Vasomotor Research Articles

Treating Hot Flashes with an Anticonvulsant

Menopausal vasomotor symptoms, which appear to originate in the hypothalamus, can be effectively treated with estrogens and progestins. It can be

Cerebral Vasomotor Reserve in Hypertension during Head-up Tilt

P44 Objective: To evaluate cerebral vasomotor reserve in hypertension during head-up tilt with hypo- and hypercapnia. Background: Cerebral vasoregulation determines degree of perfusion during increased metabolic demands such as orthostatic stress, hypo- and hypercapnia. With hypertension, silent hypoperfusion may develop if vasomotor reserve is compromised due to remodeling of the vessel wall and impaired vasodilation. Methods: We studied 15 mild hypertensive (BP 145/95 mm Hg) and 15 control men and women (aged 35–65 years) using Transcranial Doppler. Blood flow velocities (BFV) from both middle cerebral arteries (MCA), brachial artery (BRA), heart rate, blood pressure (BP), respiration and carbon dioxide (CO 2 ) were simultaneously recorded during: hyperventilation (3 min), apnea (1 min) and CO 2 rebreathing (3 min) in supine rest and head-up tilt at 80 O . Vasomotor reserve (VMR) was calculated from systolic (VMRS), diastolic (VMRD) and mean BFVs (VMRM) using regression analysis as percentual increment between hypo-, normo- and hypercapnia. Results: In controls, BFVs and VMR reserve were symmetric in both MCAs and there were no significant differences between rest and head-up tilt. In hypertensive patients, VMRM and were significantly reduced during supine rest (p Conclusions: Vasomotor reserve was reduced even with mild hypertension due to impaired vasodilation. Impaired vasoregulation during orthostatic stress may be associated with silent cerebral hypoperfusion.

Low-Dose Endotoxin Reduces Human Cerebrovascular Reactivity and Produces Procoagulant State

P118 Stroke risk is increased in the presence of some infections. We studied potential mechanisms linking infections and stroke risk. We used endotoxin, a component of gram negative bacteria, as a standardized inflammatory stimulus. We infused low-dose endotoxin (1ng/kg) as a bolus in four healthy men, and analyzed cerebrovascular and hemostatic effects over 24 hours. We measured cerebral vasomotor reactivity, using transcranial Doppler ultrasonography to calculate breath-holding index (BHI); the latter consists of the percent change of middle cerebral artery blood flow velocity over time during breath holding. We also measured thrombin-antithrombin complexes (TAT, an index of thrombin generation), and soluble e-selectin (a marker of endothelial activation). Following infusion of endotoxin, there were substantial physiological changes primarily at three to six hours post-infusion. Temperature peaked at 100 °F (p

Impaired cerebral vasoreactivity correlates with recent symptomaticity in severe carotid artery disease

P62 OBJECTIVE: Impaired cerebral vasomotor reactivity has been proposed as a measure of exhausted vascular reserve in patients with carotid artery stenosis or occlusion. We tested this hypothesis by measuring vasoreactivity in patients with asymptomatic or recently symptomatic severe carotid artery disease. METHODS: Fourteen patients with severe carotid artery disease (5 with occlusion, 9 with stenosis 80–99%, 8 symptomatic, 6 asymptomatic within 2 years) and 7 healthy controls had continuous bilateral monitoring of mean flow velocity (MFV) in the MCAs by transcranial Doppler (TCD). End-tidal CO2 was measured continuously with an in-line capnometer connected via snorkel mouthpiece, nasal airway occluded by noseclip. After baseline measurements, subjects held their breath for 30 seconds. A breath holding index (BHI) was calculated (% change in MFV/seconds held). After return to baseline MFV, subjects breathed a 5% CO2 gas mixture for 2 minutes. CO2 reactivity was calculated as percent rise in MFV per mmHg PCO2 once the MFV curve plateaued. ANOVA was used to calculate differences between symptomatic, asymptomatic and control groups for CO2 reactivity and BHI. RESULTS: There was a highly significant difference in vasoreactivity by CO2 inhalation in the symptomatic group (2.02±.80 %/mmHg) versus the asymptomatic group (4.45±1.9 %/mmHg) and controls (3.69±.95 %/mmHg) (F 2,18 =7.85, p=.004). A linear relationship was seen between MFV and PCO2, taking multiple MFV measurements at various PCO2 levels throughout the study period (average r 2 =.60 for patients, .77 for controls). BHI did not distinguish between the groups (p=.37). CONCLUSIONS: Measuring cerebral vasoreactivity by CO2 inhalation with continuous TCD monitoring provides an important physiological index of the clinical status of patients with carotid artery disease which may help guide treatment algorithms. The linear relationship between MCA MFV and end-tidal CO2 enables confirmation of the baseline and maximum measurements used to calculate CO2 reactivity, and provides the opportunity to investigate further the link between physiology and clinical state.

The dose effect of propofol on cerebrovascular reactivity to carbon dioxide in rabbits.

Propofol has several properties beneficial to intracranial operation such as reduction in cerebral metabolic rate and cerebral blood flow (CBF) in a dose-dependent manner while leaving autoregulation intact. Several studies have demonstrated that the responsiveness of CBF to changes in arterial carbon dioxide tension (PaCO2) is maintained during propofol anesthesia in both humans and animals. These studies showed a significant difference in the CBF-CO2 reactivity slope between awake and propofol anaesthetized groups, but no comparison with different doses of propofol was made. To determine the dose effect of propofol on cerebrovascular CO2 reactivity, we used laser Doppler flowmetry (LDF) to detect the changes of CBF during propofol anesthesia. Ten rabbits were studied using LDF on the parietal cortex. After surgical preparation, anesthesia was maintained with 66% N2O in O2, morphine 10 mg/kg and pancuronium. Three experimental conditions were studied sequentially with intravenous administration of the following drugs: (1) normal saline (control), (2) propofol 20 mg/kg/h i.v., (3) propofol 40 mg/kg/h i.v. Mean arterial pressure, rectal temperature and hematocrit were kept constant. The arterial carbon dioxide tension (PaCO2) was adjusted to three levels during each condition: 20-25 mmHg (hypocapnia), 35-40 mmHg (normocapnia) and 45-50 mmHg (hypercapnia). CBF was measured continuously and recorded after the target PaCO2 had been reached. There were no differences among all conditions in mean arterial pressure and heart rate. The changes of CBF as PaCO2 increased at the three different CO2 levels during each of the conditions were significantly different. The slope of CBF-CO2 reactivity among three different propofol doses was not significantly different. These data indicate that cerebral vasomotor responsiveness to CO2 during propofol anesthesia is preserved and that the slope of CBF-CO2 reactivity is independent of propofol doses as mean arterial blood pressure is maintained.

The role of comparison questions in physiological detection of deception.

Comparison questions in physiological detection of deception were studied with 60 "guilty" and 60 "innocent" participants in a mock crime experiment. Different types of comparison questions were used in four conditions: relevant-irrelevant (R-I) participants answered only relevant and neutral questions; trivial directed lie participants were instructed to lie to three of the six neutral questions; personal directed lie participants were instructed to lie to personally relevant questions; and probable lie participants received traditional probable lie comparison questions. Respiration, cardiovascular, vasomotor, and electrodermal activity were recorded. Manipulation of the comparison questions produced different patterns of physiological responses for innocent but not for guilty participants. The R-I test produced an unacceptable rate of false positive decisions.

Effect of ambient temperature on power spectral density of arterial pressure during sleep in the rat.

Power spectral density (PSD) of arterial pressure (AP) during sleep was observed at various ambient temperatures (Ta: 16, 22 and 28 degrees C). Average AP and heart rate (HR) during sleep increased with lowering of Ta. PSD of AP during slow wave sleep (SWS) decreased over the entire range of frequency with increasing of Ta. Low frequency component (approximately 0.1 Hz) in PSD of AP during paradoxical sleep (PS) increased, while higher frequency component (0.1 Hz approximately) decreased with increasing of Ta. This study suggests that Ta affects the PSD of AP during sleep, and that vasomotor sympathetic tone during PS might increase with increasing of Ta.

Hypothalamic homeothermy across the ultradian sleep cycle.

In the ambient thermal zone for the vasomotor regulation of body temperature hypothalamic temperature changes across the states of the ultradian sleep cycle are the result of state-dependent heat production-heat loss imbalances affecting the temperature of the arterial blood perfusing the brain. However, the changes in arterial blood temperature are efficiently buffered, at a low energetic cost, by the thermal inertia of the mass of body water. Thus, the oscillations in hypothalamic temperature are maintained within a width of a few tenths of a degree and are so small as to be subliminal as thermal feedback stimuli for thermoregulatory responses. This passive hypothalamic homeothermy would support the hypothesis that a phylogenetic pressure was operative early on in mammals in order to limit the duration of the ultradian sleep cycle so as to fit the thermal inertia of the different masses of body water in mammals of different sizes.

Plasma Endothelin as a Predictor of Outcome in Unstable Angina

Although the role of plaque rupture and platelet activation in acute coronary ischemia has been studied extensively, the importance of coronary vasomotor tone abnormalities has only recently become the subject of clinical investigation. This study prospectively examined the prognostic significance of circulating plasma levels of …

LIPID-LOWERING AND ANTIOXIDANT THERAPIES REDUCE CORONARY VASOCONSTRICTION.

The clinical effects of hypercholesterolemia may be mediated not only by the promotion of atherosclerosis, but also by alterations in endothelium-mediated vasomotor function. For example, oxidized LDL cholesterol might interfere with the release of natural vasodilators from the coronary endothelium. To assess …

Psychophysiological activity and reactivity and concept identification performance in alcoholics and controls

Detoxified alcoholics and controls were tested on the Concept Identification (CI) task as seven measures of psychophysiological activity and reactivity were recorded. On the CI task, subjects initially learned, by trial and error, to classify geometric patterns until the criterion of 16 consecutive correct responses was reached in 80-160 trials. Fewer alcoholics solved the CI problem than did controls. While working on the CI problem, alcoholics had higher skin conductance level (SCL) and vasomotor (VM) activity than controls. Only alcoholics had significant negative correlations between SCL and VM activity. Also, alcoholics who did not solve the problem had significant negative correlations between response latency and systolic blood pressure. The alcoholics’ abstraction deficit and their sensitivity to failure could explain why they had more psychophysiological activity on the CI problem than did controls.

Response of the microcirculation in rat cremaster muscle to peripheral and central sympathetic stimulation.

Microvascular diameter and flow responses to peripheral and central sympathetic stimulation were measured in different segments of the arteriolar network in rat cremaster muscle. For peripheral stimulation, a bipolar electrode was placed on the internodal segment of the lumbar sympathetic chain between ganglia L1 and L2. For central stimulation, a bipolar electrode was stereotaxically implanted in the posterior hypothalamus. Inside vessel diameter, red blood cell velocity, and volumetric flow rate were recorded in response to electrical stimulations of varying magnitude in four series-coupled segments of the arteriolar network: 1A, 2A, 3A, and 4A. Systemic arterial pressure was also monitored. The vasoconstriction and flow reduction produced by stimulation of the lumbar chain was graded with the frequency of stimulation over the range of 0.5-16.0 Hz in all arteriolar segments. Examination of the relation between stimulation frequency and vasoconstrictor response measured as percent of control diameter indicated a sequence of responsiveness to peripheral stimulation where 4A = 3A greater than 2A = 1A. No changes in diameter were recorded in the venous microcirculation at any level of stimulation. Stimulation of the posterior hypothalamus with currents of 38-300 microA for 60 seconds produced graded vasoconstriction in only 3A and 4A vessels. Fluorescence histochemistry for biogenic amines was used to examine the distribution of innervation to the microvasculature. All segments of the arteriolar network from 1A to 4A possessed an adrenergic innervation; no vessels of the venous network were found to be innervated. The results indicate that the pattern of response of the arteriolar network in rat cremaster muscle to peripheral and central sympathetic stimulation is segmentally differentiated and consistent with the distribution of the vasomotor innervation.

Vasoactive effects of serotonin on proximal coronary arteries in awake dogs.

This study evaluates the vasoactive effects and mechanisms of action of serotonin on epicardial arteries in awake dogs chronically instrumented with miniature piezoelectric dimension crystals on the proximal circumflex coronary artery. Serotonin (2-16 micrograms) infused as a bolus in the left atrium effected a dose-related biphasic response, which was characterized by an initial increase in vessel dimension with a peak response at 45-75 seconds, followed by a delayed and more sustained vasoconstriction, with a maximum response at 2-8 minutes. The magnitude of the initial vasodilation was generally greater than the delayed vasoconstriction. The initial vasodilation remained unchanged after selective S2 blockade with ketanserin (0.3 mg/kg) and was only minimally but insignificantly attenuated when flow was held constant but was reduced after S1 and S2 blockade with methysergide (0.25 mg/kg). Selective S2 blockade with ketanserin (0.3 mg/kg) attenuated the delayed vasoconstriction in most but not all dogs; the effect of ketanserin was, however, not significant when the entire group was considered. Selective endothelial denudation effectively eliminated the initial vasodilation response to serotonin and significantly augmented the delayed vasoconstriction when the dogs were studied 1-2 days after denudation. The data indicate that in the awake dog, serotonin effects a biphasic vasomotor response characterized by an initial vasodilation that is mediated primarily through a direct endothelium-dependent S1 mechanism followed by a delayed vasoconstriction that is probably mediated via a direct S2 effect on the vascular smooth muscle and is attenuated by the normal endothelium.

Increased vascular contraction and sensitivity to norepinephrine after endothelial denudation is inhibited by prazosin.

The vasomotor function of rabbit aorta was examined after deendothelialization with a Fogarty balloon catheter and during the subsequent development of intimal hyperplasia. Helical strips of injured lower abdominal aortic tissue showed an increase in norepinephrine-induced contraction when compared with control strips from normal upper abdominal aorta. This increase was 235% +/- 40% of control immediately after injury and 341% +/- 51% at 28 days after injury. Standardized dose-response curves demonstrated that the injured tissue was increasingly sensitive over time to norepinephrine and that this was more marked at physiologic levels of norepinephrine. Contraction was blocked by prazosin hydrochloride but not by yohimbine or propranolol. Furthermore, a single intramuscular dose of prazosin hydrochloride 2 hours before injury significantly (p = 0.001) reduced the maximal contraction and sensitivity. These results imply an increase in vasomotor reactivity after deendothelialization mediated through the alpha 1-adrenergic receptor. These functional changes are related to the pertinent morphologic observations.

Bronchomotor and vasomotor activities of physiologically active amines administered into the bronchial artery

Bronchomotor and vasomotor activities of physiologically active amines administered into the bronchial artery

Vascular effects of cigarette smoke in isolated pig lungs.

To determine the local effects of cigarette smoke on the pulmonary vasculature, we measured pulmonary artery pressure--flow curves in isolated, blood-perfused pig lungs before and after 4 exposures to cigarette smoke. During each exposure, smoke was administered into the trachea for 3 to 4 min at a rate of 20 to 25 puffs/min and a puff volume of 35 to 50 ml with a smoking machine. During hypoxia (inspired PO2, 50 mmHg), when baseline vasomotor tone was high, cigarette smoke caused an acute transient vasodilation. During control (inspired PO2, 200 mmHg), when baseline tone was low, no significant effect was observed. In addition to this acute effect, cigarette smoke caused a depression of the pulmonary pressor response to hypoxia, which developed gradually during the course of the experiment. Indomethacin, at perfusate concentrations of 20 and 100 micrograms/ml, did not significantly alter the acute vasodilating effect of smoking, suggesting that prostaglandins synthesized by cyclooxygenase were not the mediators of this response. Indomethacin did, however, prevent the gradual depression of the pulmonary vasoconstrictor response to hypoxia.

Sensation Seeking and Psychophysiological Responses to Auditory Stimulation

ABSTRACTThis study tested the hypothesis that the orienting response (OR) is one of the biological correlates of sensation seeking. Skin conductance (SC), heart rate (HR), and peripheral vasomotor (VM) activity were recorded while ten 60dB, 1000 Hz, slow‐rise‐time tones were presented to male subjects with high (N = 16) and low (N = 15) total scores on Form V of the Sensation Seeking Scale (SSS).There were no significant differences between groups in the SC or VM responses to the first (novel) tone or in the rate at which these responses habituated. The HR response to the first tone was deceleration (an OR) for the high SS group (as well as for a high Disinhibition subgroup), while the response of the low SS group (and a low Disinhibition subgroup) included what appeared to be startle components—a short‐latency accelerative response that habituated rapidly on subsequent trials. It is suggested that individuals with low sensation seeking tendencies may be unusually prone to startle, and that subsequent research on the biological correlates of sensation seeking should take into account individual differences in the tendency to give orienting, defensive, and startle responses.

Inhibition of the baroreceptor reflex on stimulation in the brain stem defence centre.

1. In anaesthetized cats, the pattern of cardiovascular response characteristic of the defence reaction has been elicited by localized electrical stimulation within the appropriate region of the hypothalamus. The baroreceptor reflex response has been elicited by raising the pressure in a blind sac preparation of the carotid sinus or by electrical stimulation of the sinus nerve.2. In addition to arterial blood pressure, heart rate and regional blood flows, activity was recorded in cardiac and renal sympathetic nerves, to assess more precisely the cardiomotor and vasomotor changes during interactions between brain stem stimulation and baroreceptor activation.3. The sympatho-inhibitory and depressor effects of carotid sinus stimulation or electrical stimulation of the sinus nerve could be completely suppressed by stimulation within the hypothalamic defence area, as could the reflex bradycardia. It is concluded that this suppression is effected through the central nervous system.4. Stimulation at points in the hypothalamus close to, but outside, the defence area, and which elicited increases in arterial pressure and sympathetic activity of similar magnitude to those from the defence area itself, did not abolish the sympatho-inhibitory or depressor effects of baroreceptor activation, though the reflex bradycardia was usually inhibited. It is suggested that this less localized change results from augmentation of the central inspiratory drive which inhibits the vagal outflow to the heart.

Convergence of preganglionic fibers on the vasomotor neurons of the sympathetic ganglia of cats

By means of intracellular recordings from the neurons of isolated lumbar ganglia III-IV it is shown that B1-, B2- and C-preganglionic fibres widely converge on these neurons. The neurons antidromically activated by stimulation of muscular and cutaneous branches were identified as vasomotor ones. The latter had distinct features of preganglionic fibre convergence. Only B2- and C-preganglionic fibres were able to activate them, but the efficacy of the B2-fibres excitatory action was considerably higher. The vasomotor neurons had a lower conduction velocity in its axons (0.95 +/- 0.05 m/s) as compared to other postganglionic neurons (1.30 +/- 0.15 m/s).

Autonomic Vasomotor Tone in the Pulmonary Circulation

Autonomic Vasomotor Tone in the Pulmonary Circulation