Predictive factors for neonatal morbidity in neonates with an umbilical arterial cord pH less than 7.00

OBJECTIVE: Fewer than 50% of neonates with an umbilical arterial pH < 7.00 have neonatal complications. Our objective was to identify clinical predictive factors for adverse outcomes in this group of neonates. STUDY DESIGN: In this case-control study both cases and controls had an umbilical arterial cord pH < 7.00. Cases were defined as those neonates who had seizures, grade 3 to 4 intraventricular hemorrhage, gastrointestinal dysfunction, respiratory distress syndrome requiring intubation, sepsis, or death. Controls had an umbilical arterial cord pH < 7.00 and no complications. A multivariable prediction model was created, with variables having an association with adverse outcome by bivariate analyses, attempting to predict which neonates in this umbilical arterial pH range are at greatest risk for adverse outcomes. RESULTS: We identified 73 of 10,705 neonates born between July 1992 and October 1996 with an umbilical arterial cord pH < 7.00. Thirty-five neonates met our case definition, and the remaining 38 composed the control group. Cases had significantly lower arterial pH values and 1- and 5-minute Apgar scores, greater arterial base deficit values, and a higher incidence of abruptio placentae and maternal cocaine use. More cases were delivered before 34 weeks. There were three neonatal deaths, two cases of grade 3 or 4 intraventricular hemorrhage, five cases of gastrointestinal dysfunction, and four cases of neonatal seizures. In our predictive model for adverse neonatal outcome, an arterial base deficit > or = 16 mmol/L and a 5-minute Apgar score < 7 had a sensitivity and a specificity of 79% and 80.8%, respectively. CONCLUSION: Neonatal morbidity in neonates with an umbilical arterial cord pH < 7.00 can be predicted by a high arterial base deficit value and low 5-minute Apgar score.     

Regulation of thrombin formation by activated protein C: effect of the factor V Leiden mutation

Recent developments in arterial hemodynamics have indicated that the human arterial pressure waveform contains more information than is available from conventional sphygmomanometry. This information includes indices describing left ventricular systolic function and arterial properties. A cheap and reliable system was designed and implemented using readily available hardware for recording, analysis, and storage of arterial pressure waveforms. The system embodies an online technique for synthesizing ascending aortic pressure waveform from recordings made at different peripheral sites of the human arterial system. Eighteen indices are then derived from arterial pressure waveforms. This system can be used in an outpatient clinic for assisting in current pharmacological management of cardiovascular disease. It can also be extended to the critical care area, where the extra information provided aid in assessing the patient's condition.     

Role of endogenous carbon monoxide in central regulation of arterial pressure

We investigated the contribution of neural mechanisms to the arterial pressure increase produced by zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), an inhibitor of endogenous carbon monoxide synthesis. The arterial baroreceptor reflex control of heart rate was examined in rats with and without ZnDPBG pretreatment (45 micromol/kg IP) by analysis of the arterial pressure-heart rate relationship during infusions of phenylephrine or sodium nitroprusside to vary arterial pressure. ZnDPBG increased arterial pressure from 110 +/- 3 to 126 +/- 2 mm Hg without eliciting bradycardia. The maximum gain of the heart rate response to changes in arterial pressure was attenuated by ZnDPBG treatment (-1.9 +/- 0.3 versus -4.8 +/- 1.0 bpm/mm Hg). The possibility that ZnDPBG elevates arterial pressure by attenuating baroreceptor reflex function was addressed by comparing the pressor response to ZnDPBG (45 micromol/kg IP) in rats with and without sinoaortic denervation. The pressor effect of ZnDPBG was similar in rats with and without arterial baroreceptor deafferentation, implying that the increase in pressure is not simply the consequence of attenuated baroreceptor reflex function per se. The possibility that ZnDPBG increases arterial pressure via an effect on the nucleus tractus solitarii (NTS) also was investigated. ZnDPBG (1 nmol in 100 nL) injected into the NTS of rats increased arterial pressure from 111 +/- 4 to 126 +/- 5 mm Hg, and this effect was reversed by an ipsilateral microinjection of carbon monoxide into the NTS. Accordingly, the pressor effect of ZnDPBG may rely on inhibition of carbon monoxide production in the NTS. This implies that carbon monoxide formed by brain heme oxygenase plays a role in the central regulation of arterial pressure.     

Anesthetic management

Experiments were performed on obligatory bipeds to study the effects of an arteriovenous fistula on a devascularized ischemic limb. Retrograde flow of arterial blood entering the venous system by way of an arteriovenous fistula was demonstrated. Venous valves appeared not to interfere with retrograde arterial flow. The data from these experiments indicate that a "Y" type arteriovenous fistula can lead to functional revascularization in the ischemic limb with arterial obstruction. The dual mechanism of retrograde arterial flow in venous channels and the stimulation of collateral flow adjacent to the fistula seemed to be critical factors. Since a peripheral arteriovenous fistula is a potent stimulus to arterial collateralization in the extremity, its application is worthy of consideration in certain selected patients with advanced and otherwise inoperable arterial occlusive disease.     

Repeated hepatic arterial infusion chemotherapy using an implanted port system in patients with unresectable malignant liver neoplasms: significant factors affecting early hepatic arterial occlusion

The purpose of this study was to identify significant factors affecting early hepatic arterial occlusion in patients who received repeated hepatic arterial infusion chemotherapy using an implanted port system. Eighty-five patients with unresectable liver neoplasms who underwent implantation of the port system were studied. Arterial infusion chemotherapy was performed every 1-4 weeks. Arterial occlusion was evaluated by hepatic arteriography performed via the port every 3 months. Twenty variables were analyzed using univariate and multivariate analyses to identify significant factors affecting early hepatic arterial occlusion. Hepatic arterial occlusion was found in 25.9% (22/85) of the patients. Thirteen of them experienced early arterial occlusion within 6 months. The mean survival period was significantly worse in patients who experienced early arterial occlusion than those who did not (16 months vs. 26 months, p<0.05). In the multivariate analysis, the following 3 variables had independent value for early arterial occlusion; i). diameter of the common hepatic artery, ii). gender, and iii). previous systemic chemotherapy. Early arterial occlusion affects therapeutic effects and survival in patients who undergo arterial infusion chemotherapy with an implanted port. Factors demonstrated here are important to classify patients at risk of early hepatic arterial occlusion.     

The correlations between the arterial and venous components of the hemodynamics and cerebrospinal fluid pressure in arterial hypotension

A total of 30 patients with arterial hypotension were examined. Rheoencephalogrammes documented hypotension of the arterial and venous constituents of the brain in one third of the above patients (in those patients with physiological hypotension it was recordable more frequently): in one forth of those cases with primary arterial hypotension presenting with the cerebral crises, moderately severe venous and arterial hypotension was generally seen. In a major proportion of the examinees, a correlation was found between the drop in arterial pressure, vascular tension of the arterial vessels of the brain and an adequate state of the venous tension and liquor pressure. Roentgenography of the skull and ophthalmoscopy do not permit forming an opinion about liquor hypertension since it was not demonstrated on the computerized tomographic scans.     

Experimental study of microarterial autografts for repair of arterial defects with significant size discrepancy

On the basis of our years of clinical experience using the "unequal bite" suturing technique to perform end-to-end anastomosis of vessel with great discrepancy in diameter, an animal experimental study was performed in which an arterial defect, 1.0 to 1.4 mm in diameter, was reunited through the autogenous arterial graft, which was 0.3 to 0.4 mm in diameter. A high patency rate (95% in total) was obtained postoperatively. A small autogenous arterial graft may be used for repairing a large-caliber arterial defect clinically.     

The significance of blood vessels on both sides of the growth plate

A new 3-D presentation of the whole vasculature of the epiphyseal growth plate clearly allows for a distinction between arterial and venous sections of the blood circulation. Histological investigations using these processing methods could neither prove the connection between epiphyseal and metaphyseal vessels through the growth plate in newborns nor the concept of an arterial epiphyseal blood supply of the growth plate presented by Trueta. It is rather a question of an arterial metaphyseal perfusion and an epiphyseal venous drainage system.     

Rat model for a vascularized laryngeal allograft

A new rat model was developed to reexamine the potential for laryngeal transplantation. The final anatomic derivation evolved from two earlier developmental phases. The first model had only a single arterial anastomosis; the second had an end-to-end arterial anastomosis with an end-to-end arteriovenous shunt. The final product employed an end-to-side arterial shunt and an end-to-side arteriovenous shunt for revascularization. The allografts were sited in tandem with the intact recipient larynges and were not innervated. A total of 16 animals were studied in phase 3; 2 died and the remaining 14 had a 64% arterial patency at intervals of 1 to 14 days. Our purpose is to detail the relevant technical considerations of this new model and compare it with historical controls.     

Cell-free arterial grafts: morphologic characteristics of aortic isografts, allografts, and xenografts in rats

PURPOSE: Chronic rejection of arterial allografts and xenografts results in arterial wall dilation and rupture, making them unsuitable for long-term arterial replacement in vascular surgery. In the arterial wall, as in other organs, the cells probably carry major antigenic determinants. Arterial wall cellular components can be removed by detergent treatment to produce a graftable matrix tube. METHODS: We compared the patency and macroscopic and microscopic morphologic changes that occurred in sodium dodecyl sulfate (SDS)-treated and untreated arterial isografts, allografts, and xenografts 2 months after implantation in rats. We quantified elastin, collagen, and nuclear density in the three layers of the graft wall (intima, media, and adventitia) by morphometric methods. The SDS treatment removed endothelial and smooth muscle cells and cells in the adventitia but preserved elastin and collagen extracellular matrix. RESULTS: All arterial xenografts, whether SDS treated or untreated, were aneurysmal 2 months after grafting, with loss of the medial cellular and extracellular components. In allografts, SDS treatment prevented dilation, reduced adventitial inflammatory infiltration, and preserved medial elastin. The SDS-treated allografts had an evenly distributed, noninflammatory intimal thickening that was richer in elastin fibers than that in untreated allografts. CONCLUSIONS: These results suggest an interspecies, but not an intraspecies, graft antigenicity of arterial extracellular matrix. The SDS treatment prevented chronic rejection of the arterial allograft and led to the proliferation of an elastin-rich and adapted intima.     

Multidisciplinary treatment of chronic pulmonary insufficiency. 4. The influence of intrathoracic pressure variations on increases in pulmonary vascular pressure during exercise in patients with chronic obstructive pulmonary disease

In the present era of direct monitoring of pressure in patients with chronic obstructive pulmonary disease (COPD), an appreciation of all factors that may influence the observed pulmonary vascular pressures is essential. Our study examines the impact of respiratory variations in intrathoracic pressure on the recorded pulmonary vascular pressures in 28 patients with COPD. Althouth pulmonary hypertension was present in only nine subjects at rest, all had an abnormal increase in the mean pulmonary arterial pressure during supine exercise. In 15 subjects, this abnormal response was, in part, related to an increase in pulmonary arterial wedge pressure to 15 mm Hg or more. The increase in pulmonary arterial wedge pressure was directly related to the amplitude of the peak-to-peak respiratory variation of such wedge pressure. This variation correlated with the specific airway resistance but was not related to the arterial oxygen pressure or pulmonary vascular resistance. These findings indicate the important influence of exaggerated respiratory effort on the measurement of pulmonary arterial wedge pressure and mean pulmonary arterial pressure in patients with chronic obstructive pulmonary disease.     

Acceleration of ageing processes by ionizing radiation (author''s transl)]

The dynamics of arterial, venous, and lymphatic flow in the mesentery were studied in dogs, using an electromagnetic flowmeter for the blood and cannulation and gravimetric measurement for the lymph. Ligation of veins caused an increased venous outflow in adjacent veins and a marked increase in lymph flow. When marginal vessels were ligated, eliminating the major collateral flow, venous flow decreased, but elevated lymph flow persisted. Simultaneous ligation of arteries and veins resulted in increases of both arterial and venous flow in adjacent vessels. Lymph flow decreased unless excessive arterial collateral flow persisted. When collateral marginal vessel flow was occluded, adjacent venous and arterial blood flow decreased to control levels. With arterial ligation, collateral arterial blood flow increased slightly, but venous and lymph flow decreased sharply. When collateral marginal vessels were eliminated, adjacent arterial blood flow decreased to control levels and venous flow virtually stopped. As a result of these studies, the technic of early primary arterial ligation followed by marginal vessel ligation appears to be the most satisfactory procedure for decreasing venous and lymphatic outflow and hopefully avoiding dissemination of cancer cells during the operation. This technic is now being used as a modification of the "no touch" technic for cancer of the colon.     

Pulse oximetry in severe carbon monoxide poisoning

STUDY OBJECTIVES: To evaluate the accuracy and quantitate the error of pulse oximetry measurements of arterial oxygenation in patients with severe carbon monoxide (CO) poisoning. DESIGN: Retrospective review of patient clinical records. SETTING: Regional referral center for hyperbaric oxygen therapy. PATIENTS: Thirty patients referred for treatment of acute severe CO poisoning who demonstrated carboxyhemoglobin (COHb) levels >25%, with simultaneous determinations of arterial hemoglobin oxygen saturation by pulse oximetry (SpO2) and arterial blood gas (ABG) techniques. MEASUREMENTS AND RESULTS: COHb levels and measurements of arterial oxygenation from pulse oximetry, ABG analysis, and laboratory CO oximetry were compared. SpO2 did not correlate with COHb levels. SpO2 consistently overestimated the fractional arterial oxygen saturation. The difference between arterial hemoglobin oxygen saturation (SaO2) calculated from ABG analysis and SpO2 increased with increasing COHb level. CONCLUSIONS: Presently available pulse oximeters overestimate arterial oxygenation in patients with severe CO poisoning. An elevated COHb level falsely elevates the SaO2 measurements from pulse oximetry, usually by an amount less than the COHb level, confirming a prior observation in an animal model. Accurate assessment of arterial oxygen content in patients with CO poisoning can currently be performed only by analysis of arterial blood with a laboratory CO-oximetry.     

Disparate effects of antidiabetic drugs on arterial contraction

Type II diabetic patients and others with insulin resistance are at risk for development of hypertension characterized by elevated peripheral vascular resistance and loss of insulin's normal vasodilating activity. Oral antidiabetic drugs have recently been recognized to have disparate effects on arterial pressure in such patients and in related rodent models. Sulfonylureas (e.g., glyburide), which stimulate insulin secretion, have been reported either to increase or not to affect arterial pressure, whereas nonsulfonylurea agents with insulin-sensitizing properties, the biguanide metformin and various thiazolidinediones (eg, pioglitazone), have been reported to decrease arterial pressure in humans and rodents. To help elucidate these disparate effects, we investigated these agents for direct actions on arterial vascular contractility and its sensitivity to insulin. Preincubation of intact rat tail arterial tissue rings for 2 hours with known therapeutically effective antidiabetic concentrations of metformin and pioglitazone significantly attenuated the force of contractions produced by either potassium (membrane depolarization) or norepinephrine ([NE] adrenergic receptor activation). Glyburide did not influence these contractions. Preincubation with metformin also induced an attenuating (vasodilating-like) action of insulin on arterial tissue rings contracted by potassium. Conversely, glyburide induced an accentuating action of insulin on potassium-mediated contractions. These results are consistent with measures of vascular function obtained in the past after oral administration of the drugs, which suggested but did not prove that they may exert direct effects on arterial vascular contractility. Thus, metformin and thiazolidinediones may decrease arterial pressure partly by direct vasorelaxant mechanisms, with metformin having an additional effect of inducing vasorelaxation by insulin. In contrast, sulfonylureas may directly induce a paradoxical vasoconstrictor response to insulin.     

The development of Cop 1 (Copaxone), an innovative drug for the treatment of multiple sclerosis: personal reflections

The aim of the review is to summarize the present knowledge on determinants of transfer of low density lipoprotein (LDL) into the arterial wall, particularly in relation to the risk of development of atherosclerosis. The flux of LDL into the arterial wall (in moles of LDL per surface area per unit of time) has two major determinants, i.e. the LDL concentration in plasma and the arterial wall permeability. LDL enters the arterial wall as intact particles by vesicular ferrying through endothelial cells and/or by passive sieving through pores in or between endothelial cells. Estimates in vivo of the LDL permeability of a normal arterial wall vary between 5 and 100 nl/cm2/h. In laboratory animals, the regional variation in the arterial wall permeability predicts the pattern of subsequent dietary induced atherosclerosis. Moreover, mechanical or immunological injury of the arterial wall increases the LDL permeability and is accompanied by accelerated development of experimental atherosclerosis. This supports the idea that an increased permeability to LDL, like an increased plasma LDL concentration, increases the risk of atherosclerosis. Hypertension, smoking, genetic predisposition, atherosclerosis, and a small size of LDL may all increase the arterial wall permeability to LDL and in this way increase the risk of accelerated development of atherosclerosis. The hypothesis that atherosclerosis risk can be reduced by improving the barrier function of the arterial wall towards the entry of LDL remains to be investigated; agents which directly modulate the LDL permeability of the arterial wall in vivo await identification.     

Use of polymerase chain reaction in clinical diagnostic laboratories in viral hepatitis B and C]

alpha 1-Antitrypsin deficiency has been associated with a variety of vascular disorders including arterial aneurysms, spontaneous extracranial arterial dissections, and arterial fibromuscular dysplasia. We determined the distribution of alpha 1-antitrypsin phenotypes in patients with intracranial arterial dissections, a rare cause of subarachnoid hemorrhage. The study population consisted of 4 consecutive patients with subarachnoid hemorrhage due to spontaneous intracranial arterial dissections. The vertebral artery was involved in 3 patients and the posterior inferior cerebellar artery in 1 patient. Three of these 4 patients were found to have a heterozygous alpha 1-antitrypsin deficiency (PiMZ or PiMS phenotypes). These data support previous studies suggesting that patients with alpha 1-antitrypsin deficiency may be at an increased risk of developing spontaneous arterial dissections.     

Assessment of thrombin inhibitor efficacy in a novel rabbit model of simultaneous arterial and venous thrombosis

The importance of thrombin in arterial and venous thrombosis renders thrombin inhibition an important therapeutic target. Identification of novel inhibitors requires an appropriate animal model. We modified a previously reported rat arterial thrombosis model to allow simultaneous assessment of the arterial and venous antithrombotic efficacies of heparin, hirudin, hirulog, a novel thrombin inhibitor H-(N-Me-D-Phe)-Pro-L-trans-4-aminocyclohexyl-Gly-[CO-CO]-NHCH3+ ++ (L-370,518) and the factor Xa inhibitor tick anticoagulant peptide in rabbits. Thrombosis was induced through application of 70% ferric chloride to the femoral artery and jugular vein. Incidence of occlusion, thrombus weight, aPTT and plasma inhibitor concentrations were determined. Heparin was efficacious in preventing arterial and venous occlusive thrombosis but at a dose that profoundly elevated aPTT. On a molar dosing basis, the approximate order of potency of the thrombin and factor Xa inhibitors was similar in artery and vein: hirudin>tick anticoagulant peptide>hirulog> or =L-370,518. Data suggested that compounds tended to be more potent in preventing venous thrombosis than arterial. This thrombin-dependent model is an economical and efficient approach to arterial and venous antithrombotic efficacy screening that eliminates variabilities encountered when multiple model/multiple animal strategies are employed.     

Parallel increase in carotid, brachial and left ventricular cross-sectional areas in arterial hypertension

Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.     

Hypoxemia and arterial hypotension at the accident scene in head injury

OBJECTIVE: To quantify the occurrence of arterial hypotension and arterial oxygen desaturation in a series of patients with head trauma rescued by helicopter. DESIGN: Prospective, observational study. MATERIALS AND METHODS: Arterial HbO2 was measured before tracheal intubation at the accident scene in 49 consecutive patients with head injuries. Arterial pressure was measured using a sphygmomanometer. MAIN RESULTS: Mean arterial saturation was 81% (SD 24.24); mean arterial systolic pressure was 112 mm Hg (SD 37.25). Airway obstruction was detected in 22 cases. Twenty-seven patients showed an arterial saturation lower than 90% on the scene, and 12 had a systolic arterial pressure of less than 100 mm Hg. The outcome was significantly worse in cases of hypotension, desaturation, or both. CONCLUSIONS: Hypoxemia and shock are frequent findings on patients at the accident scene. Hypoxemia is more frequently detected and promptly corrected, white arterial hypotension is more difficult to control. Both insults may have a significant impact on outcome.     

Venous and arterial gas embolism associated with positive pressure ventilation

We report a 53-year-old woman with ARDS who required positive pressure ventilation with positive end-expiratory pressure. She sustained an acute right ventricular myocardial infarction associated with cardiovascular instability. The next day she sustained a fatal cerebral arterial gas embolism. Intravascular gas was documented within the cerebral, coronary, and pulmonary arterial circulations. Clinicians need to be aware of venous and arterial gas embolism as a complication of mechanical ventilation.