Effect Of Acute Blood Loss Research Articles

IMPACT OF ACUTE EXPERIMENTAL BLOOD LOSS ON DIURESIS AND FILTERING CAPACITY OF KIDNEYS AND EFFICACY OF CORRECTION WITH RINGER’S LACTATE SOLUTION IN COMBINATION WITH 2-ETHYL-6-METHYL-3-HYDROXYPYRIDINE SUCCINATE

Introduction: The kidneys remain one of target organs in acute blood loss of various genesis. Reduced perfusion leads to an increase in renal insufficiency, primarily characterized by decreased urine production and glomerular filtration rate. Timely restoration of lost blood volume deficit stands as a critical objective in addressing hypovolemic shock. Among the first-line therapeutic approaches, the administration of balanced crystalloids in a 1:1 ratio relative to the lost blood volume has demonstrated efficacy; the combined use of antioxidants is regarded as promising. This study aims to investigate the impact of acute experimental blood loss on diuresis and kidney filtration capacity, assess the effectiveness of correction with Ringer's lactate solution in combination with 2-ethyl-6-methyl-3-hydroxypyridine succinate.
 Materials and Methods: In our experiments, we induced acute blood loss equivalent to 2% of the body mass in rats and evaluated kidney function using a water stress method after 1, 3, and 7 days. We measured diuresis, creatinine levels in blood serum and urine, and glomerular filtration rate. To address the effects of blood loss, we administered Ringer's lactate solution separately and in combination with 2-ethyl-6-methyl-3-hydroxypyridine succinate.
 Results: Following the induction of acute blood loss, there was a significant reduction in diuresis and glomerular filtration rate, accompanied by an increase in creatinine levels in both blood serum and urine. These impairments worsened over the course of 1 to 7 days. Comparing the efficacy of infusion therapy with Ringer's lactate solution alone and in combination with 2-ethyl-6-methyl-3-hydroxypyridine succinate after 7 days revealed a significantly more pronounced increase in diuresis, glomerular filtration rate, and a reduction in urine creatinine levels in the combined therapy group. These findings suggest the promising potential of combined therapy in preventing renal dysfunction in the context of acute blood loss.
 Conclusions: Acute blood loss equivalent to 2% of body mass leads to disturbances in diuresis and renal filtration capacity. The administration of Ringer's lactate solution in conjunction with 2-ethyl-6-methyl-3-hydroxypyridine succinate mitigates the effects of acute blood loss and yields a more substantial improvement compared to rats treated with Ringer's lactate solution alone.

The Effects of Acute Blood Loss on Inflammatory and Bone Biomarkers, Acid-base Balance, Blood Gases and Hemato-biochemical Profiles in Sedated Donkeys (Equus asinus)

The current experiment was designed to investigate the possible effects of acute blood loss on the inflammatory and bone biomarkers status, acid-base balance, blood gases, and hemato-biochemical profiles in sedated donkeys (Equus asinus). For the induction of acute blood loss, collected 900mL of blood from the carotid artery of 10 male donkeys sedated with xylazine HCl (1mg/kg). For analysis, five blood samples were collected; collected the 1st (T0) before induction of blood loss and the other 4 (T1, T2, T3 and T4) collected at 30, 60, 120 and 240min post-blood loss. The serum concentrations of amyloid A (SAA) and haptoglobin (Hp) decreased at all-time points after blood loss compared to T0, but the differences were non-significant. The differences in levels of serum biomarkers osteocalcin (OC), β-alkaline phosphatase (β-ALP) and pyridinoline cross-links (PYD) at all-time points post blood loss compared to T0 values were also non-significant. Except for PCO2, the acid-base status and blood gases, including pH, PO2, HCO3, TCO2, sO2, base excess, anion gap and lactate, increased significantly after blood withdrawal. On the contrary, most of the measured hemato-biochemical parameters decreased significantly after blood loss, except for glucose. In conclusion, acute blood loss in sedated donkeys did not influence serum concentrations of the inflammatory biomarkers SAA and Hp and the markers of bone metabolism OC, β-ALP, and PYD. On the contrary, most acid-base, blood gas parameters, and hemato-biochemical parameters differed significantly after blood withdrawal compared to their values before blood loss.

The effect of acute blood loss on fibrinogen and fibrinogen "B" in plasma

Under the influence of acute blood loss in humans and animals, blood clotting increases, which contributes to the cessation of bleeding (E. Briicke, J. Cohnheim, N. Sahli, G. A. Ionkin and N. N. Popova, N. S. Javadyan, D. . M. Zubairov, R. A. Dymshits). In our previous studies (Kazan honey., 1961, 2; Folia Haematolog., 1962, 1), it was found that a sharp increase in blood clotting after acute blood loss is accompanied by the appearance of thrombin in the blood, which in some cases leads to vascular thrombosis.

The effect of acute blood loss complicated by limb ischemia-reperfusion on the induction of the apoptosis of pulmonary leukocytes and its correction by carbacetam

The development of acute lung injury is one of the severe complications of massive blood loss. Under these conditions, the apoptosis which is identified as an informative marker of the severity of the pathological process, enhances in the pulmonary leukocytes. The effect of limb ischemia and its reperfusion on the systemic mechanisms of the pathogenesis of acute massive blood loss, in particular the level of apoptosis of pulmonary leukocytes, remains understudied. There are no data concerning the efficacy of the carbacetam under these conditions.The objective of the research: to establish the effect of acute blood loss complicated by limb ischemia-reperfusion on the induction of the early apoptosis of pulmonary leukocytes and the efficacy of the carbacetam in the correction of identified abnormalities.Material and methods. The experimental studies were conducted on 216 white non-linear male rats weighing 200-220g. All procedures were carried out under thiopental sodium anesthesia. A limb ischemia-reperfusion, an acute blood loss as well as a combination of these lesions were carried out in the experimental groups. The identified abnormalities were corrected with carbacetam in the separate experimental group. After 1 and 2 hours as well as 1, 7, and 14 days, the bronchoalveolar lavage fluid of experimental animals was taken for the detection of the level of early apoptosis in the leukocyte population.The results. The simulations of a limb ischemia-reperfusion, an acute blood loss, and a combination of these lesions create the preconditions for the enhancement of early apoptosis of pulmonary leukocytes obtained from the bronchoalveolar lavage fluid. If under the conditions of simulating, solely, the limb ischemia-reperfusion the index is significantly higher than the control after 1 hour, 2 hours, and 1 day, and returns to the control level after 7-14 days, then after simulation an acute blood loss and its complication by limb ischemia-reperfusion the index is statistically significantly higher than control level at all observation periods. It has been established that the combination of massive acute blood loss and limb ischemia-reperfusion is accompanied by statistically significantly great increase in the studied parameter, as compared to the other experimental groups. The index statistically significantly decreases in all experimental groups under the effect of the carbacetam, which indicates the marked proapoptotic effect of the medication. Notwithstanding that studied parameters do not reach the level of the control group, the carbacetam is considered to be the promising medication for the correction of acute lung injury under conditions of acute blood loss complicated by limb ischemia-reperfusion.Conclusions. The simulation of a limb ischemia-reperfusion, an acute blood loss, and a combination of these lesions create the preconditions for the enhancement of early apoptosis of pulmonary leukocytes obtained from the bronchoalveolar lavage fluid. The complication of acute blood loss by limb ischemia and reperfusion is followed by statistically significantly greater abnormalities at all observation periods. Administration of the carbacetam leads to decrease in the level of early apoptosis in the bronchoalveolar lavage leukocytes after 7-14 days, which indicates the prospects of the medication for correction of identified abnormalities.

Peculiarities of impairments of absorptive-excretory and glycogen synthesis functions of the liver in the presence of acute blood loss complicated by limb ischemia-reperfusion and their correction by carbacetam

Introduction. Under conditions of massive bleeding from the extremities, both in combat and in peacetime, the only means for salvation is applying tourniquet, which completely stops the arterial blood flow. It is believed that the maximum safe time for bleeding of the limb due to the use of the tourniquet is up to two hours. The systemic effect of acute blood loss complicated by ischemia-reperfusion of the limb on the liver, which is the main organ of detoxification of the body, remains almost unexplored.Objective of research: to determine the effect of acute blood loss complicated by two-hour limb ischemia and its reperfusion on the absorption-excretory and glycogen-synthesizing function of the liver.Materials of the research and their discussion. The experiments were performed on 108 nonlinear male rats weighing 200-220 g. All animals were divided into four groups: control and three experimental. All interventions were performed under thiopental-sodium anesthesia. In the first experimental group, the animals were simulated ischemia-reperfusion of the limb by applying a strip of elastic harness "SWAT-T" (USA)10 mm wide for 120 minutes proximal to the left paw. In the second experimental group, acute blood loss (20% of the circulating blood volume) was simulated by cutting the femoral vein. In the third experimental group, these injuries were combined. In the control group, the animals were anesthetized, and then taken for research after 1 hour.After 2 and 3 hours, as well as after 1, 7 and 14 days in experimental animals were determined by the absorption-excretory and glycogen-synthesizing functions of the liver.Result of the research and their discussion. It was found that the simulation of two-hour limb ischemia after 3 h and 1 day of reperfusion is accompanied by a significant decrease in hepatic excretory function, accompanied by a slowing of bile bromosulfalein excretion and its normalization starting from 7 days of the experiment. Under conditions of acute blood loss, the disorders deepen at all times of observation. Complications of acute blood loss by ischemia-reperfusion of the limb, contributes to a greater slowing of the absorption and excretory function of the liver compared to the simulation of only acute blood loss. The result was statistically significant after 7 and 14 days of the experiment.With regard to the content of glycogen in the liver, it was found that the simulation of only ischemia-reperfusion of the limb was accompanied by a significant decrease in the content of glycogen in the liver after 3 h of the experiment. Under conditions of acute blood loss, the rate was lower than the control level for seven days of the experiment. Additional ischemia-reperfusion of the limb on the background of acute blood loss caused a more pronounced decrease in glycogen content in the liver after 1 and 7 days of the experiment, which did not return to normal by 14 days of the experiment.The use of carbacetam showed that compared with animals without correction of the drug for 14 days significantly accelerated the purification of blood from bromosulfalein and normalized glycogen content. Thus, carbacetam is a promising means of correcting the functional state of the liver in conditions of acute blood loss complicated by ischemia-reperfusion of the limb, which requires further preclinical study.Conclusions. Complications of acute blood loss by two-hour limb ischemia in the reperfusion period lead to liver dysfunction, accompanied by a greater slowing of liver blood clearance from bromosulfalein compared to the model of isolated blood loss after 7 and 14 days of the experiment and a greater decrease in glycogen in the liver.The use of carbacetam for 14 days in the reperfusion period in animals with acute blood loss complicated by limb ischemia-reperfusion, compared with animals without correction, significantly accelerates hepatic clearance of bromosulfalein and normalizes glycogen content in the liver which indicates the prospects of carbacetam as a means of systemic correction in the simulated pathology. It could be the theoretical basis for its use in the clinic.

The Effects of Acute Blood Loss on Electrocardiogram in Male and Female Swiss Albino Mice

The aim of the present study is to investigate the possible effects of acute blood loss (1% of body weight) on electrocardiogram (ECG) in male and female Swiss albino mice. Anesthesia was maintained with the ketamine-xylazine combination. The tail was cut using a scalpel blade and blood at a ratio of 1% body weight was collected in capillary tubes. ECG recording was done by using the standard lead II. P and T waves, intervals of PQ, QT, and RR, and QRS complex were measured after all ECG was recorded. The amplitude of P and QRS waves were significantly higher in males than that of females (P<0.005, P<0.05 respectively). PR intervals were also longer in male mice than those of females (P<0,001). Neither blood removal nor anesthesia affected the amplitude of the QRS complex in any gender. The duration of the QRS complex was longer in males than females in both groups (P<0,01). Blood removal led to a reduction in the duration of the QRS complex in male mice (P<0.01). Anesthesia caused the prolongation of the QT and QTc in all groups (P<0,001, P<0,05 respectively). Females had longer QT interval compared to male groups (P<0,05) and blood removal caused prolongation of the QT period in females (P<0,05). An acute blood loss of 1% of body weight in male mice led to a reduction in heart rate, whereas prolongation of the QT interval in female mice. It was concluded that gender is an important factor in terms of blood-loss associated ECG alterations.

Clinical responses to acute blood loss in goats

The response to blood loss is directly related to the degree of hemorrhage, but for the caprine species some aspects still need to be investigated. Therefore, the present study aimed to assess the clinical and hemodynamic effects of acute blood loss in goats. Eight healthy, adult male crossbred goats were subjected to external jugular puncture to remove 30% of the total blood volume. A physical examination and blood gas, biochemical, and hematologic analyses were performed at baseline, before blood loss (T0), and after one (T1h), six (T6h), 12 (T12h), 24 (T24h) and 72 (T72h) hours, and eight (T8d), 16 (T16d), 24 (T24d) and 32 (T32d) days after the acute blood loss event. The goats presented with tachycardia, tachypnea, and hyperthermia one hour after blood loss with a return to normal physiological values at T6h. Packed cell volume was decreased at T1h and red cell counts at T12h, both returning to baseline at T24d. There was a reduction in total protein and albumin levels at T1h, both remained below baseline levels until T16d and T8d, respectively. The serum calcium concentration decreased over the period T1h to T24h and glucose increased over the period T1h to T6h. The values of pH, TCO2, bicarbonate, and base excess were lower at T1h, while lactate increased markedly at this time. The pCO2 value only was reduced at T24h. Systolic (PS), diastolic (PD), and mean (PM) pressures were decreased at T1h. Acute loss of 30% of blood volume in goats caused changes in clinical, blood gas, and biochemical parameters, which were restored over a six-hour period, while hematologic changes were more persistent, with baseline values restored only after 24 days.

Content of vitamine C metabolites in rats organs at acute blood loss

There has been studied the effect of acute blood loss, which was modeled by a single loss of 30% of the circulating blood, on the fluctuations in the content of ascorbic (AA), dehydroascorbic (DAA), diketogulonic (DKGA) acid and their sum in the organs of rats in dynamics for the fifth, twelfth, nineteenth and twenty-sixth days after the blood loss. Acute blood loss caused a significant decrease in the content of all parameters of the system of metabolites of ascorbic acid – their sum, AA, DAA and DKGA – by 10–73 % compared to the control. The most significant decrease was in the content of AA, which was not restored in all organs until the end of the study period. The DAA content in all organs increased from the 12th day, and then decreased during the experiment. The content of the DKGA increased from the 19th day of the experiment. At the same time, it was found that on 26th day in the kidneys, the DAA content exceeded the control value by 42%, and the content of DKGA in the liver and blood – by 25–60 %. The content of the amount of ascorbic acid metabolites at the end of the experiment was almost restored, but this recovery occurred in various ways: in the kidneys – due to an increase in the DAA content, in other organs – by increasing the concentration of DKGA. The parts of AA from the sum of acids (in %) after blood loss significantly decreased, starting from the 5th day, and the process of its recovery began to occur only after the 19th day. The ratio of the amount of the vitamin component of the acids of the ascorbic acid system to the content of the non-vitamin DKGA was increased in the kidneys on the 12th and 26th days of the experiment, in other organs this index decreased 2.3–3.1 times in comparison with the control. The obtained data can be explained by the increased consumption of ascorbic acid to neutralize the effects of the intensification of oxidative processes under oxidative stress, which were activated by the action of acute blood loss, due to its reversible conversion to dehydroascorbic acid, and the latter irreversibly to diketogulonic acid.

Carotid Flow Time Changes With Volume Status in Acute Blood Loss

Noninvasive predictors of volume responsiveness may improve patient care in the emergency department. Doppler measurements of arterial blood flow have been proposed as a predictor of volume responsiveness. We seek to determine the effect of acute blood loss and a passive leg raise maneuver on corrected carotid artery flow time. In a prospective cohort of blood donors, we obtained a Doppler tracing of blood flow through the carotid artery before and after blood loss. Measurements of carotid flow time, cardiac cycle time, and peak blood velocity were obtained in supine position and after a passive leg raise. Measurements of flow time were corrected for pulse rate. Seventy-nine donors were screened for participation; 70 completed the study. Donors had a mean blood loss of 452 mL. Mean corrected carotid artery flow time before blood loss was 320 ms (95% confidence interval [CI] 315 to 325 ms); this decreased after blood loss to 299 ms (95% CI 294 to 304 ms). A passive leg raise had little effect on mean corrected carotid artery flow time before blood loss (mean increase 4 ms; 95% CI -1 to 9 ms), but increased mean corrected carotid artery flow time after blood loss (mean increase 23 ms; 95% CI 18 to 28 ms) to predonation levels. Corrected carotid artery flow time decreased after acute blood loss. In the setting of acute hypovolemia, a passive leg raise restored corrected carotid artery flow time to predonation levels. Further investigation of corrected carotid artery flow time as a predictor of volume responsiveness is warranted.

The effects of acute blood loss on blood pressure recovery from the Valsalva maneuver

Human baroreflex regulation plays an important role in stabilising blood pressure. Though we have several indices to quantify cardiovagal responses, sympathetic baroreflex gain remains difficult to assess. We investigated how the recently validated pressure recovery time (PRT) and sympathetic baroreflex gain (SBRS) derived from the Valsalva maneuver was influenced by acute blood loss. 26 healthy blood donors were included in the study (age 35±15years; 20 men). SBRS was derived from the blood pressure drop (SAP delta) and pressure recovery time during the Valsalva maneuver. Besides we calculated cardiovagal baroreflex parameters, the Valsalva ratio (VR) and a simplified baroreflex gain (VBRS). We compared these parameters before and after the withdrawal of 350–400ml blood. The baseline systolic blood pressure was the same before and after blood donation (123±17 vs 126±23mm Hg, NS). The minimum systolic pressure (SAP min) during phase III was significantly lower, and the SAP delta significantly greater after blood withdrawal (SAP min 83±24mm Hg vs 69±27mm Hg, p<0.001; SAP delta 41±15mm Hg vs 57±16mm Hg, p<0.001). PRT increased significantly (from 2.0 to 3.6s, p<0.006). SBRS did not change between the study conditions (24±12mm Hg/s vs 22±10mm Hg/s, NS), nor did the VR and the VBRS: In conclusion, after the acute loss of approximately 350–400ml blood there was a greater blood pressure drop in phase II and III and a slower blood pressure recovery in phase IV of the Valsalva maneuver that resulted in an unchanged SBRS.

ラットにおける遺伝子組み換えヒトエリスロポエチンの内因性エリスロポエチン産生への影響

To clarify the influence of recombinant human erythropoietin (r-HuEPO) on endogenous erythropoietin production, experiments using rats were designed as follows.Firstly, to evaluate the effect of acute blood loss on endogenous erythropoietin production, five rats (Wistar; mean body weight 280g) were bled of 1.3% of body weight (g) by cardiac puncture under pentobarbital sodium (30mg/kg, ip) anesthesia, followed by periodic blood examinations, including serum erythropoietin (s-EPO) levels, hemoglobin and reticulocyte counts. Secondly, 12 rats were divided into two groups of six rats each, control and r-HuEPO-treated groups. Rats received no r-HuEPO or 200U/kg of r-HuEPO subcutaneously once a week after the first blood sampling. All rats were given iron sulphate. Blood (0.6% of body weight) was drawn from each rat at three weekly intervals. At the fourth donation, blood volume of 1.5% of body weight was drawn. The results were as follows: 1) serum erythropoietin significantly increased at 3h after phlebotomy. s-EPO level peaked at 24h after phlebotomy, then returned to normal within 7 days; 2) mean hemoglobin level in the r-HuEPO-treated group decreased gradually during the 3 weeks of blood donation; 3) after the fourth donation, the peak in s-EPO level in control group occurred on day one, whereas in half of the rats in the r-HuEPO-treated group it occurred on day 7. On the basis of our data, however, no significant difference was found in recovery from phlebotomy-induced anemia between the two groups. In conclusion, r-HuEPO seems useful for the speed correction of anemia associated with successive phlebotomy. However, our data suggest that the administration of r-HuEPO suppres endogenous erythropoietin production after acute massive bleeding. Further study remains to be done to ascertain the clinical implications of these findings.

DOES THE HAEMODYNAMIC RESPONSE TO ACUTE CENTRAL HYPOVOLAEMIA DEPEND ON THE RATE OF FALL OF CARDIAC OUTPUT?

1. In published studies of the effects of acute blood loss in conscious rabbits, the rates of haemorrhage have ranged for 3-9% of blood volume/min. This is potentially a confounding factor when it comes to comparing the results of different studies. We have therefore tested whether the haemodynamic response to acute central hypovolaemia depends on the rate of fall of cardiac output. 2. Cardiac output in six conscious rabbits was reduced by 4, 8 and 12% of baseline levels per min by gradual inflation of a cuff around the thoracic inferior vena cava. These rates correspond approximately to blood loss at rates of 3, 6 and 9% of blood volume/min. 3. The haemodynamic responses were biphasic. In Phase I (compensatory) there was progressive systemic vasoconstriction and tachycardia, and only a small fall in blood pressure. In Phase II (decompensatory), systemic vasoconstriction failed abruptly, arterial pressure plummeted and heart rate declined. 4. We could detect no effect of rate of fall of cardiac output on the pattern of the haemodynamic responses in either Phase I or Phase II. 5. We conclude that the rate of blood loss in different studies of haemorrhage in conscious rabbits, within the range 3 to 9 per cent of blood volume per minute, need not be regarded as a confounding factor when it comes to interpreting the results. It is likely that this conclusion can be generalized to studies of haemorrhage in other mammalian species.

Respiratory system mechanics in guinea pigs after acute hemorrhage

We evaluated the effects of acute blood loss on the respiratory mechanics of guinea pigs. We measured respiratory system elastance (Ers) and resistance (Rrsmax) using the end-inflation occlusion method. Rrsmax was partitioned into its homogeneous component (Rrsmin) and that due to the unevenness within the respiratory system (Rrsu). Respiratory mechanics were studied both before and immediately after bleeding in eight animals. Another eight guinea pigs had received propranolol previously and were also submitted to hemorrhage. Propranolol-treated animals showed higher control values of Rrsmax (p less than .02) and Rrsmin (p less than .0001). Animals not treated with propranolol exhibited a decrease (p less than 0.001) in Rrsmax after hemorrhagic hypovolemia (from 0.375 +/- 0.051 to 0.323 +/- 0.042 cm H2O/ml.sec), due to a decrease (p less than 0.005) in Rrsmin (from 0.140 +/- 0.031 to 0.094 +/- 0.032 cm H2O/ml.sec), whereas Ers and Rrsu did not change. Propranolol-treated animals showed an increase (p less than .001) in Rrsmax (from 0.512 +/- 0.133 to 0.664 +/- 0.144 cm H2O/ml.sec), Rrsu (p less than 0.01) from 0.252 +/- 0.09 to 0.345 +/- 0.139 cm H2O/ml.sec, and Ers (p less than 0.001) (from 4.565 +/- 0.933 to 5.402 +/- 1.24 cm H2O/ml) after bleeding. The results indicate that the immediate effects of acute bleeding on respiratory mechanics are significantly influenced by catecholamines.

Effect of acute blood loss on glycosylated hemoglobin determinations in normal subjects.

Nondiabetic adult subjects (N = 12) were studied to determine the effect of an approximately 450-ml acute blood loss upon glycosylated hemoglobin measurements. After blood loss, the hematocrit significantly decreased by week 1 (P less than 0.001) and the reticulocyte count peaked by week 2. All glycosylated hemoglobins measured showed significant decreases post blood loss. The nadir was at week 4 for total A1, A1c, and irreversible A1c by high-pressure liquid chromatography (HPLC), and at week 6 for irreversible A1 by HPLC and A1 by electrophoresis. The mean percent decrease in glycosylated hemoglobins ranged from 4.6% (irreversible A1 by HPLC) to 8.6% (total A1c by HPLC).

Effect of acute blood loss on hepatic xenobiotic oxidizing enzymes in the rat

It was found that the loss of up to one-half of the blood volume of male Sprague-Dawley rats did not result in significant alteration of either cytochrome P-450 content or activity as measured by a reductive assay. The activity of FAD-monooxygenase was similarly found to be unaffected by acute blood loss.

Changes in Erythrocyte Metabolism Following Acute Blood Loss in Chickens

The effect of acute blood loss on erythrocyte metabolism has been studied in a number of mammals. This study was designated to provide comparative data in chickens. Twenty to 30 ml of blood were removed from 7 chickens for 3 successive days. Packed red cell volumes were restored at the rate of 1.46% per day, and a maximum reticulocyte count (26.7%) occurred on the third day after the initial phlebotomy. Fourteen of the 16 erythrocyte enzymes measured became elevated significantly. Enzymatic activity was increased when the greatest numbers of young red cells were in the circulation and declined as the erythrocytes aged. Initial enzymatic activity was not related to the subsequent magnitude of increased activity. Inositol pentaphosphate, adenosine 5′-triphosphate, and reduced glutathione, but not 2,3-diphosphoglycerate, increased significantly in the postphlebotomy period. The markedly rapid and significant rise of inositol pentaphosphate suggested that it was controlled. That could be the way hemoglobin function is controlled during changing physiologic requirements.

Acute blood loss and pulmonary host defense mechanisms in the rat

After trauma and hemorrhage, there is a high incidence of bacterial pneumonia. We have evaluated in the rat the effect of acute blood loss on intrapulmonary host defense mechanisms. Rats were phlebotomized 2.0 ml/100 g body weight and were then kept without food or water until sacrifice 15 and 38 hr later. Intrapulmonary inactivation of an inhaled inoculum of radiolabeled ( 32P) S. aureus was quantified in individual rats 14 hr after exposure in an aerosol generator system. Since dehydration and starvation by themselves might influence pulmonary phagocytic activity, separate experiments were included to evaluate these factors. The acute blood loss produced hypotension for less than 1 hr. When sham and experimental rats were challenged with S. aureus 1 hr after surgery, the phlebotomized rats had an impaired intrapulmonary bacterial inactivation when sacrificed 14 hr later. This was unrelated to changes in lung water and arterial pH, pCO 2 and pO 2. Sham and experimental rats exposed to S. aureus 24 hr after surgery had a similar depression of intrapulmonary bacterial inactivation which was related to decreases in lung water. Starvation had no effect on intrapulmonary bacterial inactivation but 38 hr of dehydration caused an impairment which was related to decreased lung water. After acute blood loss, there is a direct effect of hypotension on intrapulmonary host defense mechanisms. Since blood loss did not cause a greater impairment of bacterial inactivation at 38 hr than dehydration alone, the factor operational in the earlier hours after hemorrhage may have no longer been present. Both dehydration and blood loss may be operative in the traumatized patient and contribute to the development of posttraumatic pulmonary infections.

The hemodynamic effect of acute blood loss in normal man, with observations on the effect of the Valsalva maneuver and breath holding.

Skillman, John J. M.D.; Olson, John E. M.D; Lyons, John H. M.D; Moore, Fbanos D. M.D. Author Information

Blood volume changes in pregnancy and the puerperium: II. Red blood cell loss and changes in apparent blood volume during and following vaginal delivery, cesarean section, and cesarean section plus total hysterectomy

Blood volume changes were studied in 150 parturient women to determine the fate of the blood added to the circulation during pregnancy as well as to quantitate blood loss associated with delivery. Previously it was shown that when chromium-labeled red blood volume there was good agreement between the volume of red blood cells that disappeared from the circulation and the volume of red blood cells lost during parturition. This technique was used in the study. In 75 women during and very soon after vaginal delivery red blood cell loss from the circulation was equivalent to 505 ml of predelivery blood. In 40 women undergoing repeat cesarean section prior to labor the average loss equaled 930 ml of predelivery blood. In 35 other women subjected to cesarean section plus total hysterectomy the average loss equaled 1435 ml of predelivery blood. Between the first hour after vaginal delivery and 72 hours later in 54 women an average of 80 ml of blood was collected from the vagina. With 1 exception oxytocics were not administered except at the time of placenta delivery. In essentially normal pregnant women the loss of 20-30% of the predelivery blood volume as the result of parturition typically produced little change in the hematocrit during the puerperium. It is concluded that in general women during and after parturition can tolerate the loss of most of the blood added to the circulation during pregnancy without serious effects. In a discussion R.G. Holly notes 1) the need for studying long-term effects of acute blood loss and 2) that this study is a good example of using isotopes to obtain precise information. J.L. McKelvey comments on iron storage in patients whose hemoglobin mass does not increase. C.J. Lund notes that postpartum changes in hematocrit are not unpredictable if total blood volume is considered.

RESPONSE OF NORMAL SUBJECTS TO ACUTE BLOOD LOSS

Studies on the response of the body to acute blood loss are of both theoretic and practical importance because hemorrhage is a serious complication in many medical and surgical conditions. In man, controlled observations on the effect of hemorrhage on the circulation, the plasma volume, the protein concentration and the cell-plasma ratio are difficult to obtain because the immediate care of the patient requires the complete attention of the physician and because the amount of blood lost is not known. In addition, the underlying disease producing the hemorrhage may alter the response of the body. Although many investigators have studied the effect of acute blood loss on lower animals, few studies on human subjects have been made under controlled conditions. Keith1observed changes in hematocrit reading and blood volume as determined by the dye method after the removal of 800 cc. of blood from a normal man. He found