Hypovolemic Hypotension Research Articles

Impact of Laser Radiation on the Rate of Free Radical Oxidation in Hypovolemic Hypotension and After Reinfusion: Experimental Study

The impact of laser radiation (LR) on the rate of plasma free radical processes during hypotension and after reinfusion was studied in acute experiments on non-inbred albino rats with prior severe hypovolemic hypotension (blood pressure, 25—30 mm Hg) during 60 min. LR used before blood loss was shown to increase total plasma antioxidative activity and to promote the decreased production of lipid peroxidation products during hypotension. Inclusion of LR into a package of resuscitative measures deteriorates free radical oxidative processes. LR may be a promising method for correcting the excessive rate of free radical oxidation after reinfusion at later rehabilitative stages (after recovery of the energetic potential and adaptation mechanisms).

Treatment of hypotension in pigs with an inspiratory impedance threshold device: a feasibility study.

An inspiratory impedance threshold device was evaluated in spontaneously breathing animals with hypotension to determine whether it could help improve systemic arterial pressures when fluid replacement was not immediately available. Prospective, randomized. Animal laboratory. Thirty-nine female farm pigs (weight, 28-33 kg). A total of 39 anesthetized spontaneously breathing pigs were treated with an impedance threshold device, with cracking pressures from 0 to -20 cm H2O. Four separate experimental protocols were performed: protocol A, in which the hemodynamics of seven pigs were examined during application of an impedance threshold device at various levels of inspiratory impedance (-5, -10, -15, and -20 cm H(2)O), both before and after a severe, controlled hemorrhage to a systolic blood pressure of 50 - 55 mm Hg; protocol B, in which nine pigs bled to systolic blood pressure of 50 -55 mm Hg were treated with an impedance threshold device set at -12 cm H2O and were compared with nine others treated with a sham device; protocol C, in which the effects of the impedance threshold device on mixed venous gases were measured in seven hemorrhaged pigs; and protocol D, in which the effects of the impedance threshold device on cardiac output in seven hemorrhaged pigs were measured. During initial studies with both normovolemic and hypovolemic pigs, sequential increases in inspiratory impedance resulted in a significant increase in systolic blood pressure, whereas diastolic left ventricular and right atrial pressures decreased significantly and proportionally to the level of impedance. When comparing the sham vs. active impedance threshold device (-12 cm H(2)O) in hypotensive pigs, systolic blood pressure (mean +/- sem) with active impedance threshold device treatment increased from 70 +/- 2 mm Hg to 105 +/- 4 mm Hg (p <.01). Pressures in the control group remained at 70 +/- 4 mm Hg (p <.01). Cardiac output increased by nearly 25% (p <.01) with the active impedance threshold device when calculated using the mixed gas equation and when determined by thermodilution. These studies demonstrate that it is feasible to use a device that creates inspiratory impedance in spontaneously breathing normotensive and hypotensive pigs to increase blood pressure and enhance cardiopulmonary circulation in the absence of immediate fluid resuscitation. Further studies are needed to evaluate the potential long-term effects and limitations of this new approach to treat hypovolemic hypotension.

Injury severity and cell death mechanisms: effects of concomitant hypovolemic hypotension on spinal cord ischemia–reperfusion in rats

A number of previous studies indicated that ischemia–reperfusion injury causes two distinct types of cell death—necrosis and apoptosis—in the central nervous system. It was also implicated that the intensity of injury can somehow affect the cell death mechanisms. By occluding the descending thoracic aorta with or without simultaneously induced hypovolemic hypotension in rats, we established a model of experimental spinal cord ischemia–reperfusion (I/R) in which the injury severity can be controlled. Recordings of carotid blood pressure (CBP) and spinal cord blood flow (SCBF) showed that aortic occlusion induced dramatic CBP elevation but SCBF drop in both the normotensive (NT) and hypotensive (HT) groups of rats. However, the HT group demonstrated significantly lower SCBF during aortic occlusion, and much slower elevation of SCBF after reperfusion, and extremely poor neurological performance. Spinal cord lesions were characterized by infarction associated with extensive necrotic cell death, but little apoptosis and caspase-3 activity. In contrast, in the NT group, I/R injury resulted in minor tissue destruction associated with persistent abundant apoptosis, augmented caspase-3 activity, and favorable functional outcome. The relative sparing of motoneurons in the ventral horns from apoptosis might have accounted for the minor functional impairment in the NT group. The severity of I/R injury was found to have substantial impact on the histopathological changes and cell death mechanisms, which correlate with neurological performance. Our results implicate that injury severity and duration after injury are two critical factors to be considered in therapeutic intervention.

HYPOVOLEMIC HYPOTENSION ALTERS THE DYNAMIC BALANCE BETWEEN O2 DELIVERY AND UTILIZATION IN CONTRACTING SKELETAL MUSCLE

In healthy animals under normotensive conditions, perfusion of contracting skeletal muscle is regulated precisely to maintain microvascular PO2 (PO2m) at a level commensurate with O2 demands (Behnke et al. Respir. Physiol. 2001). However, hypovolemic hypotension (HH) impairs muscle contractile function due possibly to a reduced blood-myocyte pressure gradient for O2. PURPOSE We tested the hypothesis that HH would alter the matching of O2 delivery (QO2) and O2 utilization (VO2) as determined by PO2m following the onset of muscle contractions. METHODS PO2m in the spinotrapezius muscles of six female Sprague-Dawley rats (∼ 280 g) was measured every 2 s across the transition from rest to 1 Hz twitch contractions using phosphorescence quenching techniques (R2, 15 mg/kg, restricted to the vascular space). Measurements were made under normotensive (N; mean arterial pressure, MAP, 97±4 mmHg) and HH (induced by arterial section, MAP, 58±3 mmHg, P < 0.05) and the PO2m profiles modeled using a multi-compartment exponential fitting with independent time delays (KaleidaGraph 3.5). RESULTS At the onset of contractions, HH 1) significantly decreased resting PO2m, 2) reduced the time delay (N, 12.1±1.8; H, 5.7±0.9 s, P < 0.05) prior to the fall in PO2m, 3) tended to accelerate the rate of PO2m decrease (time constant, N, 12.8±1.6; H, 7.8±1.7 s, P> 0.05), and 4) significantly decreased the mean response time (i.e., time constant + delay, N, 24.8±2.0; H, 13.5±2.3 s, P < 0.05.). CONCLUSION These results demonstrate that hypovolemic hypotension constrains the increase of QO2 to skeletal muscle at the onset of contractions leading to a decreased PO2m which will decrease blood-myocyte O2 flux thereby reducing VO2 and exacerbating the O2 deficit generated at exercise onset. Supported by NIH Grants HL 50306, AG 19228, Merck-Merial foundation NIH training grant T35RR07064, and P20RR16475 from the BRIN program of the National Center for Research Resources.

Response by the corpuscles of Stannius to hypotensive stimuli in three divergent ray-finned fishes ( Amia calva, Anguilla rostrata, and Catastomus commersoni): cardiovascular and morphological changes

In accordance with their vital role in cardiovascular physiology ( Butler and Zhang, 2001) corpuscles of Stannius (CS) from two teleosts and an holostean species showed marked and consistent degranulation and exocytotic responses to hypotensive stimuli. In eels ( Anguilla rostrata LeSueur) acute blood withdrawal (hypovolemic hypotension) was followed by a prompt decrease in cardiac output (CO) and dorsal aortic pressure ( P DA), a compensatory tachycardic response and an increase in systemic vascular resistance ( R SYS). Isovolemic hypotension induced by papaverine i.v, led to a similar, but more prolonged, decrease in P DA but the heart rate (HR) continued to accelerate, thereby counterbalancing the severe and persistent decrease in R SYS. Both hypovolemic and isovolemic hypotension were followed by a significant depletion of cytoplasmic granules from eel CS even though plasma concentrations of Ca, Mg, Na +, and K + were normal. In an ancient holostean fish, the bowfin, Amia calva and a generalized teleost fish, Catastomus commersoni, the number of cytoplasmic granules decreased by 39% and 54%, respectively, 120 min after the acute withdrawal of 8 ml kg bw −1 of blood. These findings suggest that a primary role of the CS is to release cytoplasmic granules containing renin or isorenin into the blood circulation, in response to hypotension and/or hypovolemia.

Calpain Activity in the Rat Brain after Transient Forebrain Ischemia

Activity of the Ca2+-dependent protease calpain is increased in neurons after global and focal brain ischemia, and may contribute to postischemic injury cascades. Understanding the time course and location of calpain activity in the post-ischemic brain is essential to establishing causality and optimizing therapeutic interventions. This study examined the temporal and spatial characteristics of brain calpain activity after transient forebrain ischemia (TFI) in rats. Male Long Evans rats underwent 10 min of normothermic TFI induced by bilateral carotid occlusion with hypovolemic hypotension (MABP 30 mm Hg). Brain calpain activitywas examined between 1 and 72 h after reperfusion. Western blot analysis of regional brain homogenates demonstrated a bimodal pattern of calpain-mediated α-spectrin degradation in the hippocampus, cortex, and striatum with an initial increase at 1 h followed by a more prominent secondary increase at 36 h after reperfusion. Immunohistochemical analysis revealed that calpain activity was primarily localized to dendritic fields of selectively vulnerable neurons at one hour after reperfusion. Between 24 and 48 h after reperfusion neuronal calpain activity progressed from the dorsal to ventral striatum, medial to lateral CA1 hippocampus, and centripetally expanded from watershed foci in the cerebral cortex. This progression was associated with fragmentation of dendritic processes, calpain activation in the neuronal soma and subsequent neuronal degeneration. These observations demonstrate a clear association between calpain activation and subsequent delayed neuronal death and suggest broad therapeutic window for interventions aimed at preventing delayed intracellular Ca2+ overload and pathologic calpain activation.

Staphylococcus aureus induces release of bradykinin in human plasma.

Staphylococcus aureus is a prominent human pathogen. Here we report that intact S. aureus bacteria activate the contact system in human plasma in vitro, resulting in a massive release of the potent proinflammatory and vasoactive peptide bradykinin. In contrast, no such effect was recorded with Streptococcus pneumoniae. In the activation of the contact system, blood coagulation factor XII and plasma kallikrein play central roles, and a specific inhibitor of these serine proteinases inhibited the release of bradykinin by S. aureus in human plasma. Furthermore, fragments of the cofactor H-kininogen of the contact system efficiently blocked bradykinin release. The results suggest that activation of the contact system at the surface of S. aureus and the subsequent release of bradykinin could contribute to the hypovolemic hypotension seen in patients with severe S. aureus sepsis. The data also suggest that the contact system could be used as a target in the treatment of S. aureus infections.

Can initial distribution volume of glucose predict hypovolemic hypotension after radical surgery for esophageal cancer?

We recently reported that the initial distribution volume of glucose (IDVG) reliably measures the central extracellular fluid volume in the presence or absence of fluid gain or loss. We examined which variables, including IDVG, can predict subsequent hypovolemic hypotension produced by the continuous shift of the extracellular fluid from the central to the peripheral compartment early after radical surgery for esophageal cancer. IDVG and plasma volume were calculated after measuring cardiac index (CI), central venous pressure, and pulmonary artery wedge pressure immediately after admission to the intensive care unit. Intraoperative fluid balance and urine volume were also recorded. Postoperative hypovolemic hypotension was clinically defined as systolic blood pressure < 80 mm Hg responsive to IV fluid administration. Either IDVG < 105 mL/kg or CI < 3.4 L. min(-1). m(-2) was associated with subsequent hypovolemic hypotension (P = 0.002 for the former and P = 0.00 03 for the latter), while remaining variables were not. IDVG and CI were well correlated (r = 0.8 7, n = 25, P = 0.0001). Our results suggest that IDVG can help predict the subsequent hypovolemic hypotension early after radical surgery for esophageal cancer. Routine cardiovascular variables immediately after major surgery cannot predict the subsequent hypovolemic hypotension produced by the shift of the extracellular fluid. Glucose dilution using glucose 5 g and a one-compartment model can predict it simply and rapidly.

Immunomorphological sequelae of severe brain injury induced by fluid-percussion in juvenile pigs--effects of mild hypothermia.

Severe traumatic brain injury (TBI) often leads to a bad outcome with considerable neurological deficits. Secondary brain injuries due to a rise of intracranial pressure (ICP) and global hypoxia-ischemia are critical and may be reduced in extent by mild hypothermia. A porcine animal model was used to study the effect of severe TBI, induced by fluid percussion (FP; 3.5+/-0.3 atm) in combination with a secondary insult, i.e., temporary blood loss with hypovolemic hypotension. Six-week-old juvenile pigs were subjected to this kind of severe TBI; one group was then submitted to moderate hypothermia at 32 degrees C for 6 h, starting 1 h after brain injury. Animals were killed after 24 h. TBI and hypothermia-associated alterations in the brains were investigated by immunohistochemistry with antibodies against microtubule-associated protein 2 (MAP-2) and beta-amyloid precursor protein (betaAPP). In addition, DNA fragmentation was investigated by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method. Seven of the 13 normothermic TBI animals developed a secondary increase in ICP (TBI-NT-ICP) after an interval of several hours. None of the animals in the hypothermic trauma (TBI-HT) group exhibited a secondary ICP increase, indicating a protective effect of the treatment. TBI-HT animals showed significantly higher levels of MAP-2 immunoreactivity, lower levels of betaAPP immunoreactivity and less DNA fragmentation than the TBI-NT-ICP animals. Differences between the TBI-HT group and normothermic animals without an ICP increase (TBI-NT) were less marked. A considerable decrease in MAP-2 outside the site of TBI-FP administration was seen only in the TBI-NT-ICP animals. MAP-2 immunohistochemistry was thus a reliable marker of diffuse brain damage. Axonal injury was present in all TBI groups, indicating its special significance in neurotrauma. Thus, severe TBI caused by FP, combined with temporary blood loss, consistently produced traumatic axonal injury and focal brain damage. Mild hypothermia was able to prevent a secondary increase in ICP and its sequelae of diffuse hypoxic-ischemic brain injury. However, hypothermia did not afford protection from traumatic axonal injury.

Dry weight in hemodialysis: Volemic control

In dialysis patients the chronic fluid overload may represent a nonphysiologic condition which brings both arterial hypertension and hemodynamic instability. Volume expansion is significantly correlated to casual predialysis blood pressure and 24-hour arterial pressure. The normalization of the patient hydration status is not only followed by a reduction in pressure values but also by an improvement of the circadian blood pressure rhythm. On the other hand, hypovolemia and underhydration combined with an impaired cardiovascular regulatory response may generate the dialysis-related hypotension. Many techniques have been introduced to obtain an objective measurement of the hydration status: postdialysis radiological chest examination, plasma atrial natriuretic peptide (ANP), and plasma cyclic guanidine monophosphate (cGMP) levels, multifrequency electrical bioimpedance and the continuous plasma volume measurement. The latter, alone or in combination with provocative tests (stop and go of the ultrafiltration), may help in optimizing plasma volume contraction. The plasma volume monitoring avoids the risk of hypovolemic hypotension and facilitates the achievement of a correct dry body weight. The biofeedback system, exploiting the automatic control of the intradialytic variations, may represent an additional advantage in the formulation of an ideal postdialysis blood volume that overlaps the patient's dry weight.

Usefulness of Maalox for Detection of the Precise Bleeding Points and Confirmation of Hemostasis on Gastrointestinal Hemorrhage

For endoscopists, gastrointestinal hemorrhage is one of the major occurrences encountered in general practice as a life-threatening emergency. The first goal is to stop the bleeding endoscopically without surgical treatment [1], because hypovolemic hypotension and delay in hemostasis increase the surgical risk and adversely affect the patient9s survival [2].

Transient intrauterine hypotension: effect on newborn rat brain.

Intrauterine perfusion failure can cause cerebral malformations. We investigated the effect of transient maternal hypotension on newborn rat brain by inducing hypovolemic hypotension for 2.5 h during early embryonic day 7 (E7) or late (E15) gestation in pregnant rats. We found an increase in the number of TUNEL-positive cells within the periventricular germinative matrix in pups subjected to early gestational hypotension and within the cerebral cortex in those subjected to late gestational hypotension in comparison to sham control animals. These results suggest that episodic maternal hypovolemic hypotension may affect the fetal brain, and apoptotic mechanisms may mediate this effect.

Electrocortical brain activity, cerebral haemodynamics and oxygenation during progressive hypotension in newborn piglets

Objective: To investigate the relationships between systemic and cerebral haemodynamics and oxygenation, and electroencephalogram (EEG) amplitude and frequency analysis studied by the cerebral function analyzing monitor (CFAM) during progressive hypovolemic hypotension. Methods: Six piglets of 1 week of age, weighing 1.9–3.4 kg were mechanically ventilated under 1–1.5% halothane anaesthesia. After 1 h stabilization, blood was withdrawn in aliquots of 10 ml/kg over 15 min up to a total of 40–60 ml/kg. Arterial oxygenation was maintained at normal levels. Thereafter, the total blood volume previously withdrawn, was reinfused. Changes in near infrared spectroscopy (NIRS) parameters [cerebral oxidized cytochrome aa3 (Cytaa3), cerebral blood volume (CBV) or total haemoglobin (tHb: oxy- + deoxyhaemoglobin)], carotid blood flow (Q car), maximal EEG amplitude and EEG frequency percentages were analyzed continuously. Results: The EEG amplitude remained stable until the mean arterial blood pressure (MAP), Q car and tHb dropped below 30 mmHg (41% of baseline), 20 ml/min (33% of baseline) and 82% of baseline, respectively. Delta (δ) wave frequency percentage of the CFAM increased significantly at MAP below 30 mmHg. EEG amplitude remained depressed after blood reinfusion and haemodynamic recovery. Cytaa3 changes were not statistically significant, reflecting sufficient neuronal oxygenation. Conclusion: Our results show that electrocortical function is affected only by profound systemic hypotension. This occurred at a higher level of cerebral oxygen delivery than the level associated with neuronal hypoxia and secondary cell damage.

Evidence for a Sustained Inflammatory Response of the Hepatic Microcirculation after Hemorrhagic Shock

Defined microcirculatory disturbances have been demonstrated during the first hours after hemorrhagic shock involving complex pathophysiological mechanisms. Since clinical complications associated with the inflammatory reaction that accompanies shock and resuscitation become apparent within days, our aim was to establish an experimental model of hemorrhagic shock which simulates this clinical situation. Therefore, a nonlethal rat model was developed allowing for the investigation of the hepatic microcirculation by intravital microscopy up to 4 days after hermorrhagic shock. Anesthetized Sprague-Dawley rats were subjected to hemorrhagic hyptension by blood withdrawal reducing MAP (mean arterial blood pressure) to 40 mm Hg. After 60 min of hypovolemic hypotension, the animals were resuscitated. After 1, 2, 3, or 4 days, sinusoidal perfusion pattern and leukocyte adhesion characteristics were investigated using intravital fluorescence microscopy. In separate, but parallel experiments, the time course of TNFα (tumor necrosis factor α) and ICAM-1 (intercellular adhesion molecule-1) mRNA expressio was examined in enriched parenchymal and non-parenchymal liver cell fractions by Northern blot hybridization. At day 1, sinusoidal narrowing as seen in previous experiments a few hours after shock was not observed but occurred at days 2 and 3 after shock. Permanent adhesion of leukocytes to the sinusoidal endothelium reached a maximum at day 2 after shock and remained significantly increased until day 4 compared with controls. An early TNFα mRNA accumulation was observed in shock animals but not in sham operated controls. In contrast, a sustained expression of ICAM-1 and prolonged accumulation of white blood cells were observed. The data reflect an early transient TNFα mRNA response and a sustained inflammatory reaction associated with shock and resuscitation. The inflammatory pathological alteration of the hepatic microcirculation after hemorrhagic shock are paralleled by a sustained disturbance of the sinusoidal flow patterns.

Regulation of blood pressure in chronic renal failure: determinants of hypertension and dialysis-related hypotension

Regulation of blood pressure is of crucial importance in the management of patients with chronic renal failure. in the predialysis phase, hypertension is common. Apart from volume overload and an inappropriately activated renin-angiotensin system, overactivity of the sympathetic nervous system appears to play a role as well. Sympathetic outflow may be enhanced by elevated Angiotensin II levels. Maintenance treatment with angiotensin converting enzyme inhibition normalizes sympathetic overactivity in hypertensive patients with chronic renal failure. In view of the unfavourable role of increased sympathetic activity in cardiovascular disease and prognosis, normalization of sympathetic outflow may be a new treatment goal.Hemodialysis is often complicated by sudden hypotension, causing considerable distress and morbidity. Reduction of blood volume causes sympatho-excitation, vasoconstriction and tachycardia. Sudden hypotension, however, is accompanied by acute withdrawal of sympathetic activity, vasodilation and relative bradycardia, also known as the Bezold-Jarisch reflex. Subtle fluctuations in vasomotor tone in hypovolemic conditions can elicit this reflex. In a series of experiments we showed that reduction of blood volume plays a pivotal role in the pathogenesis of hypovolemic hypotension. Autonomic neuropathy and dysfunction of the central opioid system have been proposed as causative mechanisms in dialysis-related hypotension. We, however, could not confirm a pathogenetic role for either mechanism.

Pulmonary care of the critically ill

Summary In managing the patient requiring ventilatory support, the clinician must exercise vigilance to avoid unnecessary complications. The most obvious of these include barotrauma (pneumothorax, subcutaneous emphysema), hypovolemic hypotension, pneumonia, hypoventilation, and atelectasis. However, the clinician also must be concerned with more subtle, but nonetheless significant factors, such as oxygen toxicity and volutrauma, that may aggravate underlying lung injury. Additionally, the development of unrecognized dynamic hyperinflation, or auto-PEEP, may compromise the clinician's ability to allow adequate exhalation in the patient receiving mechanical ventilatory support. For these reasons, communication between the physician and the respiratory therapy and nursing personnel who provide care for the mechanically ventilated patient is essential. Attention to the patient's plateau airway pressure, inspired oxygen concentration, and flow mechanics is as necessary to the care of the patient as vital signs, physical examination, and chest roentgenograms.

Cerebral vasoconstriction during sustained ventricular tachycardia induces an ischemic stress response of brain tissue in rats.

Arterial hypotension can cause cerebral ischemia when the autoregulation of the cerebral circulation is exhausted. We hypothesized that sudden cerebral vasoconstriction induced by moderate hypotensive, but hemodynamically stable, sustained ventricular tachycardias (MHT-VT) further compromises cerebral blood flow (CBF) and induces an ischemic stress response of the brain. CBF-measurements and morphological studies were performed without and with blockade of alpha-adrenergic receptors in order to determine the impact of MHT-VF on brain perfusion and brain tissue. Using a model of MHT-VT, CBF was measured with colored microspheres in 71 rats during control conditions. after the onset of MHT-VT, after the onset of moderate hypotensive hypovolemia (MHH), and after additional non- selective (alpha-blockade with phentolamine and selective alpha1-blockade with prazosin, respectively (0.2-0.4 mg/kg body weight). Plasma catecholamine concentrations were measured in 18 additional rats during control conditions. during MHT-VT and during MHH. The occurrence of heat shock protein (hsp) 72 and activated microglia in the brain was analysed in 18 additional rats in controls, after MHT-VT and MHH. After 20 min of the respective induced hypotension, control conditions were restored for a period of 8 h, by stopping VT or by infusion of isotonic saline solution. CBF was 0.98+/-0.16 (mean+/-S.D.) ml/g/min during control conditions at an arterial pressure of 118+/-13 mmHg, 0.50+/-0.05 ml/g/min (P<0.05 v control) during MHT-VT (76+/-4 mm Hg) and 0.75+/-0.14 ml/g/min (P<0.05 v control and v MHT-VT ) during MHH (71 +/- 8 mm Hg). CBF was better preserved with non-selective alpha-blockade during MHT-VT (0.78+/-0.15 ml/g/min, P<0.05 v MHT-VT and control) as well as with selective alpha1-blockade (0.67+/-0.08 ml/g/min, P<0.05 v MHT-VT and control). Plasma catecholamines were elevated during MHT-VT (P<0.05 v control) but not during MHH (P = N.S. v control). hsp 72 and activated microglia were found in hippocampal regions only after MHT-VT (P<0.05 v control and MHH). These morphological changes were prevented by non-selective alpha-blockade. Stable sustained MHT-VT further reduce the already compromised CBF leading to morphological alterations in the brain which are characteristic of an early ischemic stress response. alpha-Blockade prevents alpha1-adrenergic vasoconstriction and attenuates cerebral hypoperfusion.

Hemodynamic sequelae of ventricular tachyarrhythmias on cerebral blood flow

The present experiments were designed to compare the behavior of cerebral blood flow (CBF) during acute moderate and severe hypotensive episodes induced by either ventricular tachycardias (VT) or by hemorrhage. Using the microsphere method CBF was determined in 20 Sprague-Dawley rats during sinus rhythm (Group A), in 28 animals during high-rate VT (Group B) and in 10 animals after hemorrhage (Group C). According to the decrease in blood pressure and with respect to the lower threshold of cerebral autoregulation Group B was divided into subgroups (B1: 80-130 mmHg; B2: 50-80 mmHg) retrospectively. While CBF remaIned constant In Group B1 (0.98 ± 0.3 ml g-1 min-1 vs. 1.01 ± 0.32 In controls, NS), CBF decreased markedly during severely hypotensive VT in Group B2 (0.52 ± 0.2 ml g-1 min-1, p < 0.001 vs. A; p < 0.05 vs. C) and during hypovolemic hypotension in Group C (0.77 ± 0.22 ml g-1 min-1 vs. A; NS). Cerebrovascular resistance and autoregulation indices indicated a maintenance of CBF regulation during hypovolemic hypotension and a failure during normovolemic hypotension. These findings indicate that the autoregulatory ability of the brain is substantially more stable during hypovolemic hypotension than during normovolemic hypotension. Therefore, the hemodynamic sequelae of acute hypotensive episodes on CBF depend on the underlying cause of hypotension. [Neural Res 1998; 20: 549-554]

Use and misuse of albumin infusions in neonatal care.

During the neonatal period, albumin infusions are administered in response to a variety of clinical scenarios. Review of currently available literature, however, demonstrates that crystalloid rather than colloid infusions should be used both to treat hypovolaemic hypotension and as the replacement fluid in a dilutional exchange. The role of an albumin infusion in "treating" metabolic acidosis needs further evaluation, but the practice of giving albumin to correct "asymptomatic" hypoalbuminaemia or at resuscitation should be discouraged. The neonatologist would be well advised, when reaching for an albumin infusion, to reflect that there may be a safer, certainly cheaper and equally effective alternative.

Correction of hypovolemic hypotension by centrally administered naloxone in conscious rabbits

Our goal was to test directly whether the vasoconstrictor action of naloxone during hypovolemic hypotension is centrally mediated. In eight chronically instrumented rabbits, progressive central hypovolemia and fall in cardiac output (CO) were produced by gradually inflating a cuff on the thoracic vena cava. Central hypovolemia was then sustained for 8 min by holding CO constant. In the main experiment (n = 4), each rabbit was studied eight times over 4 experimental days. Saline or naloxone treatment commenced 10 min before progressive hypovolemia (early treatment) or 2 min after the onset of sustained hypovolemia (late treatment), given by intravenous infusion or into the fourth ventricle (V4). With saline treatment, there was spontaneous recovery of systemic vasoconstriction and arterial pressure during sustained hypovolemia. Late treatment with naloxone (4 mg/kg i.v.; 4-37 micrograms/kg V4) accelerated and exaggerated these changes. Thus, under conditions of constant CO and central blood volume, the vasodilatation of the decompensatory phase of acute hypovolemia is not sustained, and intravenous nalox one's vasoconstrictor action is via a brain stem mechanism.