Redistribution Of Regional Blood Flow Research Articles

Regional redistribution of blood flow in the external and internal carotid arteries during acute hypotension

The present study examined to what extent an acute bout of hypotension influences blood flow in the external carotid artery (ECA) and the corresponding implications for blood flow regulation in the internal carotid artery (ICA). Nine healthy male participants were subjected to an abrupt decrease in arterial pressure via the thigh-cuff inflation-deflation technique. Duplex ultrasound was employed to measure beat-to-beat ECA and ICA blood flow. Compared with the baseline normotensive control, acute hypotension resulted in a heterogeneous blood flow response. ICA blood flow initially decreased following cuff release and then returned quickly to baseline levels. In contrast, the reduction in ECA blood flow persisted for 30 s following cuff release. Thus, the contribution of common carotid artery blood flow to the ECA circulation decreased during acute hypotension (-10 ± 4%, P < 0.001). This finding suggests that a preserved reduction in ECA blood flow, as well as dynamic cerebral autoregulation likely prevent a further decrease in intracranial blood flow during acute hypotension. The peripheral vasculature of the ECA may, thus, be considered an important vascular bed for intracranial cerebral blood flow regulation.

Gastrointestinal Perfusion in Septic Shock

Septic shock is characterised by vasodilation, myocardial depression and impaired microcirculatory blood flow, resulting in redistribution of regional blood flow. Animal and human studies have shown that gastrointestinal mucosal blood flow is impaired in septic shock. This is consistent with abnormalities found in many other microcirculatory vascular beds. Gastrointestinal mucosal microcirculatory perfusion deficits have been associated with gut injury and a decrease in gut barrier function, possibly causing augmentation of systemic inflammation and distant organ dysfunction. A range of techniques have been developed and used to quantify these gastrointestinal perfusion abnormalities. The following techniques have been used to study gastrointestinal perfusion in humans: tonometry, laser Doppler flowmetry, reflectance spectrophotometry, near-infrared spectroscopy, orthogonal polarisation spectral imaging, indocyanine green clearance, hepatic vein catheterisation and measurements of plasma D-lactate. Although these methods share the ability to predict outcome in septic shock patients, it is important to emphasise that the measurement results are not interchangeable. Different techniques measure different elements of gastrointestinal perfusion. Gastric tonometry is currently the most widely used technique because of its non-invasiveness and ease of use. Despite all the recent advances, the usefulness of gastrointestinal perfusion parameters in clinical decision-making is still limited. Treatment strategies specifically aimed at improving gastrointestinal perfuision have failed to actually correct mucosal perfusion abnormalities and hence not shown to improve important clinical endpoints. Current and future treatment strategies for septic shock should be tested for their effects on gastrointestinal perfusion; to further clarify its exact role in patient management, and to prevent therapies detrimental to gastrointestinal perfusion being implemented.

Trauma: physiology, pathophysiology, and clinical implications

AbstractObjective: To review the physiology, pathophysiology, and consequences of trauma. The therapeutic implications of hypovolemia, hypotension, hypothermia, tissue blood flow, oxygen delivery, and pain will be discussed.Data Sources: Human and veterinary clinical and research studies.Human and veterinary data synthesis: Trauma is defined as tissue injury that occurs more or less suddenly as a result of violence or accident and is responsible for initiating hyothalamic–pituitary–adrenal axis, immunologic and metabolic responses that are designed to restore homeostasis. Tissue injury, hemorrhage, pain, and fear are key components of any traumatic event. Trauma and blood loss result in centrally integrated autonomic‐mediated cardiovascular responses that are designed to increase heart rate, systemic vascular resistance, and maintain arterial blood pressure (ABP) to vital organs at the expense of blood flow to the gut and skeletal muscle. Severe trauma elicits exuberant physiologic, immunologic, and metabolic changes predisposing the animal to organ malfunction, a systemic inflammatory response, infection, and multiple organ dysfunctions. The combination of both central and local influences produces regional redistribution of blood flow among and within tissue beds which, when combined with impaired vascular reactivity, leads to maldistribution of blood flow to tissues predisposing to tissue hypoperfusion and impaired oxygen delivery and extraction. Gut blood flow and viability may serve as a sentinel of patient survival. These consequences are magnified in animals suffering from pain or that become hypothermic. Successful treatment of traumatized animals goes beyond the restoration of blood pressure and urine output, is dependent on a fundamental understanding of the pathophysiologic processes responsible for the animals current physical status, and incorporates the reduction of pain, stress, and the systemic inflammatory response and methods that restore microcirculatory blood flow and tissue oxygenation.Conclusions: Severe trauma is a multifaceted event and is exacerbated by hypothermia, pain, and stress. Therapeutic approaches must go beyond the simple restoration of vascular volume and ABP by maintaining tissue blood flow, restoring tissue oxygenation, and preventing systemic inflammation.

Regional blood flow during hyperoxic haemodilution

Ventilation with pure oxygen (hyperoxic ventilation, HV) increases arterial oxygen content (CaO(2)). However HV induces arteriolar constriction and thus potentially affects O(2) supply. We therefore investigated the effects of HV on regional blood flow (RBF) and O(2) supply of different vital organs during moderate normovolaemic anaemia. Twenty-two anaesthetized dogs were haemodiluted under normoxia (i.e. FiO(2) = 0.21) to a target haemoglobin concentration (Hb) of 7 g dl(-1) and were subsequently ventilated with pure O(2). RBF was determined by use of the radioactive microspheres method in the myocardium, kidney, skeletal muscle, liver, intestine, stomach, and pancreas at Hb = 7 g dl(-1) and after subsequent initiation of HV. RBF in proportion to cardiac output (RBF(relative)), the variation coefficient of RBF (VC) and regional O(2) supply (rDO(2)) were calculated. Initiation of HV at Hb = 7.0 +/- 0.3 g dl(-1) reduced cardiac index (-17%) as well as RBF within the myocardium (-21%), pancreas (-25%), and skeletal muscle (-25%), whereas renal, hepatic, and intestinal RBF remained unchanged. Consequently RBF(relative) of the latter organs increased. Heterogeneity of RBF was marginally affected by HV. The initiation of HV during moderate normovolaemic anaemia (Hb =7 g dl(-1)) was accompanied by RBF redistribution with preference for renal, hepatic and intestinal O(2) supply. Cardiac, pancreatic and muscular O(2) supply decreased, however without any critical restriction of organ function.

Muscle metaboreflex is blunted with reduced vascular resistance response of nonexercised limb in patients with chronic heart failure

Background Exercise-mediated muscle metaboreflex (MMR) activates the sympathetic nervous system afferently and may play an important role in the reduction in blood flow in nonexercised limb, thus enhancing exercised skeletal muscle blood flow (ie, normal regional blood flow redistribution during exercise). However, few data are available to describe the relationship between MMR and peripheral vascular control during exercise in congestive heart failure (CHF). The aim of this study was to determine whether MMR is impaired in CHF, and, if so, whether MMR is related to clinical severity of CHF and to changes in nonexercised limb vascular resistance in CHF. Methods and results Eleven CHF patients and 9 healthy age- and gender-matched controls were examined. All subjects performed a rhythmic handgrip exercise test at 50% of maximal voluntary contraction for 3 minutes on 2 occasions with and without postexercise upper arm regional circulatory occlusion (RCO/non-RCO). Changes in systolic blood pressure were measured and plotted against protocol time for both RCO and non-RCO. The area under each curve was estimated, and the calculating difference in the area between RCO and non-RCO was regarded as MMR. In addition, changes in calf vascular resistance were measured continuously by plethysmography after the handgrip test and the area differences between the RCO and non-RCO data was taken to represent MMR-provoked resistance changes in the nonexercised limb. During the handgrip exercise, systolic blood pressure increased similarly on the 2 occasions for both groups. MMR was significantly lower in CHF patients than in controls (68.2 ± 23.1 versus 160.4 ± 29.6 arbitrary units; P < .05). Decrease in MMR activity was related to clinical severity of CHF (controls, 160.4 ± 29.6; New York Heart Association class II, 87.6 ± 29.8; New York Heart Association class III, 34.3 ± 34.8 arbitrary units; P < .05). The increase in calf vascular resistance between RCO and non-RCO protocols in the control group was significant (+146.5 ± 38.0 arbitrary units; P < .05), whereas the difference in the CHF group was not significant (−72.9 ± 126.9 arbitrary units; not significant). Conclusions Exercise-induced MMR control in mild to moderate CHF is impaired in association with a blunted increase in nonexercised limb vascular resistance. This suggests that blunted MMR activity impairs regional blood flow redistribution and may contribute in part to exercise intolerance in this disorder.

Prenatal Hemodynamic Disturbances - Pathophysiological Background of Intestinal Motility Disturbances in Small for Gestational Age Infants

Uteroplacental insufficiency leads to fetal growth retardation which is a major cause of perinatal and postnatal morbidity. In the present study we investigated the relationship between prenatal hemodynamic disturbances and postnatal intestinal perfusion and gastrointestinal function in small for gestational age neonates. Prospectively, 124 preterm neonates with a birth weight below 1500 g were assigned to one of two groups according to the prenatal Doppler sonographic measurements: neonates with or without prenatal hemodynamic disturbances. We defined a pathological fetal perfusion using a pulsatility index of uterine arteries, umbilical artery and fetal thoracic aorta above the 90th percentile and a pulsatility index of the middle cerebral artery below the 10th percentile of a normal group. We compared intestinal adaptation in both groups as well as the blood flow velocity wave forms of the superior mesenteric artery in all neonates. Postnatally, all 42 neonates with prenatal hemodynamic disturbances were classified to be small for gestational age. Thirty-seven of these neonates developed abdominal problems with delayed meconium passage, abdominal distension, bilious vomiting and a delay in tolerating enteral feeding within the first days of life. Five of them needed surgical intervention, but none of these infants revealed typical signs of necrotizing enterocolitis. In contrast, all neonates born after normal prenatal perfusion were classified as appropriate for gestational age. Only 19 of 82 neonates of this group showed signs of intestinal disturbances postnatally. Doppler sonography demonstrated significantly lower systolic, mean and END-diastolic flow velocities, and higher pulsatility indices of the superior mesenteric artery in neonates with prenatal hemodynamic disturbances. This may occur as a result of a postnatally persistent redistribution of regional blood flow and results in gastrointestinal problems and may adversely affect gut motility.

Effects of milrinone on hemodynamics and regional blood flow in the hypoxic dog.

Milrinone, a therapeutic agent for acute congestive heart failure, has both inotropic and vasodilatory effects, but investigations of these effects of milrinone were almost all conducted under normoxia, and few reports have investigated how milrinone affects the hemodynamics and redistribution of regional blood flow under severe hypoxia. By using colored microspheres, we investigated how milrinone affects hemodynamics and the redistribution of regional blood flow under severe hypoxia. Twelve healthy mongrel dogs were divided into 2 groups. The milrinone group was infused with milrinone cumulatively at 25, 75 and 250 microg/kg for 5 min each. The intact group was infused with saline instead of milrinone. We measured the hemodynamics and cerebrum, cerebellum and kidney blood flow in both groups. Both groups were inspired with 10% oxygen. Milrinone induced significant decrease in mean pulmonary artery and pulmonary vascular resistance, compared with the intact group. In both groups slight decreases in mean arterial pressure, systemic vascular resistance and double-product were seen. In regional blood flow, milrinone-induced increases in blood flow were seen in the cerebrum, cerebellum, and especially in the kidneys. Milrinone's vasodilatory effects were sufficient even under hypoxia. And milrinone increased regional blood flow slightly in the cerebrum and cerebellum, and significantly in the kidneys. These results suggested that milrinone protects against hypoxia-induced organ damage especially in the kidneys. In addition, milrinone is very potent in improving severe congested hemodynamics which complicates hypoxic pulmonary vasoconstriction.

Beneficial haemodynamic effects of insulin in chronic heart failure

OBJECTIVETo characterise the central and regional haemodynamic effects of insulin in patients with chronic heart failure.DESIGNSingle blind, placebo controlled study.SETTINGUniversity teaching hospital.PATIENTSTen patients with stable chronic heart failure.INTERVENTIONSHyperinsulinaemic euglycaemic clamp and non-invasive haemodynamic measurements.MAIN OUTCOME MEASURESChange in resting heart rate, blood pressure, cardiac output, and regional splanchnic and skeletal muscle blood flow.RESULTSInsulin infusion led to a dose dependent increase in skeletal muscle blood flow of 0.36 (0.13) and 0.73 (0.14) ml/dl/min during low and high dose insulin infusions (p &lt; 0.05 and p &lt; 0.005 v placebo, respectively). Low and high dose insulin infusions led to a fall in heart rate of 4.6 (1.4) and 5.1 (1.3) beats/min (p &lt; 0.05 and p &lt; 0.005 v placebo, respectively) and a modest increase in cardiac output. There was no significant change in superior mesenteric artery blood flow.CONCLUSIONIn patients with chronic heart failure insulin is a selective skeletal muscle vasodilator that leads to increased muscle perfusion primarily through redistribution of regional blood flow rather than by increased cardiac output. These results provide a rational haemodynamic explanation for the apparent beneficial effects of insulin infusion in the setting of heart failure.

Liquid ventilation.

Partial liquid ventilation (PLV) developed considerably in the clinical and experimental fields during the past few years. In addition to improved oxygenation and lung mechanics by perfluorocarbon (PFC) administration, recent animal studies have tried to optimize PLV by evaluating the most appropriate ventilatory mode to use during PLV and by adjusting the best level of positive end-expiratory pressure (PEEP). Other pathophysiological aspects of acute lung injury that may be positively affected by liquid ventilation have been studied, including regional blood flow redistribution, reduction in ventilator-induced lung injury, and antiinflammatory properties of PFC. Although the precise dosing of PFC is debated, evidence from several experimental studies supports the use of smaller doses of PFC because larger doses increase the occurrence of baro- and volutrauma. In the clinical field, after promising data from preliminary studies, an international randomized controlled trial is on the verge of completion.

Postnatal intestinal disturbances in small‐for‐gestational‐age premature infants after prenatal haemodynamic disturbances

Uteroplacental insufficiency leads to fetal growth retardation, which is a major cause of perinatal and postnatal morbidity. In the present study we investigated the relationship between prenatal haemodynamic disturbances and postnatal intestinal perfusion and gastrointestinal function in small-for-gestational-age neonates. Prospectively, 114 preterm neonates with a birthweight below 1500 g were assigned to one of two groups according to their prenatal Doppler sonographic measurements: neonates with or without prenatal haemodynamic disturbances. We defined a pathological fetal perfusion by a pulsatility index of uterine arteries, umbilical artery and fetal thoracic aorta above the 90th percentile and by a pulsatility index of middle cerebral artery below the 10th percentile of a normal group. We compared the postnatal respiratory and intestinal adaptation in both groups as well as the blood flow velocity waveforms of the superior mesenteric artery in all neonates. Postnatally, all 36 neonates with prenatal haemodynamic disturbances were classified to be small for gestational age. Thirty-one of these neonates developed abdominal problems with delayed meconium passage, abdominal distension, bilious vomiting and a delay in tolerating in enteral feeding within the first days of life. Six of them needed surgical intervention, but none of these infants revealed typical signs of necrotizing enterocolitis. In contrast, all neonates after normal prenatal perfusion were classified to be appropriate for gestational age. Only 19 of 78 neonates of this group showed signs of intestinal disturbances postnatally. By Doppler sonographic investigations we found significant lower systolic, mean and end-diastolic flow velocities and higher pulsatility indices of the superior mesenteric artery in neonates with prenatal haemodynamic disturbances. This may occur as a result of postnatal persistent redistribution of regional blood flow and results in gastrointestinal problems and may adversely affect gut motility.

Renin Angiotensin System Antagonists and Anesthesia

R enin angiotensin system (RAS) antagonists, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor antagonists are increasingly used to treat cardiovascular and other diseases (1–6). These treatments induce a blockade of the RAS that may affect hemodynamics during anesthesia and surgery. In 1978, Miller et al. (7) reported that the RAS is involved in maintaining normal blood pressure during anesthesia. Although anesthesia is not invariably associated with a deleterious hemodynamic event in RAS-blocked patients (8–10), hemodynamic instability, described as unexpected episodes of hypotension, have been reported (11–13). Otherwise, stresses such as surgery or hypotension stimulate the generation of angiotensin II, which induces vasoconstriction (14) to maintain blood pressure but reduces blood flow to organs such as the kidneys and bowels. Accordingly, an angiotensin II-induced reduction in blood flow may contribute to acute renal failure (15) and splanchnic ischemia (16), which are obvious factors in postoperative morbidity (17). RAS blockade with ACE inhibitors decreases some consequences of the stress response on the regional circulation (9,18,19), which may then contribute to body protection. Much of the information regarding the physiology and pathophysiology of the RAS during anesthesia and surgery is based on the effects of ACE inhibitors. Because ACE inhibitors probably act mostly by blocking the RAS, similar effects should be obtained from angiotensin (AT) receptor antagonists. RAS antagonist pharmacology may help us to understand the hemodynamic risk of anesthesia in RAS-blocked patients, to identify predisposing factors, and to determine the potential benefit of RAS antagonists during anesthesia and surgery. Physiology of the RAS Generation of Angiotensin II

MUSCLE OXYGENATION AND FEMORAL ARTERY FLOW DURING DYNAMIC PLANTAR FLEXION EXERCISE

1173 Purpose of the study was to investigate oxygenation patterns of m. gastrocnemius, a. tibialis and 1. soleus muscle groups and common femoral artery blood flow (Qfa) during dynamic plantar flexion exercise at different contraction frequency. Six females (21±1% y.o.) in a supine position performed a 1-min dynamic plantar flexion at 30% MVC (40, 60, 80 cpm) alternated with a 15-min recovery. Then they exercised (60 cpm) until exhaustion. Qfa in the dominant leg was measured by Doppler ultrasound (HP Sonos 1000). Muscle oxygenation (mSO2) was measured by a near-infrared photometer based on spatially resolved method (OM-100AS, Shimadzu). Qfa almost doubled after the onset of exercise reaching a plateau within 30 s independently of contraction frequency. L. soleus and a. tibialis mSO2 sligthly decreased only at 80 cpm. Whilst m. gastrocnemius mSO2 reached its minimum value since the beginning of exercise at 40 cpm (from 71±3 to 29±8 at 40 cpm; from 72±2 to 29±9 at 60 cpm; from 73±2 to 29±8 at 80 cpm). At 60 cpm Qfa progressively increased throughout the duration of exhaustive exercise, whilst m. gastrocnemius mSO2 dropped at the onset of exercise and gradually recovered during the last part of exercise. These data suggest that oxygenation pattern differs in main synergists for plantar flexion at different cpm and m. gastrocnemius mSO2 recovery during exhaustive exercise is an indirect evidence of regional blood flow redistribution in the calf muscles. Supported by CNR and JSPS Exchange Program

The New Neuropsychology of Sleep: Implications for Psychoanalysis

In his 1895 “Project for a Scientific Psychology,” Sigmund Freud clearly stated his goal: to integrate the workings of the mind with the workings of the brain. But in his day, too little neurobiology was known to make his goal attainable and he tried instead to understand such fascinating normal phenomena as dreaming in exclusively psychodynamic terms. A century later, Freud’s brilliant but entirely speculative dream theory is in need of radical revision, if not complete overhaul, because dreams, as well as other unusual states of consciousness, can finally be approached from the solid foundation of modern neuroscience. In other words, the goals of Freud’s Project are at last within our grasp. Ironically, an obstacle to progress is the tenacious adherence of orthodox psychoanalysis to a theory that even by the standards of its originator, is now clearly outmoded.In this paper, recent positron emission tomography (PET) imaging and brain lesion studies in humans are integrated with new basic research findings at the cellular level in animals to explain how the formal cognitive features of dreaming may be the combined product of a shift in the neuromodulator balance of the brain and a related redistribution of regional blood flow. The human PET data indicate a preferential activation in rapid eye movement (REM) sleep of the pontomesencephalic brainstem and of limbic and paralimbic cortical structures involved in the emotional and mnemonic aspects of cognition. The pontine brainstem mechanisms controlling the neuromodulator balance of the brain in rats and cats include noradrenergic and serotonergic influences which enhance waking and impede REM via anticholinergic mechanisms, and cholinergic mechanisms which are essential to REM sleep and only come into full play when the serotonergic and noradrenergic systems are inhibited. In REM, the brain thus becomes activated but processes its internally generated data in a manner quite different from that of waking.

Regional Myocardial Blood Flow Redistribution as a Cause of Postprandial Angina Pectoris

Postprandial angina pectoris has been recognized for more than two centuries and can be identified in up to 10% of patients with chronic ischemic heart disease. Redistribution of myocardial blood flow, from a region supplied by a severely stenotic coronary artery to those supplied by less diseased or normal vessels, is a potential mechanism of postprandial angina. To test this hypothesis, we have determined the effects of a standard liquid meal on whole heart and regional myocardial blood flow, measured by means of dynamic positron emission tomography (PET) with 15O-labeled water in 14 patients with a reproducible history of postprandial angina and 7 matched control subjects. The standard liquid meal precipitated angina pectoris in all patients. Baseline whole heart blood flow was similar and increased normally after the meal in patients (0.97+/-0.14 to 1.14+/-0.25 mL.min(-1).g(-1), P<.04) as in control subjects (0.92+/-0.12 to 1.02+/-0.13 mL.min(-1).g(-1), P<.02). In contrast, the coefficient of variation of blood flow increased significantly after the standard liquid meal in patients (34+/-9%, P<.05 versus baseline) but not in control subjects (17+/-7%, P=NS versus baseline). In patients, analysis of regional myocardial blood flow demonstrated decreased myocardial blood flow in territories supplied by stenotic arteries (1.01+/-0.35 to 0.76+/-0.27 mL.min(-1).g(-1), P<.03), but there was an increase in blood flow in territories supplied by normal arteries (0.89+/-0.16 to 1.34+/-0.25 mL.min(-1).g(-1), P<.001) after the meal. The standard liquid meal induced angina pectoris in patients with coronary artery disease. Although whole heart blood flow increased appropriately for the greater cardiac work, there was a redistribution of regional blood flow from territories supplied by severely stenosed coronary arteries to those supplied by less diseased or normal arteries. This redistribution may be the cause of myocardial ischemia in postprandial angina.

The neuropsychology of REM sleep dreaming.

Recent PET imaging and brain lesion studies in humans are integrated with new basic research findings at the cellular level in animals to explain how the formal cognitive features of dreaming may be the combined product of a shift in neuromodulatory balance of the brain and a related redistribution of regional blood flow. The human PET data indicate a preferential activation in REM of the pontine brain stem and of limbic and paralimbic cortical structures involved in mediating emotion and a corresponding deactivation of dorsolateral prefrontal cortical structures involved in the executive and mnemonic aspects of cognition. The pontine brainstem mechanisms controlling the neuromodulatory balance of the brain in rats and cats include noradrenergic and serotonergic influences which enhance waking and impede REM via anticholinergic mechanisms and cholinergic mechanisms which are essential to REM sleep and only come into full play when the serotonergic and noradrenergic systems are inhibited. In REM, the brain thus becomes activated but processes its internally generated data in a manner quite different from that of waking.

Vascular reactivity and tissue oxygenation.

When blood carries less than the normal amount of oxygen (CaO2) or when blood flow (Q) decreases, oxygen delivery (DO2 = QCaO2) is gradually reduced. Compensatory adjustments occur in an attempt to satisfy the oxygen requirements of peripheral tissues. Oxygen consumption (VO2) is maintained by increases in the oxygen extraction ratio (ERO2 = VO2/DO2), until a critical point at which VO2 falls with further declines in DO2, and tissues shift toward a chemically reduced state with elaboration of reduced substrate forms such as lactate. It has been proposed that increased ERO2 is a consequence of regulation of the circulation and the result of the simultaneous activation of both central and local factors. Central factor induces a regional redistribution of blood flow among tissues via sympathetic vasoconstrictor tone while local factor induces an increase in the density of perfused capillaries within tissues via metabolic vasodilator tone. An inability to regulate blood flow distribution, between and within tissues, could result in hyperperfusion of some tissue beds at the expense of other hypoperfused areas resulting in oxygen extraction defect.

Regional Blood Flow Redistribution in Preterm Piglets with Hemorrhage and Resuscitation

Acute hemorrhage in premature infants occurs as the result of obstetrical complications, birth trauma, or operative procedures. This study evaluates the response of the preterm piglet to acute hemorrhage and resuscitation. Piglets delivered by Caesarean section 7-14 days preterm underwent acute arterial/venous hemorrhage (20 cc/kg). At 0, 15, and 60 rain after hemorrhage, hemodynamic parameters and regional blood flows (reference organ technique) were measured. Animals were then resuscitated with shed blood (20 cc/kg), crystalloid (60 cc/kg), or colloid (dextran 40, 20 cc/kg) with study parameters obtained 30 min later (statistical analysis by ANOVA). Significant decreases in blood pressure (BP) and cardiac output (CO) occurred after hemorrhage. BP and CO were reestablished to near control levels following resuscitation with blood and crystalloid. Dextran failed to return BP to baseline; however, it resulted in CO 1.7 × control. Heart and CNS blood flow were not significantly influenced by hemorrhage; however, dextran increased flows to these organs significantly above control levels. In the kidney and small bowel, flows decreased significantly following hemorrhage; blood and crystalloid restored flows to near baseline, while dextran resulted in flows significantly greater. In summary, the preterm piglet responds to hemorrhage with maintenance of blood flow to the heart and brain and significantly decreased flows to the kidney and small intestine. Flows following resuscitation with blood and crystalloid are comparable to those in control. Dextran resuscitation resulted in flows significantly greater than baseline; this response might be detrimental with ongoing hemorrhage and/or prolonged ischemia.

Nimodipine after circulatory arrest: Effects on oxygen delivery and consumption

Purpose : Evaluation of the effects of nimodipine administration during and after cardiopulmonary resuscitation (CPR) on oxygen delivery and consumption was the aim of this study. Methods : A randomized double-blind study in 32 anesthetized domestic pigs was performed. After 5 minutes of ventricular fibrillation (VF) and 5 minutes of external CPR, epinephrine (50 μg/kg) and either nimodipine or placebo (10 μg/kg bolus, 1 μg/kg/min continuously throughout 4 hours of observation) were administered. One minute later (equal to 11 minutes VF), the first countershock was given. If this failed to restore spontaneous circulation, epinephrine and countershocks were repeated for a maximum of 30 minutes. Results : Eleven of 12 nimodipine- and 7 of 14 placebo-treated pigs could be resuscitated successfully and survived the observation period ( P < .05). Hemodynamic responses to nimodipine were characterized by significant decreases in systemic vascular resistance and mean arterial pressure from 10 minutes after restoration of spontaneous circulation onwards with consequent significant increases in cardiac output. Median systemic oxygen delivery indices (Do 2I) in nimodipine-treated pigs were significantly higher at all measuring points when compared with placebo-treated animals. Median systemic oxygen consumption indices (Vo 2I) did not differ significantly between groups. Median oxygen extraction ratios in nimodipine-treated pigs were in the same range as prearrest and were lower when compared with placebo-treated pigs (at 30 minutes P < .05 and at 120 minutes P < .01). Do 2I and Vo 2I were poorly correlated in all pigs treated with nimodipine and in 3 of 7 animals treated with placebo, suggesting supply independency in these animals. This difference between groups was significant ( P < .05). Conclusions : Our findings suggest that in nimodipine-treated animals, a lower oxygen deficit or a better redistribution of regional blood flow occurred after circulatory arrest and resuscitation.

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep.

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25-60%, whereas cardiac output increased by 15-25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

Reduced exercise capacity post cardiac transplantation: Is the mechanism reduced redistribution of regional blood flow?

Reduced exercise capacity post cardiac transplantation: Is the mechanism reduced redistribution of regional blood flow?