Biomedical subjects
Publications and source records attributed to G Gutierrez.
Organ survival depends on adequate tissue oxygenation and normal metabolic function. In MSOF there are changes in O2 transport and cellular bioenergetics. These metabolic alterations may set in motion mechanisms of cellular damage that will affect microcirculatory control and the ability of the cell to maintain both function and homeostasis.
Critically ill cardiac patients often undergo mechanical ventilation. The interplay between pulmonary and cardiac mechanics is complicated and in many cases may result in impaired transfer of O2 from the atmosphere to the tissues. This article addresses the principles of pulmonary and peripheral gas exchange, as well as the mechanical effects of respiration on the circulation.
The effect of both lipolytic and antilipolytic hormones on the turnover of phosphatidylcholine in freshly isolated rat adipocytes was investigated. Treatment of adipocytes with agonists such as glucagon or isoprenaline that stimulate lipolysis through a cyclic AMP-dependent mechanism caused an increase in the incorporation of [Me-3H]choline into phosphatidylcholine. Pulse-chase studies indicated that the stimulation was due to an increase in the conversion of choline into phosphatidylcholine, which was both time- and dose-dependent. The stimulatory effect of isoprenaline was inhibited in a dose-dependent manner by oxytocin or insulin. Oxytocin inhibited the incorporation of [Me-3H]choline into phosphatidylcholine in both the presence and the absence of isoprenaline, whereas in the absence of isoprenaline insulin increased the incorporation of [Me-3H]choline into phosphatidylcholine. The effects of isoprenaline, oxytocin and insulin on the incorporation of [3H]choline into phosphatidylcholine were paralleled by changes in the activity of CTP:phosphocholine cytidylyltransferase.
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It has been proposed that an increase in the affinity of hemoglobin for O2 may be beneficial in severe hypoxemia. To test this hypothesis, we compared the response to progressive hypoxemia in dogs with normal hemoglobin affinity (P50 = 32.4 +/- 0.7 Torr) to dogs with a left shift of the oxyhemoglobin dissociation curve (P50 = 21.9 +/- 0.5 Torr) induced by chronic oral administration of sodium cyanate. Animals were anesthetized, paralyzed, and mechanically ventilated. The inspired O2 fraction was progressively lowered by increasing the inspired fraction of N2. The lowest level of O2 transport required to maintain base-line O2 consumption (VO2) was 9.3 +/- 0.8 ml.min-1.kg-1 for control and 16.5 +/- 1.1 ml.min-1.kg-1 for the sodium cyanate-treated dogs (P less than 0.01). Other measured parameters at this level of O2 transport were, for experimental vs. control: arterial PO2 19.3 +/- 2.4 (SE) Torr vs. 21.8 +/- 1.6 Torr (NS); arterial O2 content 10.0 +/- 1.2 ml/dl vs. 4.9 +/- 0.4 ml/dl (P less than 0.01); mixed venous PO2 14.0 +/- 1.5 Torr vs. 13.8 +/- 1.0 Torr (NS); mixed venous O2 content 6.8 +/- 1.0 ml/dl vs. 2.3 +/- 0.2 ml/dl (P less than 0.01); and O2 extraction ratio 32.7 +/- 2.8% vs. 51.2 +/- 3.8% (P less than 0.01). We conclude that chronic administration of sodium cyanate appears to be detrimental to O2 transport, since the experimental dogs were unable to increase their O2 extraction ratios to the same level as control, thus requiring a higher level of O2 transport to maintain their base-line VO2 values.
Rabbit hindlimb preparations perfused with blood from donor rabbits were used to determine whether O2 consumption (VO2) during hypoxemia is limited by total O2 transport (TO2) or by capillary O2 driving pressure, as reflected by the venous PO2 (PVO2). The preparations were randomized into two groups: low flow (LF) and high flow (HF), perfused at 18 and 32 ml.min-1.kg of preparation wt-1, respectively. After a 1-h base-line period with arterial PO2 (PaO2) greater than 100 Torr, both groups were exposed to progressive decrements in PaO2 to less than 10 Torr. Sequential sets of arterial and venous blood gases were obtained, and VO2, TO2, and O2 extraction ratio (ERO2) were calculated. A plot of PVO2 vs. TO2 showed higher levels of PVO2 (P less than 0.05) in LF than HF, when compared at similar levels of TO2. Therefore the experimental protocol allowed the comparison of the separate effects of TO2 or PVO2 on VO2. Plotting VO2 as a function of TO2 revealed two distinct curves (P less than 0.05), with LF having a greater VO2 than HF at a given TO2. Conversely, a plot of VO2 as a function of PVO2 did not show a difference between the groups. The ERO2 of LF was greater than HF when compared at similar levels of TO2 (P less than 0.05). We conclude from these data that during progressive hypoxemia VO2 appears to be primarily limited by factors that determine capillary O2 diffusion. This conclusion supports the Kroghian theory of capillary O2 exchange.
A blood-perfused rabbit hindlimb preparation was exposed to total ischemia (n = 4) or to severe hypoxemia (n = 4) where arterial PO2 was 5 +/- 2 (SE) Torr. O2 consumption (VO2), O2 transport (TO2), venous PO2 (PVO2), venous lactate concentration, and venous glucose concentration were measured. The relative concentration of ATP, phosphocreatine (PCr), inorganic phosphate (Pi), and intracellular pH (pHi) were monitored with 31P magnetic resonance spectroscopy. PCr/Pi decreased with the onset of ischemia or hypoxemia. The preparation was reoxygenated and allowed to recover for 30 min once PCr/Pi was less than 1.0. The periods of hypoxemia and ischemia lasted 56.0 +/- 10.0 and 63.8 +/- 2.5 min, respectively (NS). During ischemia PCr decreased and Pi increased compared with control (P less than 0.05) but returned to control with reperfusion. With hypoxemia PCr also decreased and Pi increased with respect to control (P less than 0.01) but did not recover with reoxygenation. VO2 and PVO2 in both groups returned to control during recovery. ATP did not change with ischemia but decreased with hypoxemia (P less than 0.05). Venous lactate concentration did not change with ischemia but increased with hypoxemia (P less than 0.05) and continued to rise during recovery. During recovery pHi decreased in the hypoxemic group (P less than 0.05) but not in the ischemic group. These data show that, under the conditions tested, rabbit skeletal muscle does not resynthesize PCr after a severe hypoxemic episode. Furthermore it appears that VO2 and PVO2 fail to portray the true state of cellular bioenergetics after a severe hypotemic insult.
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The time required by the red blood cells (RBC) to release the O2 needed by the tissues may be rate-limiting under conditions of reduced O2 supply (DO2). A time-dependent mathematical model of capillary O2 transport is developed to explore the effect of RBC deoxygenation kinetics on the intracapillary plasma PO2. The tissue capillaries are represented by a series of perfectly mixed compartments. In each compartment O2 is removed by the tissues as a chemical reaction takes place between O2 and oxyhemoglobin (HbO2). A system of differential equations is formulated to monitor changes in the intracapillary concentration of HbO2 and plasma O2. These equations allow for changes in blood flow, arterial oxygenation, capillary transit time, rate of O2 uptake, hemoglobin concentration and the position of the oxyhemoglobin dissociation curve. The predicted capillary PO2 for conditions of normal O2 supply is less than the PO2 calculated assuming an instantaneous rate of RBC deoxygenation. This difference in plasma PO2 is not present in the venous end of the capillary, since at this point oxyhemoglobin and plasma O2 have sufficient time to re-establish equilibrium. The discrepancy in PO2 profiles is magnified by anemia, [( Hemoglobin] = 5 g/dl), and hypoxemia, (PaO2 = 25 Torr). For these conditions of severe DO2 reduction, the end-capillary PO2 is significantly less than the venous PO2. These results suggest that (1) the kinetics of RBC deoxygenation can play an important role in the delivery of O2 to the tissues, and (2) the venous PO2 is not always an accurate measure of the end capillary PO2.
Hypothermia produces a decrease in metabolic rate that may be beneficial under conditions of reduced O2 delivery (Do2). Another effect of hypothermia is to increase the affinity of hemoglobin for O2, which can adversely affect the release of O2 to the tissues. To determine the overall effect of hypothermia on the ability of the peripheral tissues to extract O2 from blood, we compared the response to hypoxemia of hypothermic dogs (n = 8) and of normothermic controls (n = 8). The animals were anesthetized, mechanically ventilated, and paralyzed to prevent shivering. The inspired concentration of O2 was progressively reduced until the dogs died. The core temperatures of the control and hypothermic dogs were 37.7 +/- 0.3 and 30.5 +/- 0.1 degree C, respectively (P less than 0.01). The O2 consumption (VO2) of the control dogs was significantly greater than that of the hypothermic dogs (P less than 0.05), being 4.7 +/- 0.4 and 3.2 +/- 0.3 ml X min-1 X kg-1, respectively. Hypothermia produced a left shift of the oxyhemoglobin dissociation curve (ODC) to a PO2 at which hemoglobin is half-saturated with O2 of 19.8 +/- 0.7 Torr (control = 32.4 +/- 0.7 Torr, P less than 0.01). The O2 delivery at which the VO2 becomes supply dependent (DO2crit) was 8.5 ml X min-1 X kg-1 for control and 6.2 ml X min-1 X kg-1 for hypothermia. The hypothermic dogs maintained their base-line VO2's at lower arterial PO2's than control.(ABSTRACT TRUNCATED AT 250 WORDS)
Our prospective study attempted to better define the reciprocal relation between pregnancy and systemic lupus erythematosus (SLE), to reduce maternal morbidity/mortality, and fetal loss. Our protocol included all the pregnancies in our total of patients with SLE between the years 1974-1983. There were 102 pregnancies in 75 patients during this period; SLE was exacerbated in 59.7% that started with inactive disease, most with mild episodes. Hematologic manifestations and renal disease, however, required moderate or high doses of steroids. There were no maternal deaths. There were 49% premature newborns in the entire group and this increased to 59% in mothers with active SLE; 23% of newborns were small for gestational age in the entire group and the rate increased to 65% in mothers with active SLE. There was a 16% spontaneous abortion rate with no difference between mothers with active or inactive disease, 5 stillbirths and one neonatal death, with a total fetal loss of 22% (compared with 6.7% in the control group p less than 0.001). There were 32 cesarean sections with live outcomes and 14 newborn infants with a weight below 1.5 kg survived. Our study shows that in patients with SLE planned rheumatologic care of the mother, with special obstetrical and perinatal attention, may reduce the high maternal and fetal morbidity/mortality.
We compared the hemodynamic and blood gas data from anesthetized dogs given 0.15% carbon monoxide (CO) to breathe (INH group) and from dogs injected with 100% CO intraperitoneally while breathing room air (ITP group). The animals were observed for a period of 150 min after reaching a level of 50% carboxyhemoglobin (HbCO). The time required to reach this level was similar for both groups, i.e., 102 +/- 54 and 90 +/- 21 min for the ITP and INH groups, respectively. The average HbCO% for the duration of the experiment was 58.3 +/- 2.4 and 62.9 +/- 1.5% for the ITP and INH groups, respectively. All the animals survived in each group. There was no significant difference in their hemodynamic response to CO, except for a higher mean systemic blood pressure in the INH group. This difference was also present during the base-line measurements, suggesting that it was not related to the effects of CO. Following the 150-min comparison period, we attempted to precipitate a terminal cardiovascular crisis by increasing the amount of CO given. The animals in the ITP group lived indefinitely as the result of a "plateau" effect in the level of HbCO%. The measured HbCO% level did not rise above 70% regardless of the amount of CO injected into the peritoneal space. Those in the inhalation group died with an average HbCO% of 80.0 +/- 3.5%. It is concluded that the toxic effect of CO is the result of impaired O2 delivery to the peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
Concentrations of lactate and pH were determined in the CSF of 20 normal children, 36 with viral meningitis, 16 with purulent meningitis and six with tuberculous meningitis. No differences were found between normal cases and those with viral meningitis. In patients with purulent meningitis concentration of lactate was above 30 mg/100 ml and pH below 7.3. Both determinations allowed differentiation between viral meningitis and purulent meningitis after 48 hr of treatment with antibiotics in 80% of the cases.
We are confronted with the case of a patient who presents a clinical and histopatologic diagnostic of granuloma multiforme, it is considerated as the first of this illness published in report of american literature.
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A hybrid finite-difference/finite-element technique for the thermal analysis of blood vessels embedded in perfused tissue has been developed and evaluated. This method provides efficient and accurate solutions to the conjugated heat transfer problem of convection by blood coupled to conduction in the tissue. The technique uses a previously developed 3D automatic meshing method for creating a finite element mesh in the tissue surrounding the vessels, coupled iteratively with a 1-D marching finite difference method for the interior of the vessels. This hybrid technique retains the flexibility and ease of automated finite-element meshing techniques for modelling the complex geometry of blood vessels and irregularly shaped tissues, and speeds the solution time by using a simple finite-difference method to calculate the bulk mean temperatures within all blood vessels. The use of the 1D finite-difference technique in the blood vessels also eliminates the large computer memory requirements needed to accurately solve large vessel network problems when fine FE meshes are used in the interior of vessels. The accuracy of the hybrid technique has been verified against previously verified numerical solutions. In summary, the hybrid technique combines the accuracy and flexibility found in automated finite-element techniques, with the speed and reduction of computational memory requirements associated with the 1D finite-difference technique, something which has not been done before. This method, thus, has the potential to provide accurate, flexible and relatively fast solutions for the thermal analysis of coupled perfusion/blood vessel problems, and large vessel network problems.
Two new cases of phenotypic males with 46,XX karyotype are presented. Fluorescence, autoradiographic and centromeric heterochromatin studies in several lines, including testicular cells, failed to demonstrate the existence of the Y chromosome or the existence of distal Yq material translocated to another chromosome in the two patients. The Xg study in one of the patients and his family provided direct evidence of transmission of an X chromosome from father to son. We present indirect evidence favoring the mutation theory to explain the XX male phenotype.
In many critically ill patients, systemic measures of hemodynamic and O2 transport variables may not be sufficiently sensitive to portray the complex interaction between energy requirements and energy supply in all tissues. Gastric or intestinal tonometry has been proposed as a relative noninvasive index of the adequacy of aerobic metabolism in the gut mucosa, a tissue that is particularly vulnerable to alterations in perfusion and oxygenation. The gut mucosa lacks some of the microvascular control mechanisms that allow other tissues, such as the heart, skeletal muscle, and the brain, to increase tissue perfusion during times of stress, and, just like the canary, it will display metabolic changes indicative of dysoxia earlier than those more "vital" tissues. The tonometric measurement of mucosal PCO2 rests on the premise that equilibrium exists between mucosal and luminal PCO2. Increases in mucosal PCO2, or conversely, decreases in mucosal pH (pHi), are associated with the development of intestinal mucosa ischemia. The clinical utility of pHi to detect intestinal mucosal ischemia has been demonstrated in patients undergoing abdominal aortic surgery. Further, a low gastric mucosal pHi on admission to the ICU appears to be predictive of mortality and pHi-guided resuscitation may improve outcome in a subpopulation of patients admitted to the ICU with normal pHi, perhaps by preventing splanchnic ischemia and the development of a systemic oxygen deficit.