-rapid-eye-movement sleep in unanesthetized dogs. Eight dogs were chronically instrumented so that ventilation, heart rate, and blood pressure could be measured while pressure in the isolated carotid sinus was rapidly changed by means of an extracorporeal perfusion circuit. Raising Pcs 35–75 mmHg consistently reduced ventilation 15–40% in a dose-response fashion, with little or no further diminution in minute ventilation as Pcs was further increased > 75 mmHg above control level. This decrease in minute ventilation was immediate, due primarily to a decrease in tidal volume, and was sustained over the 20-s period of elevated Pcs. Increases in Pcs also caused immediate sustained reductions in systemic blood pressure and heart rate, both of which also fell in a dose-dependent fashion. The ventilatory and systemic cardiovascular responses to increased Pcs were the same during wakefulness and non-rapid-eye-movement sleep. Decreasing Pcs 40–80 mmHg caused a sudden carotid chemoreceptor-mediated hyperpnea that was eliminated by hyperoxia. We conclude that increasing Pcs causes a reflex inhibition of ventilation and that this reflex may play a role in sleep-disordered breathing.

Baroreceptor influence on postural changes in blood pressure and carotid blood flow

1963 ◽  
Vol 205 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Francis L. Abel ◽  
John H. Pierce ◽  
Warren G. Guntheroth
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Sinus ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Carotid Blood Flow ◽  
Postural Changes ◽  
Nembutal Anesthesia

The effects of 30° head-down and head-up tilting on mean systemic blood pressure, carotid blood flow, and heart rate were studied in 16 dogs under morphine and Nembutal anesthesia. The tilting procedure was further repeated after denervation of the carotid sinus and aortic arch baroreceptors and after administration of a dihydrogenated ergot alkaloid mixture (Hydergine). The results indicate that the drop in pressure in the head-down position is primarily due to baroreceptor activity and that the baroreceptors are necessary for compensatory vasoconstriction on head-up tilting. Carotid blood flow decreased in both tilted positions in the control animals; the possible relationship to cerebral blood flow is discussed.

The effect of Adrenaline upon Cardiovascular and Metabolic Functions in Man

1985 ◽  
Vol 69 (2) ◽  
pp. 215-222 ◽  
Author(s):  
I. W. Fellows ◽  
T. Bennett ◽  
I. A. Macdonald
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Metabolic Rate ◽  
Plasma Potassium ◽  
Glycerol Concentration ◽  
Plasma Adrenaline ◽  
Metabolic Functions ◽  
Circulatory Effects ◽  
Solution Saline ◽  
And Control

1. On three separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline, 50 ng min−1 kg−1 (high A), adrenaline, 10 ng min−1 kg−1 (low A) or sodium chloride solution (saline :154 mmol of NaCl/1) plus ascorbic acid, 1 mg/ml (control), over 30 min. 2. Venous adrenaline concentrations of 2.19 ± 0.15 nmol/l, 0.73 ± 0.08 nmol/l and 0.15 ± 0.03 nmol/l were achieved during the high A, low A and control infusions respectively. 3. Heart rate rose significantly by 19 ± 3 beats/min (high A) and by 6 ± 1 beats/min (low A). Heart rate remained significantly elevated 30 min after cessation of the high A infusion, despite venous plasma adrenaline concentration having fallen to control levels. 4. The diastolic blood pressure fell during the high A and low A infusions, but the systolic blood pressure rose only during the high A infusion. 5. Vasodilatation occurred in the calf vascular bed during both high A and low A infusions. The changes in hand blood flow and hand vascular resistance were not statistically significant, although there was a tendency to vasoconstriction during the infusion of adrenaline. 6. Metabolic rate rose significantly by 23.5 ± 1.8% (high A) and by 11.8 ± 1.6% (low A). Metabolic rate remained elevated between 15 and 30 min after termination of the high A infusion. There was an initial transient increase in respiratory exchange ratio (RER) during the adrenaline infusions. During the later stages of the adrenaline infusions and after their cessation, RER fell, probably reflecting increased fat oxidation. 7. Blood glucose, glycerol and lactate concentrations all rose significantly during the high A infusion, but only the blood glycerol concentration rose during the low A infusion. Plasma potassium concentration fell during and after the high A infusion but only after cessation of the low A infusion. 8. When adrenaline was infused intravenously at rates that elevated the plasma adrenaline concentration within the physiological range, peripheral circulatory effects were observed similar to those previously described for larger doses of adrenaline. The persistent tachycardia noted after stopping the high A infusion may, at least in part, have been a consequence of the concomitantly elevated metabolic rate.

P504 HEMODYNAMIC RESPONSE TO NON-SELECTIVE BETA BLOCKERS DESPITE LACK OF EFFECTS ON HEART RATE AND SYSTEMIC BLOOD PRESSURE

2014 ◽  
Vol 60 (1) ◽  
pp. S237
Author(s):  
S. Bota ◽  
M. Mandorfer ◽  
P. Schwabl ◽  
P. Salzl ◽  
A. Ferlitsch ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Beta Blockers ◽  
Systemic Blood Pressure ◽  
Hemodynamic Response ◽  
Systemic Blood
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