Biomedical subjects

J Hartikainen

Publications and source records attributed to J Hartikainen.

At least 19 recordsLinked to original sources

PubMed1996

Sympathetic reinnervation after acute myocardial infarction.

Myocardial infarction produces sympathetic denervation of the necrotic myocardium and noninfarcted myocardium apical to the injury. Proof of sympathetic reinnervation after myocardial infarction has, however, remained elusive. In this study, we investigated whether cardiac sympathetic reinnervation occurs in men recovering from myocardial infarction. I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid, and Tc-99m sestamibi scintigraphic imaging were conducted in 13 men 3 and 12 months after a first myocardial infarction to determine the extent of denervated myocardium, the size of the infarct, and the size of the myocardium with reduced perfusion, respectively. A defect was determined as regional uptake of < or = 30% of the maximal myocardial activity. The size of the MIBG defect was not significantly different between 3 and 12 months after infarction (17 +/- 8% and 18 +/- 8% of left ventricular mass, respectively). There was also no significant change in the extent of viable but denervated myocardium at 3 and 12 months (average 9 +/- 6% and 10 +/- 5%, respectively). MIBG activity of the infarct zone (expressed as a percentage of MIBG activity of the myocardium with normal perfusion) did not change (17 +/- 13% and 20 +/- 16%), whereas MIBG activity of the periinfarct zone increased during follow-up (32 +/- 11% and 41 +/- 14%, p < 0.01). This was associated with an increase in periinfarct I-123 paraphenylpentadecanoic acid activity (40 +/- 11% and 48 +/- 9%, p < 0.05), but not Tc-99m sestamibi activity (48 +/- 10% and 48 +/- 11%). In conclusion, we did not observe sympathetic reinnervation in the infarct zone between 3 and 12 months after myocardial infarction. However, MIBG activity of the periinfarct zone increased, suggesting partial reinnervation, and this was associated with a recovery of myocardial metabolic activity of the periinfarct zone.

3-Iodobenzylguanidine↗

PubMed1996

External DCR.

Explore the source record for details and available documents.

Dacryocystorhinostomy↗

PubMed1996

Is vagal innervation to the atrioventricular node impaired after radiofrequency ablation of the slow atrioventricular nodal pathway?

To assess the potentially adverse effects of RF catheter ablation (RFCA) of the slow AV nodal pathway on the parasympathetic innervation to the AV node in patients with AV nodal reentrant tachycardia (AVNRT), AV nodal conduction was evaluated following vagal stimulation by means of a phenylephrine bolus injection (200 micrograms) before and after RFCA in ten patients (mean age, 37 +/- 14 years). Nine patients with AV reentrant tachycardia (AVRT) due to a left free wall accessory pathway served as a control group (mean age of 37 +/- 12 years). Whereas no prolongation of the AH interval was observed in the AVNRT group following the phenylephrine bolus during sinus rhythm, despite a significant slowing in sinus rate, phenylephrine administration in AVRT patients was associated with both slowing of the sinus rate and prolongation of the AH interval. Following successful RFCA, the same responses were observed. To delineate the indirect effect of heart rate on AV conduction in response to the phenylephrine bolus, the AH interval was also measured during fixed atrial pacing. A marked prolongation of the AH interval occurred in both groups following phenylephrine administration. This prolongation was biphasic in 50% of AVNRT patients before ablation, suggesting a predominant effect of vagal stimulation on the fast AV nodal pathway. RFCA was associated with disappearance of discontinuous AV conduction in all but one patient with AVNRT. Vagal stimulation caused the same amount of AH interval prolongation as before RFCA in both study groups. In conclusion, patients with AVNRT have a preserved modulation of AV nodal conduction in response to vagal stimulation during sinus rhythm. In addition, vagal stimulation seems to exert a predominant effect on the fast AV nodal pathway. RFCA of the slow AV nodal pathway in patients with AVNRT does not cause detectable damage to the vagal innervation to the AV node.

Adult↗

PubMed1996

Lacrimal bone thickness at the lacrimal sac fossa.

BACKGROUND AND OBJECTIVE: Because laser dacryocystorhinostomy techniques have become more popular during the past few years, interest has grown concerning the anatomic structures that need to be penetrated in these procedures. The authors therefore studied the thickness and the histologic type of the lacrimal bone at the lacrimal sac fossa. PATIENTS AND METHODS: The thickness of 69 lacrimal bones at the lacrimal sac fossa from 48 patients was measured. RESULTS: The mean thickness was 106 microns. In 67% of the patients the mean thickness of individual lacrimal bone was less than 100 microns and in 4% it was more than 300 microns. The thinnest measured cross section of the lacrimal bone sample was 11 microns and the thickest was 722 microns. The lacrimal bone was composed of a thin plate of lamellar bone. CONCLUSION: In most cases the lacrimal bone at the lacrimal sac fossa is so thin that it can be easily penetrated with most surgical instruments.

Adult↗

PubMed1995

Prediction of atrioventricular block during radiofrequency ablation of the slow pathway of the atrioventricular node.

BACKGROUND: Selective radiofrequency (RF) ablation of the slow pathway is an effective treatment for atrioventricular (AV) nodal reentry tachycardia. A previous report showed that rapid junctional tachycardia (JT) caused by RF associated with loss of ventriculoatrial (VA) conduction is related to increased risk for AV block. However, this can be difficult to detect during energy delivery, and more importantly, it cannot be measured before the onset of RF energy delivery. The aim of our study was to determine whether measurements made from electrograms could be used to predict the risk of AV block before RF energy is delivered. METHODS AND RESULTS: Fifty-eight patients underwent 63 selective slow pathway RF ablation procedures. In 46 (26.9%) of 172 JTs caused by RF, VA block was observed, and in 11 this was followed by AV block of various degrees. Electrograms before each application of RF were analyzed for the interval between the atrial signals in the His bundle catheter and in the distal mapping catheter [A(H)-A(Md)], the interval between the atrial signals in the His bundle catheter and in the proximal coronary sinus catheter [A(H)-A(CS)], the AV ratio, and the presence of a slow pathway potential or a fractionated atrial signal in the distal mapping catheter. Mean cycle length (CL) of JT was calculated if it consisted of at least 10 beats. These parameters were compared between patients with JT who developed VA block and subsequent AV block (group 1), patients with JT and VA block but without subsequent AV block (group 2), and patients with JT without VA block (group 3). The A(H)-A(Md) interval was significantly shorter in group 1 (17 +/- 8 ms) than in groups 2 (33 +/- 8 ms, P < .001) and 3 (32 +/- 10 ms, P < .001), whereas the A(H)-A(Md) intervals of groups 2 and 3 did not differ from each other. CL of JT, A(H)-A(CS) interval, AV ratio, presence of a slow pathway potential, or a fractionated atrial electrogram were not related to the occurrence of AV block. CONCLUSIONS: The A(H)-A(Md) interval provides an electrophysiological marker that can be used in addition to the radiological catheter position to assess the risk for AV block before onset of RF delivery. CL of JT and occurrence of VA block are not related to the risk of AV block.

Atrioventricular Node↗

PubMed1995

Good exercise capacity at hospital discharge predicts recovery of baroreflex sensitivity after myocardial infarction.

Myocardial infarction results in depressed baroreflex sensitivity, which has been shown to be associated with increased risk of ventricular arrhythmias and sudden death. We measured baroreflex sensitivity in 37 patients with acute myocardial infarction before hospital discharge and 3 months after the infarction to find out whether the baroreflex sensitivity recovers during that period. In addition, baroreflex sensitivity was assessed in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in R-R interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. There was a wide inter-individual variation in the change of baroreflex sensitivity (delta baroreflex sensitivity) in infarction patients, but the average baroreflex sensitivity showed no significant change during the 3-month follow-up (10.2 + 5.6 to 11.8 +/- 7.5 ms.mmHg-1, ns) and remained lower than the baroreflex sensitivity of the controls (16.4 +/- 9.7 ms.mmHg-1, P < 0.05). delta Baroreflex sensitivity correlated significantly with exercise capacity measured before hospital discharge. When the patients were divided into tertiles according to the delta baroreflex sensitivity (-3.3 +/- 1.5 ms.mmHg-1 in the lowest tertile, 1.0 +/- 1.0 ms.mmHg-1 in the middle tertile and 7.5 +/- 4.0 ms.mmHg-1 in the highest tertile) the exercise capacity was found to increase from the lowest to the highest tertile (exercise time 357 +/- 115 s, 418 +/- 126 s and 461 +/- 141 s, respectively; P < 0.05 lowest vs highest tertile). Patients with a low exercise tolerance (exercise time < 360 s) showed a significantly smaller delta baroreflex sensitivity than patients with a good exercise tolerance (exercise time > or = 480 s) (-0.5 +/- 4.4 vs 5.3 +/- 5.4 ms.mmHg-1, P < 0.05), respectively. delta Baroreflex sensitivity was not related to the location or type of infarction, thrombolytic therapy, presence of angina pectoris or left ventricular function at the time of discharge. In conclusion, exercise capacity assessed before hospital discharge seems to be a predictor of baroreflex sensitivity recovery in patients with a recent myocardial infarction.

Aged↗

PubMed1995

Metabolic stress modifies the thermogenic effect of dobutamine in man.

OBJECTIVE: To study if metabolic stress modifies the thermogenic effect of dobutamine. DESIGN: Prospective, increasing dose, pharmacologic study. SETTING: Laboratory of the Department of Intensive Care Unit at a university hospital. SUBJECTS: Twelve normal volunteers. INTERVENTIONS: Dobutamine hydrochloride was infused to 12 healthy male volunteers starting at a dose of 2 micrograms/min/kg and gradually increased to 4 and 6 micrograms/min/kg. Each dose of dobutamine was infused for 20 mins. Metabolic stress was induced in six of the 12 volunteers using a triple hormone infusion (epinephrine, cortisol, and glucagon) before dobutamine, and was continued at a constant rate during the dobutamine infusion. The remaining six volunteers served as the control group and received only dobutamine. MEASUREMENTS AND MAIN RESULTS: Oxygen consumption (VO2) was measured using a metabolic monitor. Arterial blood pressure was measured noninvasively, and cardiac output was monitored by Doppler echocardiography. Plasma concentrations of dopamine, norepinephrine, and epinephrine were measured in both groups. In the triple hormone group, blood was sampled to measure concentrations of insulin, glucagon, cortisol, free fatty acids, and glycerol to ensure the presence of a metabolic stress reaction. At the maximum dose, dobutamine induced a 19% increase (from 140 +/- 17 to 166 +/- 17 mL/min/m2) in VO2 in the control group and an 11% increase (from 167 +/- 10 to 184 +/- 13 mL/min/m2) in the triple hormone group (p < .05 between the two groups) compared with baseline. No change in the respiratory exchange ratio was seen. The triple hormone infusion alone induced hypermetabolism, a marked hemodynamic response, and increased lipolysis. CONCLUSIONS: Stress, induced by a triple hormone infusion, diminishes the thermogenic effect of dobutamine. In the clinical setting, a > 10% to 15% increase in VO2 in response to dobutamine may not be explained just by the thermogenic effect of the drug.

Adult↗

PubMed1995

Day-to-day variability of cardiac autonomic regulation parameters in normal subjects.

We examined the reproducibility of day-to-day variability in cardiovascular autonomic nervous function parameters (classical clinical tests and domain analysis of heart rate variability) in four healthy men during a period of 1 working week. The results did not show any significant difference in any of the parameters over the five repeated measurements. The maximum-minimum difference as percentage of the mean was under 15% for expiration to inspiration (E/I) ratio, Valsalva ratio, tachycardia ratio, 30/15 ratio, acceleration index and brake index; about 45% for baroreflex sensitivity for systolic and diastolic blood pressure and for root mean square difference (RMSSD) of successive R-R intervals; about 65-85% for low and high frequency bands, total power and medium to high frequency ratio; and about 125% for medium frequency band. The intraclass correlation coefficient (ICC) values showed that the agreement for classical autonomic parameters (except for brake index) was good. ICC for RMSSD, baroreflex sensitivity for systolic blood pressure and the spectral estimates of heart rate variation were less good. Coefficient of variation (CV) was 4% for E/I ratio, 2% for 30/15 ratio, 6% for Valsalva, 3% for tachycardia ratio, 4% for acceleration index and 5% for brake index. CV for baroreflex sensitivity and for RMSSD was about 20%. It is concluded that the variation in baroreflex sensitivity is clearly larger than in the classical autonomic nervous function parameters. One-minute fixed pace breathing period seems to be too short to allow reproducible measurement of RMSSD and the spectral parameters of heart rate variation. Learning effect could be excluded.

Adult↗

PubMed1995

Effect of posture on baroreflex sensitivity in healthy subjects.

In this study we investigated whether body position has significant effects on baroreflex sensitivity in healthy subjects. Baroreflex sensitivity was calculated from pressure overshoot after the release of a Valsalva strain in the supine and sitting positions in 10 subjects. At rest, no difference was found in supine and sitting mean R-R intervals (837 +/- 82 and 858 +/- 86 ms, respectively), whereas systolic and diastolic blood pressures were lower in the supine position (111.3 +/- 24.6 vs. 141.2 +/- 12.6 mmHg, P < 0.01 and 54.8 +/- 14.7 vs. 75.6 +/- 13.4 mmHg, P < 0.001, respectively). Baroreflex sensitivity in the supine (9.0 +/- 4.1 ms x mmHg-1) and sitting positions (8.8 +/- 4.9 ms x mmHg-1) did not differ significantly from each other. The correlation between supine and sitting baroreflex sensitivity was 0.96 (P < 0.001) and in 9 out of 10 subjects the discrepancy between supine and sitting baroreflex sensitivity was < 2.0 ms x mmHg-1. We conclude that baroreflex sensitivity measured in the supine and sitting positions do not differ significantly from each other.

Adult↗

PubMed1995

Phospholipase A2 content of aqueous humour in cataract patients.

In order to determine the content of group II phospholipase A2 in the aqueous humour we studied 41 cataract patients including 8 men and 33 women with age ranging between 65 and 92 (mean +/- SD being 77.0 +/- 6.7) years. In all patients preoperative biomicroscopy showed neither aqueous flare nor cells. Eleven patients (26.8%) had pseudoexfoliation syndrome. Aqueous humour tap was done at the beginning of cataract surgery before perforating the corneoscleral wound. We used time-resolved fluoroimmunoassay for the detection of group II phospholipase A2 in the aqueous humour. The group II phospholipase A2 content in the aqueous humor varied between less than measurable (in 23 patients) and 3.3 ng/ml, with an interquartile range from less than measurable to 1.4 ng/ml. There was no significant difference in the group II phospholipase A2 content of the aqueous humour whether or not the patient had pseudoexfoliation syndrome. The results show that the aqueous humour of cataract patients contains only minute amounts of group II phospholipase A2.

Aged↗

PubMed1995

Baroreflex sensitivity and neurohormonal activation in patients with acute myocardial infarction.

OBJECTIVE: To examine the relationship between baroreflex sensitivity and neurohormonal activation in patients with an acute myocardial infarction. METHODS: Baroreflex sensitivity, plasma noradrenaline, atrial natriuretic factor, endothelin-1, and plasma renin activity were measured in 37 male patients about 10 days after their first myocardial infarction, and in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in RR interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. The measurements were repeated after a follow up of three months. RESULTS: There was a significant inverse correlation between baroreflex sensitivity and plasma noradrenaline measured before hospital discharge (r = -0.43, P < 0.01). Patients with increased plasma noradrenaline (> or = 2SD above the mean of the age matched control group) had significantly lower baroreflex sensitivity than patients with normal plasma noradrenaline (8.7 (SD 4.6) v 12.1 (6.1) ms/mm Hg, P < 0.05). The change in baroreflex sensitivity during the follow up showed a significant inverse correlation with the change of plasma noradrenaline (r = -0.450, P < 0.01). Furthermore, when patients with increased plasma noradrenaline before hospital discharge were analysed separately, baroreflex sensitivity at three months in patients in whom plasma noradrenaline had decreased to normal values was significantly higher than in patients in whom plasma noradrenaline had remained increased (14.6 (5.7) v 8.1 (8.1) ms/mm Hg, P < 0.05). On the other hand, baroreflex sensitivity was not related to the levels of plasma atrial natriuretic factor, plasma endothelin-1, or plasma renin activity. Neither was any relationship found between change in baroreflex sensitivity and change in plasma atrial natriuretic factor, endothelin-1, or plasma renin activity during the follow up. CONCLUSIONS: The impairment baroreflex sensitivity after myocardial infarction was associated with increased concentration of plasma noradrenaline, that is, sympathetic activation, but not with plasma atrial natriuretic factor, endothelin-1, or plasma renin activity. Baroreflex sensitivity provides information about cardiac vagal control as well as about the balance of cardiac sympathetic-parasympathetic regulation.

Adult↗

PubMed1995

[Heart-related chest pain without manifest coronary disease].

Chest pain is a common reason for consulting a physician. Although the underlying cause of the chest pain varies, the most frequent cause is coronary disease. In many cases the diagnosis emerges from the case history, the clinical picture or non-invasive examination procedures. In cases of severe symptoms or unclear diagnosis, coronary angiography is performed which often shows the coronary arteries to be patent. In a large proportion of these patients the chest pain is of non-cardiac origin. In addition to coronary disease, other heart-related conditions may give rise to chest pain.

Chest Pain↗

PubMed1995

Myocardial sympathetic nervous dysfunction detected with iodine-123-MIBG is associated with low heart rate variability after myocardial infarction.

UNLABELLED: The association between myocardial sympathetic innervation and heart rate variability after myocardial infarction was studied in a group of 12 men (aged 30-65 yr) 3 mo after their first myocardial infarction. METHODS: Viable myocardium was imaged using 123I-phenylpentadecanoic acid (pPPA). Functioning myocardial sympathetic nervous tissue was imaged using [123I]-metaiodobenzylguanidine (MIBG). Heart rate variability was measured as the ratio of maximum-to-minimum RR intervals in ECG during deep breathing. RESULTS: The patients were divided into normal (n = 6) and low (n = 6) heart rate variability groups. Myocardial infarction size (pPPA defect) was comparable in the normal and low heart rate variability groups. Even the MIBG defect size was not significantly different in the normal and low groups, the portion of viable myocardium with impaired sympathetic innervation (MIBG defect minus pPPA defect) was significantly greater in the low heart rate variability group than in the normal group. CONCLUSION: The extent of viable myocardium with disturbed sympathetic innervation was greater in patients with low heart rate variability as compared to those with normal heart rate variability 3 mo after myocardial infarction.

3-Iodobenzylguanidine↗

PubMed1994

Extent of cardiac autonomic denervation in relation to angina on exercise test in patients with recent acute myocardial infarction.

According to the current concept, anginal pain results from stimulation of sympathetic nerves within the heart. In this study, we evaluated the role of cardiac adrenergic denervation in exercise-induced angina pectoris in 15 men with recent acute myocardial infarction. Before discharge from the hospital, the patients were subjected to a symptom-limited exercise test. Three months after the infarction, cardiac scintigraphic studies using I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid (pPPA), and Tc-99m sestamibi (MIBI) were performed in order to determine the extent of denervated myocardium, the size of infarction, and myocardium with reduced perfusion, respectively. MIBG defect (17.2 +/- 7.6% of left ventricular mass) (defect defined as an activity distribution < or = 30% of the maximal myocardial activity) was larger than pPPA defect (8.3 +/- 8.8%, p < 0.001) in all patients, which indicates that the area of myocardial necrosis was surrounded by viable myocardium with sympathetic denervation. The extent of viable but denervated myocardium was significantly greater in patients who developed angina pectoris than in patients without angina pectoris during the early exercise test (13.3 +/- 4.4% vs 5.0 +/- 2.4%, p < 0.001). In addition, patients with silent ischemia tended to have smaller areas of viable but denervated myocardium than patients with painful ischemia (5.7 +/- 3.8% vs 13.8 +/- 5.1%, p = 0.07). Thus, contrary to expectations, the extent of viable but denervated myocardium seems to be associated with increased pain sensitivity in patients with recent myocardial infarction.

Adrenergic Fibers↗

PubMed1994

Baroreflex sensitivity in men with recent myocardial infarction; impact of age.

We investigated the effect of age on baroreflex sensitivity (BRS) in 39 male patients, who had survived their first myocardial infarction (MI) and in 15 age-matched controls. BRS was inversely related to age in both MI patients (r = -0.632, P < 0.0001) and controls (r = -0.706, P < 0.0001). The relationship between BRS and age, however, was significantly different in MI patients as compared with healthy controls: BRS was markedly higher and the BRS-age regression slope was significantly steeper in controls than in MI patients. As a consequence, the decrease in BRS caused by MI (delta BRS = age-specific expected BRS--measured BRS) was related inversely to age (r = -0.66, P < 0.05) i.e. delta BRS was greatest among young MI patients. However, the relative BRS (BRS% = measured BRS divided by the age-specific expected BRS) did not correlate with age. The average BRS% of MI patients was 37% lower than that of controls. MI size and left ventricular (LV) systolic function did not correlate with BRS. BRS correlated with variables related to cardiac diastolic function (peak late LV filling rate r = -0.43, P < 0.05), exercise capacity (r = 0.31, P < 0.05) and the extent of ST-depression during exercise (r = -0.40, P < 0.05), but all these correlations lost their significance after the adjustment for age. In conclusion, age is a factor that should be taken into consideration when evaluating the mechanisms of BRS impairment associated with different diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Endonasal CO2-Nd:YAG laser dacryocystorhinostomy.

A preliminary series of endonasal dacryocystorhinostomy was carried out on 12 patients with nasolacrimal obstruction using a recently developed combined CO2-Nd:YAG laser that was guided by a fiberoptic light pipe inserted into the lacrimal sac through lacrimal canaliculi. The lacrimal passages were stented using silicone tubing that was kept in place for 6 months postoperatively. At an average follow-up time of 14.3 months the success rate was 83%. The advantages of the operation include a relatively short operation time, quick rehabilitation, absence of a skin wound, good hemostasis, and preservation of canthal anatomy.

Adult↗

PubMed1993

Circadian variation of cardiac autonomic regulation during 24-h bed rest.

We examined the effect of circadian variation on cardiac autonomic regulation in 11 young and middle-aged, healthy men during 24-h bed rest. Cardiac parasympathetic regulation expressed significant circadian variation: sensitivity of baroreceptor reflex, standard deviation of R-R intervals and the power of high frequency component of R-R interval variability (HFP) increased during the evening (2000-2100 h), were highest during the night (0200-0300 h), and gradually decreased again towards afternoon (1400-1500 h). Cardiac sympathetic regulation, the power of medium frequency component of R-R interval variability (MFP), did not show any significant circadian variation. The autonomic response to orthostatic stress changed after the 24-h bed rest; the sympathetic dominance in response to assuming upright position was before bed rest principally attributable to increased sympathetic activity (MFP increase), whereas after bed rest this was due to withdrawal of parasympathetic activity (HFP decrease). We conclude that the effect of circadian variation must be taken into account, while assessing cardiac autonomic regulation in patients with acute cardiovascular disorders.

Adult↗

PubMed1990

Haemodynamic information encoded in the aortic baroreceptor discharge during haemorrhage.

This study concerns the function of aortic baroreceptors during slow haemorrhage, in particular the mechanisms by which baroreceptors respond to hypovolaemia in the absence of hypotension and the manner in which haemodynamic information is encoded in the aortic nerve discharge. Beagle dogs, anaesthetized with morphine and chloralose, were instrumented for the recording of aortic pressure, aortic diameter, aortic flow and aortic nerve activity. The animals were subjected to slow haemorrhage (0.4 ml kg-1 min-1) of 20% of the estimated blood volume. Mean aortic pressure remained unchanged, whereas mean aortic diameter, mean aortic tension and aortic baroreceptor activity decreased during the haemorrhage. Baroreceptor sensitivity to mean aortic pressure, mean aortic diameter and mean aortic tension decreased as the haemorrhage proceeded. Also, the sensitivity of baroreceptors to mean aortic pressure and mean aortic diameter during acute pressure stimulation was attenuated. The results indicate that during non-hypotensive haemorrhage aortic baroreceptor discharge is reduced by two mechanisms: firstly, via constriction and stiffening of aortic smooth muscle and, secondly, via direct effects of the compensatory mechanisms on the baroreceptors. The reduced sensitivity renders the baroreceptors capable of responding to hypovolaemia prior to the onset of hypotension. In the regression analysis, systolic aortic diameter proved to be the best determinant of baroreceptor activity (r = 0.877). Of the neural variables, impulses per cardiac cycle and average discharge rate were the most reliable, but no difference in the relative importance of these two parameters could be observed.

Acid-Base Equilibrium↗