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Computer simulation of circulation in patient with total cavo-pulmonary connection: inter-relationship of cardiac and vascular pressure, flow, resistance and capacitance.

The aim is to develop a computer model representative of the circulation in a patient with a uni-ventricular heart surgically palliated by a total cavo-pulmonary connection (TCPC). The effects of known hazardous exposures on this type of circulation are investigated. A model of the cardiovascular system is built using standard components such as transmission lines, restrictors and capacitances. The chamber of the heart consists of a volume connected to checkvalves, and an oscillating source flow connected to the volume represents the pumping of the heart. The following are simulated: exposure to cold, heat, high altitude, accelerating forces, blood loss, reduction in ventricular function, atrioventricular-valve regurgitation and treatment with afterload-reducing agents. During simulations, all the parameters can be changed, independently of each other, and the resulting changes in flow, resistance and pressure are recorded. Exposure to cold, reduced ventricular function and atriventricular-valve regurgitation result in a decrease in cardiac output (14, 58 and 45%, respectively). At high altitude, an increase of 18% is noted in the central venous pressure. Afterload-reducing agents increase the cardiac output by 8% and reduce central aortic pressure by 23%. Blood loss results in a marked reduction in perfusion pressure. It is concluded that the computer model is a useful instrument for simulation of a TCPC or Fontan circulation. The original criteria for this surgical procedure are those showing the most marked haemodynamic responses to different stimulus.

Computer Simulation↗

Investigation of blood-brain barrier permeability to magnetite-dextran nanoparticles (MD3) after osmotic disruption in rats.

The permeability of experimentally disrupted blood-brain barrier (BBB) to superparamagnetic nanoparticles (MD3) was studied in rats. BBB opening was induced by intracarotid injection of mannitol. One hundred eighty rats were used for the study. Rats were examined at two time points, 30 minutes and 12 hours after intracarotid mannitol injection. Different preparations intravenously injected 30 minutes before rat sacrifice were used for characterization of BBB disruption. BBB integrity was determined with 99mTc-diethylenetriamine pentaacetic acid (DTPA) and 99mTc-albumin. Iron oxide-glucose particles (12-nm mean diameter), 99mTc-labeled lecithin-cholesterol liposomes of three different sizes (50, 100, and 200 nm), and polyethylene glycol (PEG)-coated 99mTc liposomes (50 nm) were used for investigations of the dependence of BBB permeability on particle system size or surface. Magnetite-dextran nanoparticles (MD3) were evaluated as superparamagnetic contrast agent to monitor with magnetic resonance imaging (MRI) the BBB breakdown. In vitro T1 and T2 relaxation times of the brain tissue were measured at 40 MHz and 37 degrees C, and T2-weighted MR images were acquired at 0.5 T. After intracarotid mannitol infusion, as expected, the BBB breakdown was immediate and temporary as judged by soluble molecule diffusion. MD3 nanoparticles crossed the BBB 12 hours after intravenous mannitol injection, at a time when brain permeability for molecules or small particles returns to normal. Magnetite crystals were found in cytoplasmic vesicles of glial cells. On MRI, signal intensity decreased after injection of MD3, even 12 hours after mannitol injection. This particularity could be useful in the study of focal pathological lesions accompanied by BBB permeability modifications. In such conditions, superparamagnetic particle contrast agents could be caught by the BBB, allowing the observation of impaired BBB areas without detectable cellular lesions.

Animals↗

Changes in systemic and regional haemodynamics during 5-HT7 receptor-mediated depressor responses in rats.

The 5-hydroxytryptamine (5-HT)-induced late depressor response in rats is mainly mediated by vascular 5-HT7 receptors. The present study was devoted to determining the systemic and regional haemodynamic changes during this response, with particular emphasis on localising vascular beds that may contribute to the increase in total systemic vascular conductance. In vagosympathectomised, pentobarbital-anaesthetised rats pretreated with the 5-HT2 receptor antagonist ritanserin (50 microg kg(-1), i.v.), 5-HT (1, 3 and 10 ug kg(-1) min(-1) during 10 min; i.v.) produced a dose-dependent decrease in mean arterial blood pressure by up to 46+/-3%. This decrease was accompanied by increases in systemic vascular conductance by up to 83+/-15%; cardiac output was unaffected. 5-HT increased regional vascular conductance in skeletal muscle, carcass, mesentery/pancreas and adrenals by up to 740+/-14%, 117+/-18%, 135+/-26% and 88+/-22%, respectively, but decreased 'lung' (mainly arteriovenous anastomotic) conductance by up to 81+/-2%. Pretreatment with R(+)lisuride (100 microg kg(-1), i.v.) abolished all 5-HT-induced systemic and regional haemodynamic effects. In contrast, i.v. pretreatment with S(-)lisuride (100 microg kg(-1)) or GR127935 (300 microg kg(-1)) did not affect the 5-HT-induced systemic haemodynamic changes. The above results suggest that hypotension induced via 5-HT7 receptor activation was exclusively caused by vasodilatation of the systemic vasculature, confined to skeletal muscle, carcass, mesentery/pancreas and adrenal vascular beds. Furthermore, this study shows that blockade of vasorelaxant 5-HT7 receptors by lisuride is stereoselective.

Adrenal Glands↗

Influence of infusion flow rates on central venous pressure measurements through multi-lumen central venous catheters in intensive care.

OBJECTIVE: To study the influence on central venous pressure (CVP), measured at the distal port, of crystalloid infusions administered through the proximal port(s) of a central venous multi-lumen catheter. PATIENTS: Thirty-one intensive care patients. INTERVENTIONS: CVP was measured at the distal port of a multi-lumen catheter inserted in the subclavian or internal jugular vein. Using the proximal port(s), saline (0.9%) was infused at rates varying from 2 ml/h to 14,340 ml/h. RESULTS: CVP measured before the infusion and during infusion (after 30 s to 1 min) were not significantly different. Positive pressure ventilation with PEEP (5.6 +/- 2.5 cmH(2)O) and/or norepinephrine infusion (0.25 +/- 0.21 microg kg(-1) min(-1)) did not produce any significant change in CVP during infusion. CONCLUSION: The administration of crystalloids at different flow rates through the proximal port(s) of a multi-lumen catheter placed in the superior vena cava does not affect CVP measurement at the distal port, even in mechanically ventilated patients or patients receiving vasopressors.

Aged↗

Numerical simulation of the blood flow in the human cardiovascular system.

This paper describes a numerical model of the human cardiovascular system. The model is composed of 15 elements connected in series representing the main parts of the system. Each element is composed of a rigid connecting tube and an elastic reservoir. The blood flow is described by a one-dimensional time-dependent Bernoulli equation. The action of the ventricles is simulated with a Hill's three-element model, adapted for the left and right heart. The closing of the four heart valves is simulated with the aid of time-dependent drag coefficients. Closing is achieved by letting the drag coefficient approach infinity. The resulting system of 32 non-linear ordinary differential equations is solved numerically with the Runge-Kutta method. The results of the simulation (pressure-time and volume-time dependence for the atria and ventricles and pressure forms in the aorta at a heart rate of 70 beats per minute) agree with the physiological data given in the literature. The model's input aortic impedance is 31.5 dyn s cm-5 which agrees with literature data given for aortic input impedance in man 26-80 dyn s cm-5). Long-term stability of the system was achieved. The cardiovascular system presented here can also be simulated at higher and varying heart rates--up to 200 beats per minute. The results of calculations for some pathological changes (e.g. valvular abnormalities) are discussed.

Algorithms↗

Investigations of the peripheral vascular mechanisms implicated in congestive heart failure by the non-invasive evaluation of radial artery compliance and reactivity.

The viscoelastic, muscular and endothelial components of the vessel wall may be altered in patients with congestive heart failure (CHF). In order to investigate the relative contribution of each of these components to the peripheral vascular mechanisms of the disease, we have studied post-ischemic (endothelial-dependent) and post-nitroglycerin (endothelial-independent) vasodilatation as well as the response to cold pressure test and the geometry and compliance of the radial artery using a non-invasive echotracking method coupled to digital photoplethysmography. Thirty-nine patients with congestive heart failure (ejection fraction = 28 +/- 2%) were compared to age- and sex-matched healthy controls. Baseline therapy was unchanged during the study. In congestive heart failure patients, cross-sectional compliance and volumic distensibility were greater (P < 0.05) but isobaric compliance which is independent of blood pressure value was unchanged. Post-ischemic and post-nitroglycerin vasodilatation were lower (7 +/- 1 vs. 11 +/- 1%, P < 0.01 and 6 +/- 1 vs. 14 +/- 2%, P < 0.001, respectively) and both of the arterial diameter and pressure responses to cold pressor test were blunted (-5 +/- 1 vs. -8 +/- 1%, P = 0.058 and 6 +/- 3 mmHg vs. 13 +/- 2 mmHg, P < 0.01, respectively) in congestive heart failure. These changes were similar in primary and ischemic congestive heart failure, suggesting that they are more likely related to common neuro-hormonal factors rather than to an atherosclerotic process.

Blood Pressure↗

Effects of calcium entry blockers on distribution of blood volume.

To evaluate the effects on hemodynamics and the distribution of blood volume of various calcium entry blocker (CEB) agents, we invasively studied 24 hypertensive patients before and after treatment with isradipine, diltiazem, and verapamil. All three agents reduced arterial pressure through a significant fall in total peripheral resistance without causing reflex tachycardia, while preserving stroke volume and cardiac output. Verapamil reduced the central blood volume (CBV) and the ratio of CBV to total blood volume (TBV) in the supine position (P < .05), suggesting peripheral venodilatation. Isradipine and verapamil modified the responses to head-up tilt. The orthostatic decrease in stroke volume was accentuated following treatment, and it was associated with a greater fall in the ratio of CBV to TBV, suggesting that these two agents attenuate the reflex venoconstriction induced by postural change. In contrast to verapamil and isradipine, diltiazem did not affect volume distribution in the supine or head-up positions. These results suggest that the effect of CEBs varies in order of venodilatory effect from verapamil to isradipine to diltiazem, with verapamil having the greatest effect.

Blood Volume↗

Moderate cerebral venous congestion induces rapid cerebral protection via adenosine A1 receptor activation.

Stroke is a devastating complication in cardiovascular surgery, and neuronal damage is worsened by intracranial pressure elevation caused by cerebral venous circulatory disturbances (CVCD). However, we have previously reported that CVCD before cerebral ischemia decreases the infarct area. In the present study, focal cerebral ischemia was induced in spontaneously hypertensive rats by filament insertion through the carotid artery. Rats were divided into the following four groups: sham-operated, mild or severe venous congestion (VC), and DPCPX. The DPCPX group received the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) prior to mild VC. Behavior, infarct volume, edema and S-100 protein were evaluated among the four groups. The infarct volume rates in mild VC and severe VC groups were significantly less than that in sham-operated and DPCPX groups. However, the mortality of the severe VC group worsened in a time-dependent manner. We observed a significant decrease in edema in the mild VC group compared to the DPCPX group. Behavioral scores also indicated that the mild VC group had fewer neurological deficits than the other three groups, including the DPCPX group. We were able to induce rapid cerebral protection via adenosine A1 receptor activation by administering an appropriate degree of VC prior to cerebral ischemia produced by middle cerebral artery occlusion. Our work suggests possible mechanisms by which such effective VC may lead to cerebral protection and adenosine A1 receptor activation.

Adenosine A1 Receptor Antagonists↗

Rotational in vitro compliance measurement of diverse anastomotic configurations: a tool for anastomotic engineering.

Anastomotic configurations with a small internal diameter are prone to intimal hyperplasia which can cause occlusion within weeks or months. A link between intimal hyperplasia and inhomogenities of the elastic profile of the anastomosis has been established, making anastomotic engineering directed towards smoothing the compliance profile at the anastomotic site essential. Methods to date restrict the anastomotic compliance measurement to one plane. We present a method by which the anastomotic configurations are rotated, thereby allowing an anastomotic elastic profile assessment in multiple planes. Eight end-to-end anastomoses (ovine common carotid artery) and three end-to-side anastomoses (e-PTFE graft to ovine common carotid artery) were prepared and mounted in an artificial circulation system. Anastomotic circumferential compliance (maximal-minimal diameter/(maximal-minimal pressure.minimal diameter)) was measured by means of a laser-scan-micrometer and a Statham pressure transducer. By rotating end-to-end anastomoses, the compliance was measured in three, and in end-to-side anastomoses in four different planes. Multiplanar compliance variability in areas remote to both end-to-end and end-to-side anastomoses was approximately 9%. At the suture line the variability was approximately 22% in end-to-end anastomoses and 78% in end-to-side anastomoses. These results show that local factors result in different compliance profiles when utilizing a multiplanar technique, particularly in end-to-side anastomoses. The rotational apparatus is a tool which can be used to more accurately engineer a homogeneously compliant anastomosis, with the ultimate goal of prolonging anastomotic patency.

Anastomosis, Surgical↗

Effect of long-term beta-blockade on aortic root compliance in patients with Marfan syndrome.

BACKGROUND: This study was undertaken to assess the effect of long-term beta-blockade on the aortic root stiffness index and distensibility in patients with Marfan syndrome. METHODS: Aortic root stiffness index and distensibility were calculated according to the formulas of Stefanadis and Hirai, respectively, with 2-dimensional guided M-mode echocardiogram before and after an average of 26 months of atenolol administration. RESULTS: Twenty-three asymptomatic patients were studied (11 men and 12 women, aged 31 +/- 14.2 years). The follow-up was 4 +/- 2.2 years. The dose of atenolol was individualized (mean 43.5 +/- 21.6 mg/d). Heart rate decreased from 79 +/- 9 beats/min to 64 +/- 9 beats/min (P =. 01), and systolic blood pressure decreased from 124 +/- 13 mm Hg to 114 +/- 2 mm Hg (P =.01). Distensibility increased from 1.85 +/- 0. 70 x 10(-6) cm2/dynes-1 to 2.21 +/- 0.76 x 10-6 cm2/dynes-1 (P =.02), and the stiffness index decreased from 9.68 +/- 3.78 to 8.85 +/- 3. 15 ( P =.2). Two groups of responses to treatment were identified. Compared with baseline values 15 (65%) patients who responded to treatment had increased distensibility and decreased stiffness index of the aortic root (P =.05). Eight patients (35%) who did not respond to treatment had no significant change. Body weight >91 kg and baseline end-diastolic aortic root diameter >40 mm were significantly associated with no response (P =.05). Two patients in the nonresponding group had echocardiographic progression of aortic insufficiency. CONCLUSIONS: There was a heterogeneous response in the aortic root elastic properties after long-term treatment with atenolol in asymptomatic patients with Marfan syndrome. Stiffness index and distensibility are more likely to respond when the baseline end-diastolic aortic root diameter is <40 mm.

Adrenergic beta-Antagonists↗

Mechanical blood-tissue interaction in contracting muscles: a model study.

A finite element (FE) model of blood perfused biological tissue has been developed. Blood perfusion is described by fluid flow through a series of 5 intercommunicating vascular compartments that are embedded in the tissue. Each compartment is characterized by a blood flow permeability tensor, blood volume fraction and vessel compliance. Local non-linear relationships between intra-extra vascular pressure difference and blood volume fraction, and between blood volume fraction and the permeability tensor, are included in the FE model. To test the implementation of these non-linear relations, FE results of blood perfusion in a piece of tissue that is subject to increased intramuscular pressure, are compared to results that are calculated with a lumped parameter (LP) model of blood perfusion. FE simulation of blood flow through a contracting rat calf muscle is performed. The FE model used in this simulation contains a transversely isotropic, non-linearly elastic description of deforming muscle tissue, in which local contraction stress is prescribed as a function of time. FE results of muscle tension, total arterial inflow and total venous outflow of the muscle during contraction, correspond to experimental results of an isometrically and tetanically contracting rat calf muscle.

Animals↗

Intradialytic and interdialytic effects of treatment with 1.25 and 1. 75 Mmol/L of calcium dialysate on arterial compliance in patients on hemodialysis.

Arterial compliance (AC) is an important determinant of vascular structure, and abnormalities of AC can greatly affect the cardiovascular system. Given the vasoconstrictive properties of increased levels of serum ionized calcium (iCa), we investigated the way that dialysate calcium level can influence AC in the hemodialysis (HD) population. In a crossover randomized design, 19 dialysis patients undergoing regular bicarbonate HD (three times weekly) underwent two cycles of four successive HD sessions each with a low (LdCa; 1.25 mmol/L) and high dialysate calcium concentration (HdCa; 1.75 mmol/L). At the fourth session of each cycle, iCa level and hemodynamic parameters (systolic blood pressure [SBP], diastolic blood pressure, mean arterial pressure [MAP], pulse pressure [PP], heart rate, and AC) were measured pre-HD and post-HD. AC was measured noninvasively at the brachial artery by arterial pulse waveform analysis. The dialysate calcium level was a significant determinant of both pre-HD (r = 0.335; P < 0.05) and post-HD iCa level (r = 0.767; P < 0.001). Pre-HD AC increased significantly (P < 0.05) by 0.01+/- 0.02 mL/mm Hg (7% +/- 19%) on switching from HdCa to LdCa treatment. Multiple regression analysis showed that both pre-HD PP and iCa level were major inverse determinants of pre-HD AC in both the LdCa (R(2) = 0.65; P < 0.001) and HdCa (R(2) = 0.51; P < 0.01) treatment groups. AC increased by 32% (P < 0.01) and 37% (P < 0.05) during LdCa and HdCa dialysis, respectively. Intradialytic changes in AC were inversely correlated with changes in SBP and PP. In the HdCa group, changes in iCa level related significantly to MAP (r = 0.464; P < 0.05). The results show that changes in AC during HD are mainly mediated through concurrent changes of systemic hemodynamics, which are largely affected by dialysate calcium level through parallel changes in iCa level. Interdialytically, a significant, blood pressure-independent, inverse relationship between AC and iCa level exists. Therefore, HD with LdCa, by reducing the incidence of HD-induced hypercalcemia, may have a beneficial role in preventing the ongoing reduction of AC in HD patients and thus improving cardiovascular prognosis.

Aged↗

Downregulation of myocardial contractility via intact ventriculo--arterial coupling in the brain dead organ donor.

OBJECTIVE: To test the hypothesis that altered loading conditions play a key role in hemodynamic instability and cardiac dysfunction in the brain dead (BD) organ donor. METHODS: BD was induced by inflation of a subdural balloon catheter. In the first part of the study, left ventricular function was assessed in a canine in situ cross-circulated heart model (n=6). Pre- and afterload and coronary perfusion pressure were kept identical in all hearts throughout the experiment. In the second part of the study, hearts (n=6) were investigated in vivo allowing the interaction between left ventricular contractility and arterial load. Left ventricular pressure--volume loops were obtained by a combined conductance-pressure catheter and the slope of the endsystolic pressure--volume relationship (Ees), arterial elastance (Ea), stroke work (SW), pressure--volume area, ventriculo--arterial coupling ratio (VAC) and mechanical efficiency (Eff) were calculated. RESULTS: Induction of BD led to a hyperdynamic response in both models with a significant increase of most hemodynamic parameters. In the in situ isolated heart model, left ventricular contractility returned to baseline without any further deterioration. In contrast, in the intact circulation the hemodynamic parameters declined significantly in comparison to baseline 4 h after BD (Ees: 4.07+/-0.51 vs. 8.06+/-1.09 mmHg/ml, P<0.05, Ea: 3.17+/-0.39 vs. 4.42+/-0.30 mmHg/ml, P<0.05). However, VAC (0.78+/-0.09 vs. 0.65+/-0.14 n.s.) and Eff (73.4+/-2.1 % vs. 76.8+/-3.7 %, n.s.) remained constant over the time. CONCLUSION: BD induction leads to an initial hyperdynamic reaction followed by hemodynamic instability. The facts that no cardiac dysfunction occurred if loading conditions were kept constant and the ventriculo--arterial coupling ratio and mechanical efficiency remained constant in the intact animal model indicate that decreased contractility reflects to decreased arterial elastance after brain death. Therefore, reduced contractile function after brain death at a decreased afterload may contribute to stroke work optimization.

Animals↗

Density gradient of the lung parenchyma at computed tomographic scanning in patients with pulmonary hypertension and systemic sclerosis.

RATIONALE AND OBJECTIVES: Pulmonary hypertension may complicate systemic sclerosis in the absence of fibrosing alveolitis. Abnormal pulmonary perfusion is known to result in regional differences in lung density at computed tomographic (CT) scanning. We assessed possible disturbances in the normal CT density gradient in patients with systemic sclerosis and reduced gas transfer but no clinical or radiologic evidence of fibrosing alveolitis. METHODS: We analyzed the CT scans of 15 patients with systemic sclerosis. Regions of interest were drawn in the most dependent and nondependent zones in the upper and lower lobes of each lung. Average densities for the most dependent and nondependent zones were calculated for the upper and lower lobes, and a global lung density measurement was derived. Zonal and global density gradients were derived from mean density measures (mean density of dependent areas minus mean densities of nondependent areas). RESULTS: Five of the 15 patients had pulmonary hypertension, defined as an estimated systolic pressure in the pulmonary artery of greater than 30 mm Hg shown by Doppler echocardiography. Patients with pulmonary hypertension were characterized by higher global lung density for nondependent zones (median, -821 H versus -853 H; p = .07) but not for dependent zones (-800 H versus -815 H, p = .71). The lung density gradient was reduced globally and in the lower zones in patients with pulmonary hypertension (p = .05). CONCLUSION: In cases of systemic sclerosis without fibrosing alveolitis, we found a significantly smaller density gradient between dependent and nondependent lung regions in patients with pulmonary hypertension compared with patients without pulmonary hypertension. This finding suggests that the normal CT density gradient depends in part on normal compliance of the pulmonary vasculature.

Absorptiometry, Photon↗

Propagation of nitric oxide pools during controlled mechanical ventilation.

OBJECTIVE: Infusing nitric oxide at a constant rate into a breathing circuit with intermittent mainstream flow causes formation of nitric oxide pools between successive breaths. We hypothesized that incomplete mixing of these pools can confound estimates of delivered nitric oxide concentrations. METHODS: Nitric oxide flowed at a constant rate into the upstream end of a standard adult breathing circuit connected to a lung model. One-milliliter gas samples were obtained from various sites within the breathing system and during various phases of the breathing cycle. These samples were aspirated periodically by a microprocessor controlled apparatus and analyzed using an electrochemical sensor. RESULTS: The pools of nitric oxide distorted into hollow parabolic cone shapes and remained unmixed during their propagation into the lungs. In our preparation, time-averaged nitric oxide concentrations were minimal 60 cm downstream of the infusion site (18 ppm) and maximal 15 cm upstream of the Y-piece (36 ppm). The concentrations were mid-range within the lung (23 ppm), yet were substantially less than predicted by assuming homogeneity of the gases (31 ppm). Generally, nitric oxide concentrations within the lung were different from all other sites tested. CONCLUSION: Incomplete mixing of nitric oxide confounds estimates of delivered nitric oxide concentrations. When nitric oxide is infused at a constant rate into a breathing circuit, we doubt that any sampling site outside the patient's lungs can reliably predict delivered nitric oxide concentrations. Strategies to ensure complete mixing and representative sampling of nitric oxide should be considered carefully when designing nitric oxide delivery systems.

Adult↗

Hyperaemic response to cigarette smoking in healthy gingiva.

BACKGROUND AND AIM: Cigarette smoking is currently considered as a risk factor for periodontal disease. Controversy exists as to whether the vasoconstrictive property of nicotine is one of the pathogenic mechanisms. To this end we tested the hypothesis that cigarette smoking is causing vasoconstriction in the healthy human gingiva. MATERIALS AND METHODS: Gingival blood flow was continuously measured with laser Doppler flowmetry in healthy (n=13) casual consumers of tobacco. Simultaneously, recordings were made of skin blood flow in the forehead and the thumb as well as heart rate (HR) and blood pressure (BP). In another session infraorbital nerve block anaesthesia (INB) with 1.0 ml of Carbocain without vasoconstrictive additives was used to identify nervously mediated vascular responses to cigarette smoking (n=8). RESULTS: Cigarette smoking induced a modest hyperaemic response in the gingiva that was lower than the relative increases in BP and HR, and the calculated gingival vascular conductance decreased. In the forehead, flow responses were similar to those in the gingiva, while in the thumb a powerful vasoconstriction was observed. During the later part of the 10-min recovery period, BP and HR tended to decrease while blood flow in the gingiva and forehead remained high. INB potentiated the hyperaemic response to cigarette smoking in gingiva. CONCLUSIONS: The present results help to shed some light on the understanding of the vasoactive mechanisms induced by cigarette smoking, and to support the hypothesis that cigarette smoking causes nervously mediated vasoconstriction in the healthy human gingiva. However, the degree of vasoconstriction was far less than in the thumb skin, and in our subjects was overcome by the evoked rise in arterial perfusion pressure. As a consequence, gingival blood flow increased during smoking. It is speculated that small repeated vasoconstrictive attacks due to cigarette smoking may in the long run contribute to gingival vascular dysfunction and periodontal disease.

Adult↗

Neonatal chronic sympathectomy in normotensive rats affects pial arteries: enhanced stiffness and reduced capacity to dilate.

The functional implication of previously shown effects on pial wall morphology by sympathectomy was tested. Following either ganglionic or pre-ganglionic denervation in 1-week-old rats the passive arterial compliance was reduced in basal cerebral arteries of 20-week-old normotensive, but not of hypertensive animals. The magnitude of the denervation induced stiffness was similar to the alteration seen in spontaneously hypertensive rats when compared with normotensive animals. No difference was seen between the two types of denervation. Following ganglionic sympathectomy in 1-week old normotensive rats-and examined 19 weeks later-the increase in cerebral blood flow (measured with the [14C]butanol sampling technique) induced by high arterial CO2 concentration was attenuated compared with control, whereas basal cerebral blood flow of 20-week-old animals was not different from control. The results indicate a long-term role by the sympathetic nerves not only on vessel wall composition, but also on the regulatory capacity of the cerebral circulation.

Animals↗