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BACKGROUND: Hypotension during dialysis arises from vasomotor tone alterations and hypovolemia, with disrupted counterregulatory mechanisms in acute kidney injury (AKI) patients. This study investigated the predictive value of preload dependency, assessed by the passive leg raising (PLR) test, and arterial tone, measured by dynamic elastance (Eadyn), for intradialytic hypotension (IDH). METHODS: In this prospective observational study conducted in a tertiary hospital ICU, hemodynamic parameters were collected from critically ill AKI patients undergoing intermittent hemodialysis using the FloTrac/Vigileo system. Baseline measurements were recorded before KRT initiation, including the PLR test and Eadyn calculation. IDH was defined as mean arterial pressure (MAP)

Abstract Background Atelectasis can occur in many clinical practices. One way to prevent this complication is through the alveolar recruitment maneuver (ARM). However, hemodynamic compromise can accompany ARM. This study aims to predict ARM-induced hypotension using a non-invasive method. Methods 94 American Society of Anesthesiologists physical status I–II patients aged 19 to 75 with scheduled spinal surgery were enrolled. After anesthesia, we performed a stepwise ARM. Data on perfusion index, mean arterial pressure, heart rate, pleth variability index, cardiac index, and stroke volume variation was collected before induction of anesthesia (T0), just before ARM (T1), at the start of ARM (T2), 0.5 min (T3), 1 min (T4), 1.5 min (T5, end of ARM), and 2 min after the beginning of ARM (T6). Hypotension was defined as when the mean arterial pressure at T5 decreased by 20% or more compared to the baseline. The primary endpoint is that the perfusion index measuring before induction of anesthesia, which reflects the patients’ own vascular tone, was correlated with hypotension during ARM. Results Seventy-five patients (79.8%) patients developed hypotension during ARM. The pre-induction persufion index (Pi) (95% confidence interval) was 1.7(1.4–3.1) in the non-hypotension group and 3.4(2.4–3.9) in the hypotension group. (p

Objective: Perfusion index has shown to be helpful in the operative and critical care settings to monitor peripheral tissue perfusion. Randomised controlled trials quantifying different agents' vasodilatory properties using perfusion index has been limited. Therefore, we undertook this study to compare the vasodilatory effects of isoflurane and sevoflurane using perfusion index. Methods: This is a pre-specified sub-analysis of a prospective randomised controlled trial on the effects of inhalational agents at equipotent concentration. We randomly allocated patients scheduled for lumbar spine surgery to either isoflurane or sevoflurane groups. We recorded values of perfusion index at age-corrected 1 Minimum Alveolar Concentration (MAC) concentration at baseline, pre- and post-application of a noxious stimulus. The primary outcome of interest was the measure of vasomotor tone with perfusion index, and the secondary outcomes which were analysed were mean arterial pressure and heart rate. Results: At age-corrected 1.0 MAC, there was no significant difference in the pre-stimulus haemodynamic variables and perfusion index between both groups. During the post-stimulus period, there was a significant increase in heart rate in the isoflurane group compared to the sevoflurane group, with no significant difference in the mean arterial pressure values between both groups. Though the perfusion index decreased during the post-stimulus period in both groups, there was no statistically significant difference between the 2 groups (P = .526, repeated-measures analysis of variance). Conclusion: In a steady state of age-corrected 1.0 MAC, isoflurane and sevoflurane had a similar perfusion index before and after a standardised nociceptive stimulus, which suggests that both of these agents have similar effect on peripheral perfusion and vasomotor tone. [ABSTRACT FROM AUTHOR]

Coronary artery disease with healthy coronaries In this review, we show how the physiology of the coronary circulation is complex and multifactorial. Its regulation involves mechanical, nervous, metabolic factors and substances synthesized and released by the endothelium. In addition to anatomical abnormalities that may impact all the downstream compartments of the coronary network, functional coronary microvascular dysfunction, decreased diastolic time and elevated extravascular tissue pressure may also contribute to the development of myocardial ischemia. Many patients with typical anginal chest pain do not have evidence of obstructive atherosclerosis of the large coronary arteries that could explain the severity of the symptoms and electrical abnormalities. In this setting, coronary microvascular dysfunction should be suspected and investigated. [ABSTRACT FROM AUTHOR]

Background: Atelectasis can occur in many clinical practices. One way to prevent this complication is through the alveolar recruitment maneuver (ARM). However, hemodynamic compromise can accompany ARM. This study aims to predict ARM-induced hypotension using a non-invasive method. Methods: 94 American Society of Anesthesiologists physical status I–II patients aged 19 to 75 with scheduled spinal surgery were enrolled. After anesthesia, we performed a stepwise ARM. Data on perfusion index, mean arterial pressure, heart rate, pleth variability index, cardiac index, and stroke volume variation was collected before induction of anesthesia (T0), just before ARM (T1), at the start of ARM (T2), 0.5 min (T3), 1 min (T4), 1.5 min (T5, end of ARM), and 2 min after the beginning of ARM (T6). Hypotension was defined as when the mean arterial pressure at T5 decreased by 20% or more compared to the baseline. The primary endpoint is that the perfusion index measuring before induction of anesthesia, which reflects the patients' own vascular tone, was correlated with hypotension during ARM. Results: Seventy-five patients (79.8%) patients developed hypotension during ARM. The pre-induction persufion index (Pi) (95% confidence interval) was 1.7(1.4–3.1) in the non-hypotension group and 3.4(2.4–3.9) in the hypotension group. (p < 0.004) The hypotension group showed considerably higher Pi than the non-hypotension group before induction. The decrease of Pi (%) [IQR] in the non-hypotensive group (52.8% [33.3–74.7]) was more significant than in the hypotensive group. (36% [17.6–53.7]) (p < 0.05) The area under the receiver operating characteristic curve of Pi for predicting hypotension during ARM was 0.718 (95% CI 0.615–0.806; p = 0.004), and the threshold value of the Pi was 2.4. Conclusion: A higher perfusion index value measuring before induction of anesthesia can be used to predict the development of hypotension during ARM. Prophylactic management of the following hypotension during ARM could be considered in high baseline Pi patients. [ABSTRACT FROM AUTHOR]

Despite significant advances in surgical technique and strategies for tissue/organ protection, cardiac surgery involving cardiopulmonary bypass is a profound stressor on the human body and is associated with numerous intraoperative and postoperative collateral effects across different tissues and organ systems. Of note, cardiopulmonary bypass has been shown to induce significant alterations in microvascular reactivity. This involves altered myogenic tone, altered microvascular responsiveness to many endogenous vasoactive agonists, and generalized endothelial dysfunction across multiple vascular beds. This review begins with a survey of in vitro studies that examine the cellular mechanisms of microvascular dysfunction following cardiac surgery involving cardiopulmonary bypass, with a focus on endothelial activation, weakened barrier integrity, altered cell surface receptor expression, and changes in the balance between vasoconstrictive and vasodilatory mediators. Microvascular dysfunction in turn influences postoperative organ dysfunction in complex, poorly understood ways. Hence the second part of this review will highlight in vivo studies examining the effects of cardiac surgery on critical organ systems, notably the heart, brain, renal system, and skin/peripheral tissue vasculature. Clinical implications and possible areas for intervention will be discussed throughout the review.

Vasomotor tone-associated factors play important roles in normal pregnancy, but their roles in the pregnancy outcome of women who undergo in vitro fertilization and embryo transfer (IVF-ET) remain unclear. A total of 82 infertile women who underwent successful IVF-ET were enrolled, including 18 pregnancy losses, 11 complications, and 53 normal deliveries. The serum NO and iNOS levels were significantly higher in the pregnancy loss group and significantly lower in the complication group than in the normal delivery group (p < 0.05). Significantly increased ET-1 and decreased PGI2 were found in both the pregnancy loss and complication groups compared with those in the normal delivery group (p < 0.05). NO, iNOS, and ET-1 are risk factors and PGI2 is a protective factor for pregnancy loss. ET-1 + PGI2 (AUC, 0.897; sensitivity, 90.6%; specificity, 83.3%) showed a relatively good predictive value for pregnancy loss following IVF-ET. [ABSTRACT FROM AUTHOR]

Background We have previously found that hyperkalemic cardioplegic arrest in the setting of cardiopulmonary bypass (CP/CPB) is associated with impairment of the coronary arteriolar response to phenylephrine in nondiabetic (ND) patients. We hypothesized that diabetes may alter coronary arteriolar response to alpha-1 adrenergic agonist in the setting of CP/CPB. In this study, we further investigated the effects of diabetes on the altered coronary arteriolar response to phenylephrine in patients undergoing cardiac surgery. Methods Coronary arterioles (90-150 μm in diameter) were harvested pre- and post-CP/CPB from the ND and diabetic mellitus (DM) patients ( n = 8/group) undergoing cardiac surgery. In-vitro microvascular reactivity was examined in response to phenylephrine. The protein expression/localization of the alpha-1 adrenergic receptors in the atrial myocardium was measured by Western blotting and immunohistochemistry. Results Phenylephrine (10 −9 to 10 −4 M) induced a dose-dependent contractile response in both ND and DM vessels pre- and post-CP/CPB. There was no significant difference in the pre-CP/CPB contractile responses to phenylephrine between ND and DM groups. The post-CP/CPB contractile response was significantly diminished in both ND and DM groups compared with the respective pre-CP/CPB response ( P < 0.05 versus pre-CP/CPB). This diminished contractile response was more pronounced in vessels from DM patients compared with vessels from ND patients ( P < 0.05 versus ND). There were no significant differences in the protein expression of alpha-1A and alpha-1B receptors in the atrial myocardium between the ND and DM groups or tissue harvested pre- or post-CP/CPB. Conclusions Diabetes is associated with a decreased contractile response of coronary arterioles to phenylephrine in the setting of CP/CPB versus that observed in ND patients. This alteration may contribute to the vasomotor dysfunction of coronary microcirculation seen early after CP/CPB in patients with diabetes. [ABSTRACT FROM AUTHOR]

Ginseng is widely used for its promising healing and restorative properties as well as for its possible tonic effect in traditional medicine. Nowadays, many studies focus on purified individual ginsenoside, an important constituent in ginseng, and study its specific mechanism of action instead of whole-plant extracts on cardiovascular diseases (CVDs). Of the various ginsenosides, purified ginsenosides such as Rb1, Rg1, Rg3, Rh1, Re, and Rd are the most frequently studied. Although there are many reports on the molecular mechanisms and medical applications of ginsenosides in the treatment of CVDs, many concerns exist in their application. This review discusses current works on the countless pharmacological functions and the potential benefits of ginseng in the area of CVDs. Results: Both in vitro and in vivo results indicate that ginseng has potentially positive effects on heart disease through its various properties including antioxidation, reduced platelet adhesion, vasomotor regulation, improving lipid profiles, and influencing various ion channels. To date, approximately 40 ginsenosides have been identified, and each has a different mechanism of action owing to the differences in chemical structure. This review aims to present comprehensive information on the traditional uses, phytochemistry, and pharmacology of ginseng, especially in the control of hypertension and cardiovascular function. In addition, the review also provides an insight into the opportunities for future research and development on the biological activities of ginseng.

Early investigation on blood circulation by Hertzman (1937) leads to the observation of vital body signs such as respiration rate, heart rate (HR), blood oxygenation and vascular assessment using photoplethysmographic (PPG) device. PPG is a noninvasive, painless optical technique used to monitor the pulsations linked to alteration in the blood volume. The PPG waveform is a summation of pulsatile and nonpulsatile components and contains useful information about the physiological systems. With the breakthrough in technology and development of powerful analytical tools, PPG devices are constantly being used in advanced medical equipments such as smart-watches and smart-wristbands for HR monitoring, pulse oximeters for measuring respiratory rate and noncontact PPG device for blood oxygen saturation measurement. This paper presents description on PPG and its characteristic waveform and working principle. It also includes brief explanation on nonlinear analysis of PPG signals and salient applications of PPG followed by its advantages and limitations. [ABSTRACT FROM AUTHOR]

The sympathetic preganglionic neurons (SPN) in the thoracic spinal cord regulate vasomotor tone via norepinephrine released from sympathetic terminals and adrenal medulla. We assessed the hypothesis that nitric oxide synthase I (NOS I)- and NOS II-derived nitric oxide (NO) in the thoracic spinal cord differentially modulate sympathetic outflow and that the adrenal medulla may be involved in those modulatory actions. In Sprague- Dawley rats, NOS I immunoreactivity was distributed primarily in the perikaryon, proximal dendrites, or axons of SPN, and small clusters of NOS II immunoreactivity impinged mainly on the circumference of SPN. Intrathecal administration of 7-nitroindazole (7-NI), a specific NOS I antagonist, into the thoracic spinal cord significantly reduced arterial pressure, heart rate, and basal or baroreflex-mediated sympathetic vasomotor tone. On the other hand, intrathecal application of S-methylisothiourea (SMT), a specific NOS II antagonist, elevated arterial pressure with a transient reduction of heart rate, induced a surge of plasma norepinephrine, and reduced baroreflex-mediated but not basal sympathetic vasomotor tone. Bilateral adrenalectomy significantly exacerbated the cardiovascular responses to 7-NI but antagonized those to SMT. We conclude that both NOS I and NOS II are present in the thoracic spinal cord and are tonically active under physiological conditions. Furthermore, the endogenous NO generated by NOS I-containing SPN exerts a tonic excitatory action on vasomotor tone mediated by norepinephrine released from the adrenal medulla and sympathetic nerve terminals. On the other hand, NO derived from NOS II exerts a tonic inhibitory action on sympathetic outflow from the SPN that targets primarily the blood vessels. [ABSTRACT FROM AUTHOR]

The rostral ventrolateral medulla (RVLM) contains neurons involved in tonic and reflex control of arterial pressure. We describe the effects of gamma-aminobutyric acid (GABA) and anesthetics injected into the RVLM of conscious and urethane (1.2 g/kg, iv) anesthetized Wistar rats (300-350 g). In conscious rats, bilateral microinjection of GABA (50 nmol/200 nl) induced a small but significant decrease in blood pressure (from 130 ± 3.6 to 110 ± 5.6 mmHg, N = 7). A similar response was observed with sodium pentobarbital microinjection (24 nmol/200 nl). However, in the same animals, the fall in blood pressure induced by GABA (from 121 ± 8.9 to 76 ± 8.8 mmHg, N = 7) or pentobarbital (from 118 ± 4.5 to 57 ± 11.3 mmHg, N = 6) was significantly increased after urethane anesthesia. In contrast, there was no difference between conscious (from 117 ± 4.1 to 92 ± 5.9 mmHg, N = 7) and anesthetized rats (from 123 ± 6.9 to 87 ± 8.7 mmHg, N = 7) when lidocaine (34 nmol/200 nl) was microinjected into the RVLM. The heart rate variations were not consistent and only eventually reached significance in conscious or anesthetized rats. The right position of pipettes was confirmed by histology and glutamate microinjection into the RVLM. These findings suggest that in conscious animals the RVLM, in association with the other sympathetic premotor neurons, is responsible for the maintenance of sympathetic vasomotor tone during bilateral RVLM inhibition. Activity of one or more of these premotor neurons outside the RVLM can compensate for the effects of RVLM inhibition. In addition, the effects of lidocaine suggest that fibers passing through the RVLM are involved in the maintenance of blood pressure in conscious animals during RVLM inhibition.

Regional myocardial blood flows are markedly heterogeneous. Fractal analysis shows strong near-neighbor correlation. In experiments to distinguish control by vascular anatomy vs. local vasomotion, coronary flows were increased in open-chest dogs by stimulating myocardial metabolism (catecholamines + atropine) with and without adenosine. During control states mean left ventricular (LV) myocardial blood flows (microspheres) were 0.5-1 ml·g-1·min-1 and increased to 2-3 ml·g-1·min-1 with catecholamine infusion and to ~4 ml·g-1·min-1 with adenosine (Ado). Flow heterogeneity was similar in all states: relative dispersion (RD + SD/mean) was ~25%, using LV pieces 0.1-0.2% of total. During catecholamine infusion local flows increased in proportion to the mean flows in 45% of the LV, "tracking" closely (increased proportionately to mean flow), while ~40% trended toward the mean. Near-neighbor regional flows remained strongly spatially correlated, with fractal dimension D near 1.2 (Hurst coefficient 0.8). The spatial patterns remain similar at varied levels of metabolic stimulation inferring metabolic dominance. In contrast, adenosine vasodilation increased flows eightfold times control while destroying correlation with the control state. The Ado-induced spatial patterns differed from control but were self-consistent, inferring that with full vasodilation the relaxed arterial anatomy dominates the distribution. We conclude that vascular anatomy governs flow distributions during adenosine vasodilation but that metabolic vasoregulation dominates in normal physiological states. [ABSTRACT FROM AUTHOR]

Tubuloglomerular feedback (TGF) describes the negative relationship between ( a) NaCl concentration at the macula densa and ( b) glomerular filtration rate or glomerular capillary pressure. TGF-induced vasoconstriction of the afferent arteriole results from the enhanced effect of several vasoconstrictors with an effect size sequence of adenosine = 20-HETE > angiotensin II > thromboxane = superoxide > renal nerves > ATP. TGF-mediated vasoconstriction is limited by the simultaneous release of several vasodilators with an effect size sequence of nitric oxide > carbon monoxide = kinins > adenosine. The sum of the constrictor effects exceeds that of the dilator effects by the magnitude of the TGF response. The validity of the additive model used in this analysis can be tested by determining the effect of combined inhibition of some or all agents contributing to TGF. Multiple independent contributors to TGF are consistent with the variability of TGF and of the factors contributing to TGF resetting. [ABSTRACT FROM AUTHOR]

Hypertension is associated with pathologically increased sympathetic drive to the vasculature. This has been attributed to increased excitatory drive to sympathetic preganglionic neurons (SPN) from brainstem cardiovascular control centers. However, there is also evidence supporting increased intrinsic excitability of SPN. To test this hypothesis, we made whole cell recordings of muscle vasoconstrictor-like (MVClike) SPN in the working-heart brainstem preparation of spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) rats. The MVClike SPN have a higher spontaneous firing frequency in the SH rat (3.85± 0.4 vs. 2.44±0.4 Hz in WKY; P=0.011) with greater respiratory modulation of their activity. The action potentials of SH SPN had smaller, shorter afterhyperpolarizations (AHPs) and showed diminished transient rectification indicating suppression of an A-type potassium conductance (IA). We developed mathematical models of the SPN to establish if changes in their intrinsic properties in SH rats could account for their altered firing. Reduction of the maximal conductance density of IA by 15-30% changed the excitability and output of the model from the WKY to a SH profile, with increased firing frequency, amplified respiratory modulation, and smaller AHPs. This change in output is predominantly a consequence of altered synaptic integration. Consistent with these in silico predictions, we found that intrathecal 4-aminopyridine (4-AP) increased sympathetic nerve activity, elevated perfusion pressure, and augmented Traube-Hering waves. Our findings indicate that IA acts as a powerful filter on incoming synaptic drive to SPN and that its diminution in the SH rat is potentially sufficient to account for the increased sympathetic output underlying hypertension. [ABSTRACT FROM AUTHOR]

The purpose of this study was to examine whether the forearm-finger skin temperature gradient (Tforearm-finger), an index of vasomotor tone during resting conditions, can also be used during steady-state exercise. Twelve healthy men performed three cycling trials at an intensity of ~60% of their maximal oxygen uptake for 75 min separated by at least 48 h. During exercise, forearm skin blood flow ( BFF) was measured with a laser-Doppler flowmeter, and finger skin blood flow ( PPG) was recorded from the left index fingertip using a pulse plethysmogram. Tforearm-finger of the left arm was calculated from the values derived by two thermistors placed on the radial side of the forearm and on the tip of the middle finger. During exercise, PPG and BFF increased ( P<0·001), and Tforearm-finger decreased ( P<0·001) from their resting values, indicating a peripheral vasodilatation. There was a significant correlation between Tforearm-finger and both PPG ( r = −0·68; P<0·001) and BFF ( r = −0·50; P<0·001). It is concluded that Tforearm-finger is a valid qualitative index of cutaneous vasomotor tone during steady-state exercise. [ABSTRACT FROM AUTHOR]

Senescence marker protein-30 (SMP30) decreases with aging. Mice with SMP30 deficiency, a model of aging, have a short lifespan with increased oxidant stress. To elucidate SMP30's effect on coronary circulation derived from myocytes, we measured the changes in the diameter of isolated coronary arterioles in wild-type (WT) mice exposed to supernatant collected from isolated paced cardiac myocytes from SMP30 KO or WT mice. Pacing increased hydrogen peroxide in myocytes, and hydrogen peroxide was greater in SMP30 KO myocytes compared to WT myocytes. Antimycin enhanced and FCCP (oxidative phosphorylation uncoupler in mitochondria) decreased superoxide production in both groups. Addition of supernatant from stimulated myocytes, either SMP30 KO or WT, caused vasodilation. The degree of the vasodilation response to supernatant was smaller in SMP30 KO mice compared to WT mice. Administration of catalase to arterioles eliminated vasodilation in myocyte supernatant of WT mice and converted vasodilation to vasoconstriction in myocyte supernatant of SMP30 KO mice. This vasoconstriction was eliminated by olmesartan, an angiotensin II receptor antagonist. Thus, SMP30 deficiency combined with oxidant stress increases angiotensin and hydrogen peroxide release from cardiac myocytes. SMP30 plays an important role in the regulation of coronary vascular tone by myocardium. [ABSTRACT FROM AUTHOR]

Background The use of vasoconstrictor can affect the dynamic indices to predict fluid responsiveness. We investigate the effects of an increase of vascular tone on dynamic variables of fluid responsiveness in a rabbit model of hemorrhage, and to examine the ability of the arterial pressure surrogates dynamic indices to track systolic volume variation (SVV) during hypovolemia under increased vasomotor tone. Methods Eighteen anesthetized and mechanically ventilated rabbits were studied during normovolemia (BL) and after blood progressive removal (15 mL/kg, BW). Other two sets of data were obtained during PHE infusion with normovolemia (BL + PHE) and during hypovolemia (BW + PHE). We measured central venous and left ventricular (LV) pressures and infra diaphragmatic aortic blood flow (AoF) and pressure. Pulse pressure variation (PPV), systolic pressure variation (SPV) and SVV were estimated manually by the variation of beat-to-beat PP, SP and SV, respectively. We also calculated PPVapnea as 100 × (PPmax-PPmin)/PP during apnea. The vasomotor tone was estimated by total peripheral resistance (TPR = mean aortic pressure/mean AoF), dynamic arterial elastance (Eadyn = PPV/SVV) and arterial compliance (C = SV/PP). We assessed LV preload by LV end-diastolic pressure (LVEDP). We compared the trending abilities between SVV and pressure surrogate indices using four-quadrant plots and polar plots. Results Baseline PPV, SPV, PPVapnea, and SVV increased significantly during hemorrhage, with a decrease of AoF (P < 0.05). PHE induced significant TPR and Eadyn increase and C decrease in bled animals, and a further decrease in AoF with a significant decrease of all dynamic indices. There was a significant correlation between SVV and PPV, PPVapnea and SPV in normal vasomotor tone (r2 ≥ 0.5). The concordance rate was 91 %, 95 % and 76 % between SVV and PPV, PPVapnea and SPV, respectively, in accordance with the polar plot analysis. During PHE infusion, there was no correlation between SVV and its surrogates, and both four-quadrant plot and polar plot showed poor trending. Conclusion In this animal model of hemorrhage and increased vasomotor tone induced by phenylephrine the ability of dynamic indices to predict fluid responsiveness seems to be impaired, masking the true fluid loss. Moreover, the arterial pressure surrogates have not the reliable trending ability against SVV. [ABSTRACT FROM AUTHOR]

Abstract: Background: The causes of cardiovascular collapse (CC) during hemorrhagic shock (HS) are unknown. We hypothesized that vascular tone loss characterizes CC, and that arterial pulse pressure/stroke volume index ratio or vascular tone index (VTI) would identify CC. Methods: Fourteen Yorkshire-Durock pigs were bled to 30 mmHg mean arterial pressure and held there by repetitive bleeding until rendered unable to compensate (CC) or for 90 min (NoCC). They were then resuscitated in equal parts to shed volume and observed for 2 h. CC was defined as a MAP < 30 mmHg for 10 min or <20 mmHg for 10 s. Study variables were recorded at baseline (B0), 30, 60, 90 min after bleeding and at resuscitation (R0), 30, and 60 min afterward. Results: Swine were bled to 32% ± 9% of total blood volume. Epinephrine (Epi) and VTI were low and did not change in NoCC after bleeding compared with CC swine, in which both increased (0.97 ± 0.22 to 2.57 ± 1.42 mcg/dL, and 173 ± 181 to 939 ± 474 mmHg/mL, respectively), despite no differences in bled volume. Lactate increase rate (LIR) increased with hemorrhage and was higher at R0 for CC, but did not vary in NoCC. VTI identified CC from NoCC and survivors from non-survivors before CC. A large increase in LIR was coincident with VTI decrement before CC occurred. Conclusions: Vasodilatation immediately prior to CC in severe HS occurs at the same time as an increase in LIR, suggesting loss of tone as the mechanism causing CC, and energy failure as its probable cause. [Copyright &y& Elsevier]