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PubMed1999

Pretreatment with allopurinol in cardiac hypoxic-ischemic reperfusion injury in newborn lambs exerts its beneficial effect through afterload reduction.

The aim of this study was to determine whether allopurinol (ALLO) reduces reperfusion injury inflicted upon the heart resulting from excess production of free oxygen radicals after hypoxia and ischemia (HI) in newborn animals. We, therefore, produced severe HI in 13 newborn lambs by low O2-ventilation and blood volume reduction. One hour before HI seven lambs received ALLO (20 mg/kg i.v.), six received a placebo (CONT). Cardiac function and hemodynamic parameters were assessed by sequential measurement of left ventricular (LV) contractility through the end-systolic pressure-volume relation (ESPVR) using the conductance catheter method. Stroke volume (SV), cardiac output (CO), and aortic pressure (Pao) were measured and ejection fraction and total peripheral resistance (TPR) were calculated before HI, upon resuscitation (UR), and at 60 and 120 min post-HI. To estimate the effect of ALLO on redox status and anti-oxidative capacity, we measured concentrations of uric acid, sulfhydryl (SH), malondialdehyde (MDA), ascorbic acid (AA), and dehydroxylated ascorbic acid (DHAA) in plasma obtained from the coronary sinus and calculated the AA/DHAA ratio. Compared to CONT lambs, TPR in ALLO treated lambs decreased significantly, accompanied by a rise in CO and SV. ALLO did not affect myocardial contractility, because the ESPVR showed no significant differences between groups. AA/DHAA and SH showed a significant decrease in ALLO animals vs pre-HI, but not in CONT animals. Uric acid was significantly decreased in ALLO as compared to pre-HI and CONT animals. MDA was significantly increased in CONT animals at 15 min post-HI as compared to pre-HI, whereas in ALLO animals MDA showed a significant increase at 120 min post-HI vs CONT. We conclude that pretreatment with ALLO has a beneficial effect on the pump function by afterload reduction but not by changes in contractility. Furthermore, ALLO inhibited uric acid formation with a consequent decrease in anti-oxidative capacity.

Allopurinol↗

PubMed2005

Differences in overshoot of blood pressure after head-up tilt in two groups with chronic autonomic failure: pure autonomic failure and multiple system atrophy.

On head down tilt to the supine horizontal position (tilt reversal) after head up tilt (HUT), patients with orthostatic hypotension may show an increase in blood pressure (BP) relative to baseline readings. We assessed this BP overshoot in 8 patients with pure autonomic failure (PAF, 64+/-13 years) and 8 patients with multiple system atrophy (MSA, 66+/-10 years). BP was intermittently measured during pre-tilt supine, HUT (60 degrees , 10 min), and post-tilt supine periods. In addition, beat-to-beat BP was measured continuously using the Portapres model 2 device to calculate stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR). There was systolic BP overshoot of > or = 15 mmHg after tilt reversal in 5 out of 8 PAF, but in only one of 8 MSA. A mean increase of systolic BP in PAF was significantly higher than that in MSA (p<0.01). TPR increased over baseline level after tilt reversal, although there was no significant difference. SV and CO levels during the post-tilt supine period were similar to baseline levels. In conclusion, BP overshoot was prominent in the PAF group but not in the MSA group. The phenomenon of BP overshoot while supine, especially in PAF, may have implications for long term cardiac and vascular damage in such patients.

Aged↗

PubMed2003

Regulation of arterial blood pressure in humans during isometric muscle contraction and lower body negative pressure.

Previous studies have shown that the blood pressure response to isometric handgrip remains unchanged during reductions in preload induced by lower body negative pressure (LBNP). The purpose of the present study was to assess the beat-by-beat haemodynamic mechanisms allowing for precise control of mean arterial pressure (MAP). We have followed the cardiovascular variables involved in the regulation of MAP during isometric handgrip with and without additional application of LBNP during defined periods of the ongoing contraction. Sixteen subjects participated. Mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO), blood flow velocity in the brachial artery, acral skin blood flow, as well as total (TPR) and local (LPR) peripheral resistance were continuously recorded/calculated before, during and after 2 min of handgrip both with and without concomitant LBNP. The main finding was that MAP increased at the same rate and to the same absolute level whether or not LBNP was applied. A uniform increase in MAP was observed even though the cardiovascular variables evolved differently in the periods with and without LBNP. At the onset of LBNP at -20 mmHg, there was a transient drop in MAP and a transient increase in HR, but within seconds, MAP was regulated back to the slope caused by the isometric handgrip proper. CO and SV, which were declining gradually, showed an additional marked but gradual reduction upon LBNP application. At the same time, both LPR and TPR increased markedly and continuously. In summary, the increase in MAP during isometric handgrip remained essentially unchanged by LBNP-induced alterations in preload. The increase in MAP was caused by a marked increase in peripheral resistance. This supports the concept of a central set point, continuously regulated upwards as long as the isometric handgrip persists. Furthermore, it reveals a considerable flexibility in the cardiovascular control mechanisms used to achieve the desired arterial pressure.

Adaptation, Physiological↗

PubMed2004

Cardiovascular responses to head-out water immersion in Korean women breath-hold divers.

Head-out water immersion (HOI) increases cardiac output (CO) for a given oxygen consumption. To investigate whether professional breath-hold divers show a similar response, cardiovascular responses to HOI were compared between six Korean women breath-hold divers, six non-diving housewives and six non-diving young women at rest and while performing leg cycle exercise of moderate intensity (Deltametabolic rate = approximately 100 W m(-2)) in water at a thermoneutral temperature (34.5 degrees C). In all three groups, HOI increased CO markedly due to a rise in stroke volume, with no significant change in heart rate (HR) and arterial blood pressure (BP). Thus, total peripheral resistance (TPR) and arterio-venous oxygen content difference fell significantly. During dynamic exercise in water CO increased mainly due to a rise in HR. The arterial systolic BP rose slightly with no significant change in diastolic BP, and the TPR fell 20-40% with similar responses among the three groups of subjects. This study showed that both at rest and during exercise, cardiovascular responses to immersion do not vary significantly with age and water immersion experience.

Adaptation, Physiological↗

PubMed2005

Interactions between exposure to hypoxia and the training-induced autonomic adaptations in a "live high-train low" session.

The autonomic and cardiovascular adaptations to hypoxia are opposite to those resulting from aerobic training. We investigated (1) whether exposure to hypoxia in a live high-train low (LHTL) session limits the autonomic and cardiovascular adaptations to training, and (2) whether such interactions remain 15 days after the end of the LHTL. Eighteen national swimmers trained for 13 days at 1,200 m, living (16 h day(-1)) either at 1,200 m (live low-train low, LLTL) or at a simulated height of 2,500-3,000 m (LHTL). Subjects were investigated at 1,200 m before and at the end of the training session, and after the following 15 days of sea-level training. Cardiovascular parameters and the autonomic control assessed by spectral analysis of R-R and diastolic blood pressure (DBP) variability were obtained in the resting supine position and in response to an orthostatic test. At the end of the 13-day training, resting heart rate (HR) and sympathetic modulation on heart decreased in LLTL (-10.1% and -25.4%, P<0.01, respectively) but not in LHTL (-5.8, -15.5%, respectively). Total peripheral resistance (TPR) and DBP became higher in LHTL than in LLTL (P<0.05). Stroke index decreased in both groups during the tilt test, counteracted by an increase in HR and sympathetic modulation to the heart and vasculature, and a decrease in vagal modulation to the heart. After the following 15-day sea-level training, differences in TPR and DBP between groups disappeared. During an LHTL session, adaptations to hypoxia interacted with the autonomic and cardiovascular adaptations to training. However, these interactions did not limit the adaptations to the following sea-level training.

Adaptation, Physiological↗

PubMed2005

Leg vascular resistance increases during head-up tilt in paraplegics.

Despite loss of centrally mediated sympathetic vasoconstriction to the legs, spinal cord-injured individuals cope surprisingly well with an orthostatic challenge. This study assessed changes in leg vascular resistance following head-up tilt in healthy (C) and in paraplegic (P) individuals. After 10 min of supine rest, subjects were tilted 30 degrees head-up. Mean arterial pressure (MAP) and total peripheral resistance (TPR) increased in C (MAP from 76.7 +/ -6.6 mmHg to 80.6 +/- 8.2 mmHg; TPR from 1.12 +/- 0.26 AU to 1.19 +/ -0.31 AU) while both remained unchanged in P. Echo Doppler ultrasound determined red blood cell velocity in the femoral artery, which decreased (P from 18.9+/-6.2 cm/s to 12.5 +/- 4.5 cm/s, P = 0.001; C from 16.3 +/- 6.2 cm/s to 10.8 +/- 5.0 cm/s, P = 0.001) and leg vascular resistance, which increased (P from 402 +/- 137 AU to 643 +/- 274 AU, P = 0.001; C from 238 +/- 68 AU to 400 +/- 122 AU, P = 0.003) from supine to upright. The present study shows that independent of supraspinal sympathetic control, humans are able to increase leg vascular resistance and maintain blood pressure during head-up tilt.

Adult↗

PubMed2005

Effects of inspiratory impedance on hemodynamic responses to a squat-stand test in human volunteers: implications for treatment of orthostatic hypotension.

Recent studies in our laboratory demonstrated that spontaneous breathing through an inspiratory impedance threshold device (ITD) increased heart rate (HR), stroke volume (SV), cardiac output (Q), and mean arterial blood pressure (MAP) in supine human subjects. In this study, we tested the effectiveness of an ITD as a countermeasure against development of orthostatic hypotension, provoked using a squat-to-stand test (SST). Using a prospective, randomized blinded protocol, 18 healthy, normotensive volunteers (9 males, 9 females) completed two-counterbalanced 6-min SST protocols with and without (sham) an ITD set to open at 0.7 kPa (7-cm H(2)O) pressure. HR, SV, Q, total peripheral resistance (TPR), and MAP were assessed noninvasively with infrared finger photoplethysmography. Symptoms were recorded on a 5-point scale (1 = normal; 5 = faint) of subject perceived rating (SPR). The reduction in TPR produced by SST (-35 +/- 5 %) was not affected by the ITD. Reduction in MAP with ITD during the transient phase of the SST (-3.6 +/- 0.5 kPa or -27 +/- 4 mmHg) was less (P = 0.03) than that measured while breathing through a sham device (-4.8 +/- 0.4 kPa or -36 +/- 3 mmHg) despite similar (P < 0.926) elevations in HR of 15 +/- 2 bpm. SV (+2 +/- 4 %) and Q (+22 +/- 5 %) with the ITD were higher (P < 0.04) than SV (-8 +/- 4 %) and Q (+10 +/- 6 %) without the ITD. SPR was 1.4 +/- 0.1 with ITD compared to 2.0 +/- 0.2 with the sham device (P < 0.04). This reduction in orthostatic symptoms with application of an ITD during the SST was associated with higher MAP, SV and Q. Our results demonstrate the potential application of an ITD as a countermeasure against orthostatic hypotension.

Adult↗

PubMed2000

Continuous monitoring of haemodynamic parameters in humans during the early phase of simulated diving with and without breathholding.

This study examined the integrative changes of blood pressure (BP) and stroke volume (SV) leading to the initial biphasic heart rate (fc) response (first 15 s) in simulated diving manoeuvres with and without breathholding (BH). Simulated diving was studied in ten young healthy volunteers by application of a gel-filled pack at 0 degree C and 18 degrees C on the forehead with and without BH. Beat-by-beat and second-to-second fc, BP, SV, and total peripheral vascular resistance (TPR) were followed by continuous non-invasive monitoring. In all conditions (BH with forehead cooling at 0 degree and 18 degrees C) there was an early rise in BP triggering the first tachycardial response (fc acceleration) which was immediately counteracted by the concurrent further increase of SV leading to the second phase of early bradycardic response (fc deceleration). Furthermore, the continuous beat-by-beat and second-to-second monitoring allowed the documentation of a highly significant increase of TPR within the first few seconds of the manoeuvres. Our data further indicated that the differences in haemodynamics observed during the stimuli at different temperatures was overruled by BH. Detailed comparisons of the beat-by-beat and second-to-second analyses were unable to show that one method was better than the other. Using continuous non-invasive monitoring of haemodynamic variables during simulated diving manoeuvres it was possible to provide better insights into the physiological principles and meaning of the diving reflex in humans.

Adult↗

PubMed1997

Physiological and biomechanical responses during treadmill walking with graded loads.

Eleven healthy men [mean (SD) for age, height, body mass and maximum oxygen consumption: 25.1 (3.0) years, 1.79 (0.06) m, 78.2 (10.5) kg and 56.9 (7.1) ml x kg(-1) x min(-1), respectively) completed two treadmill walking tests at their self-selected velocity while bilaterally carrying 15-kg and 20-kg loads (in a boxed container) for 4 min in front of the body. Each handle of the boxed container was fitted with a load cell so as to allow quantification of the load supported by each hand during load carriage. During the tests, oxygen uptake (VO2), heart rate (HR), and blood pressure (BP) were monitored using standardized procedures, and cardiac output (Qc) was measured using the carbon dioxide rebreathing method. Stroke volume (SV), arterio-venous oxygen difference (C(a-v)O2), rate pressure product (RPP) and total peripheral resistance (TPR) were calculated from the above measurements. The results showed that the two extremities sustained approximately 60% to 70% of the total load, with the balance being supported by the body. Significant increases (P < 0.05) in VO2, HR, Qc, and mean BP were observed during both of the load carriage walks compared to unloaded walking. However, SV, C(a-v)O2, RPP and TPR were unchanged (P > 0.05) during load carriage. Although VO2 was significantly higher during the 20-kg load carriage walk, no significant differences were observed between the two loads for any of the cardiovascular responses monitored. Contrary to our hypothesis, these results suggest that increasing the load from 15 kg to 20 kg during treadmill walking does not significantly increase the cardiovascular stress that occurs in healthy subjects.

Adult↗

PubMed1998

Effect of enalapril on proteinuria, phosphaturia, and calciuria in insulin-dependent diabetes.

Elevated urinary calcium and phosphate excretion have been observed in children with insulin-dependent diabetes mellitus (IDDM). This may be related to a defect in tubular reabsorption. It is well known that converting enzyme inhibition decreases microalbuminuria and may prevent or retard diabetic nephropathy. We investigated whether enalapril also improves the defect in calcium and phosphate reabsorption. We studied 16 children and young adults (age 12-21 years) with IDDM and persistent microalbuminuria before and during 12 weeks of enalapril treatment. Before treatment microalbuminuria, urinary calcium excretion, and fractional tubular phosphorus reabsorption (TPR) were 153+/-53 microg/min, 5.5+/-0.9 mg/kg per day, and 71.4+/-3.6%, respectively. At the end of the 12th week, microalbuminuria had decreased to 20.3+/-7.9 microg/min and calcium excretion to 3.3+/-0.4 mg/kg per day (P<0.01), while the TPR increased to 80.1+/-3.8% (NS). The renal threshold phosphate concentration increased from 1.8+/-0.15 to 2.92+/-0.23 mg/dl (P<0.01). The fasting serum glucose and hemoglobin Alc levels did not change significantly during the study. Systolic and diastolic blood pressures were 120.4+/-2.2 / 79.3+/-1.4 mm Hg and 110.5+/-1.8 / 71.3+/-0.9 mm Hg before and after 12 weeks, respectively. We conclude that enalapril treatment improves not only microalbuminuria but also abnormal calcium and phosphate excretion in microalbuminuric children with IDDM.

Adolescent↗

PubMed1992

Hemodynamic responses during induction of anesthesia with halothane-nitrous oxide in children with or without atropine premedication.

Forty three children ranged from 1 yr. to 6 yr. were randomly assigned to non-atropinized group (n = 20; A(-)) and atropinized group (0.015 mg.kg(-1) i.m., n = 23; A(+)). Control hemodynamics were measured under 0.5% halothane and 67% nitrous oxide and 33% oxygen for three minutes, and then halothane was increased to 2.5% and maintained for 15 min. In the A(-) group, stroke volume (SV) decreased to 64%, heart rate (HR) increased from 100/min to 111/min, and blood pressure (BP) decreased from 65 mmHg to 62 mmHg. Skin blood flow (SBF) concomitantly measured by a laser doppler flowmeter decreased to 48% and total peripheral resistance (TPR) increased to 128%. In the A(+) group, HR increased from 117/min to 132/min ( P < 0.05, vs. A(-) group), BP decreased from 67 mmHg to 66 mmHg. SV decreased to 71% ( P < 0.05, vs. A(-) group). Changes in SBF and TPR were 68% and 128% respectively. End-expired halothane concentration in the A(+) group increased slower than in the A(-) group but not significantly. The results indicate increased sympathetic tone would work as a compensating mechanism for decreased SV and CO. Atropine premedication attenuated cardiovascular depression by maintaining HR and possibly by delaying induction speed of anesthesia. In conclusion, halotane-nitrous oxide anesthesia decreased SV without a marked decrease in heart rate and blood pressure in children. This decrease in SV and BP was attenuated by atropine premedication.

Clinical Trial↗

PubMed1993

Effects of halothane on carotid occlusion in rabbits.

Effects of halothane on the carotid sinus baroreflex control of circulation were studied in chronically instrumented rabbits. The carotid sinus baroreflex was evaluated by the hemodynamic responses to bilateral carotid occlusion (BCO). Either 0.5 or 1.0 MAC of halothane inhalation did not alter mean arterial pressure (MAP) or total peripheral resistance (TPR), but significantly increased heart rate (HR). Carotid occlusion produced a significant increase in MAP and HR, and both responses were attenuated dose-dependently by halothane. Halothane depressed the reflex gain of arterial pressure from 3.5 +/- 0.3 at conscious state to 1.3 +/- 0.2 at 1.0 MAC halothane. Response of cardiac output (CO) to BCO was attenuated significantly only at 1.0 MAC compared with those responses at conscious state and at 0.5 MAC. Response of TPR was attenuated at both 0.5 and 1.0 MAC halothane as compared with at conscious state but no significant difference existed between the two concentrations of halothane. These data suggested that halothane could attenuate the carotid occlusion responses to various degrees in the involved effector components. 0.5 MAC halothane attenuated MAP response to BCO predominantly by attenuating reflex peripheral vasoconstriction. The reduced CO response was mainly responsible for further attenuation of MAP response at 1.0 MAC halothane.

Journal Article↗

PubMed1988

The effect of RO15-1788 on cardiovascular depression caused by fentanyl and diazepam.

Cardiovascular depression occurring when diazepam is combined with fentanyl has been investigated using the benzodiazepine antagonist RO15-1788 in the dog. After the initial administration of fentanyl (40 mcg/kg), the mean arterial pressure (MAP) decreased to 89% of its control value. Following the administration of diazepam (1.2 mg/kg), the MAP and the total peripheral resistance (TPR) decreased significantly, to 75% and 83% of their control values respectively. After the administration of RO15-1788 (0.4 mg/kg), the MAP increased significantly to 90% and the TPR to 102% of their control values and, lastly, the administration of naloxone (40 mcg/kg) increased the MAP to 108% of its control value. No relationship was found between the changes in the catecholamines and the changes in the MAP after the administration of fentanyl, diazepam, and RO15-1788. The mechanism of circulatory depression when diazepam was used with fentanyl is interpreted as being a peripheral vasodilatory effect of diazepam acting by way of the benzodiazepine receptors since RO15-1788 was found to antagonize this effect.

Journal Article↗

PubMed2006

A two-stage design for multiple testing in large-scale association studies.

Modern association studies often involve a large number of markers and hence may encounter the problem of testing multiple hypotheses. Traditional procedures are usually over-conservative and with low power to detect mild genetic effects. From the design perspective, we propose a two-stage selection procedure to address this concern. Our main principle is to reduce the total number of tests by removing clearly unassociated markers in the first-stage test. Next, conditional on the findings of the first stage, which uses a less stringent nominal level, a more conservative test is conducted in the second stage using the augmented data and the data from the first stage. Previous studies have suggested using independent samples to avoid inflated errors. However, we found that, after accounting for the dependence between these two samples, the true discovery rate increases substantially. In addition, the cost of genotyping can be greatly reduced via this approach. Results from a study of hypertriglyceridemia and simulations suggest the two-stage method has a higher overall true positive rate (TPR) with a controlled overall false positive rate (FPR) when compared with single-stage approaches. We also report the analytical form of its overall FPR, which may be useful in guiding study design to achieve a high TPR while retaining the desired FPR.

Cost-Benefit Analysis↗

PubMed2002

Thoracic sympathectomy: effects on hemodynamics and baroreflex control.

UNLABELLED: Endoscopic thoracic sympathectomy at T2-T4 is an effective and safe treatment for primary axillary and palmar hyperhidrosis and facial blushing refractory to conventional treatment. T2 and T4 ganglia however are in the direct pathway of sympathetic innervation of the heart and part of the vasomotor nerves. In this study we investigate possible changes in steady-state hemodynamics as well as in beat-to-beat cardiovascular control after thoracoscopic sympathectomy of T2-T4. In 12 patients we measured continuously heart rate (HR) and blood pressure (BP) (non-invasively with Finapres) during rest and during deep inspiration, in supine and sitting position as well as during a change from lying to standing. Stroke volume (SV) and total peripheral resistance (TPR) were estimated from the BP recordings by the Modelflow method. Markers for cardiovascular control were obtained from power and cross-spectra of BP and HR. After sympathectomy, only in the sitting position was mean HR decreased, while TPR and BP (diastolic and mean) were lower in the supine as well as sitting positions. SV clearly increased. Low frequency power in HR and BP was significantly decreased, just like the max/min ratio in HR after standing up, indicating a diminished capacity in sympathetic vasomotor control. High frequency power of HR as well as baroreflex sensitivity, both parasympathetic markers, did not change in a statistically significant manner. CONCLUSION: Besides altering steady-state hemodynamics, a thoracic sympathectomy causes relatively small, though measurable changes in cardiovascular control, in particular of peripheral vasomotion.

Adult↗

PubMed1991

Chemical stimulation of the locus coeruleus: inhibitory effects on hemodynamics and renal sympathetic nerve activity.

We examined the role of the locus coeruleus (LC) in the regulation of the hemodynamics and sympathetic nerve activity in anesthetized rats. Unilateral microinjection into the LC of the excitatory amino acid, L-glutamate (Glu), elicited dose-dependent decreases in arterial pressure (AP) and heart rate (HR). The bradycardic response was partially attenuated after intravenous injection of atropine sulfate, but the greater part of this response still remained. Interruption of the ascending projections of the LC by midbrain transection did not affect the depressor and bradycardic responses elicited by chemical stimulation. The renal sympathetic nerve activity showed transient but strong inhibition with this stimulation. Cardiac output was measured using an electromagnetic flowmeter implanted in the ascending aorta. The stroke volume and total peripheral resistance (TPR) were calculated. Microinjection of Glu elicited a significant decrease in TPR and slight decreases in cardiac output and stroke volume. Microinjection of the inhibitory amino acid, gamma-aminobutyric acid (GABA), or the alpha 2-adrenergic agonist, clonidine, exerted no effect on AP and HR. The present results therefore suggest that: (1) the LC neurons have an inhibitory influence on the sympathetic nervous system, and stimulation of these neurons can elicit depressor and bradycardic responses; (2) the depressor response was produced predominantly as a result of a decrease in vascular resistance, rather than a decrease in cardiac output; (3) these inhibitory responses may be provided not via the ascending projections of the LC; and (4) the LC neurons do not have a tonic influence on the cardiovascular system.

Animals↗

PubMed1993

Differential regional hemodynamic changes produced by L-glutamate stimulation of the locus coeruleus.

The locus coeruleus (LC) exerts an inhibitory influence on the cardiovascular system. Microinjection of the excitatory amino acid, L-glutamate, into the LC elicits a decrease in arterial pressure as a result of a decrease in total peripheral resistance (TPR). The aim of the present study was to examine the role of the LC in the regulation of the regional hemodynamics. Employing anesthetized rats, the blood flow to the renal, mesenteric and hind-limb vascular beds was measured with an electromagnetic flowmeter. The changes in regional blood flow and vascular resistance evoked by chemical stimulation of the LC were examined separately in each region. During the depressor response elicited by LC stimulation, the hind-limb and renal vascular resistance was significantly decreased, while the mesenteric resistance was unchanged. The vasodilatation appeared to be more prominent in the hind-limb muscle than in the systemic circulation. Renal nerve denervation attenuated the decrease in renal vascular resistance elicited by LC stimulation. However, a small part of this response still remained in the denervated kidney. The present results suggest therefore that: (1) LC neurons exert differential hemodynamic effects on the hind-limb muscle, renal and mesenteric vascular beds; (2) the largest contribution to the decrease in TPR is related to vasodilatation in the hind-limb muscles; and (3) the renal vasodilation elicited by LC stimulation is not mediated solely by the renal innervation.

Animals↗

PubMed1993

Cardiac output and regional hemodynamics during recurrent seizures in rats.

Altered cardiovascular function in status epilepticus may contribute to mortality and morbidity in patients. We investigated changes in cardiac output and regional hemodynamics during 2 h of recurrent PTZ-induced seizures in anesthetized, paralyzed rats using radioactive microspheres, thermodilution methods, and the pulsed Doppler technique. Cardiac output fell 30-60% during recurrent seizures in 17 of 27 animals. The fall in cardiac output was sudden in onset and occurred primarily in association with seizures accompanied by prolonged increases in MABP but no change in central venous pressure. Total peripheral resistance (TPR) rose during early seizures in association with vasoconstriction of renal and certain splanchnic vascular beds. Ictal increases in TPR became attenuated during late seizures, due to failure of renal and splanchnic beds to constrict. Therefore, derangements in both cardiac and vascular function occur during late seizures. These derangements may contribute to both cerebral hypoperfusion and sudden death in status epilepticus.

Animals↗