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Biomedical subjects

G J Crystal

Publications and source records attributed to G J Crystal.

At least 55 records · Page 3Linked to original sources
PubMed1992

Oxygen extraction ratio: a valid indicator of transfusion need in limited coronary vascular reserve?

We have described whole body oxygen (O2) extraction ratio (ER) as a reliable indicator of transfusion need in acute normovolemic anemia. In normal hearts, myocardial lactate production (-LACT), indicating anaerobic metabolism, does not occur until the ER greater than 50% and Hct less than 10%. It is not known if the ER is valid in the setting of limited coronary vascular reserve. This study assesses the effect of a critical left anterior descending (LAD) coronary stenosis on the compensation to acute blood loss anemia. Adult dogs were anesthetized, paralyzed, and mechanically ventilated. A critical LAD stenosis was created in seven animals (STEN). There were seven controls (CON). Animals underwent isovolemic exchange transfusion with 6% HES until cardiac failure (CF). Catheters were placed in the aorta, pulmonary artery, and anterior interventricular coronary vein. Cardiac failure occurred at Hct = 8.6% +/- 0.4% in the CON and 17.0% +/- 0.5% in the STEN animals. Cardiac output increased in the CON, but not in the STEN animals. Blood flow in the LAD increased in the CON but not the STEN animals. -LACT began in the CON and STEN animals at Hct less than 20% and coincided with an ER greater than 50% in both groups. We conclude that CF occurs at a higher hematocrit with a critical LAD stenosis. The whole body ER greater than 50% remains a valid indicator of myocardial metabolism in anemia in the presence of limited coronary vascular reserve. The ER may be a useful guide to transfusion therapy.

Anemia↗
PubMed1992

Phenylephrine does not limit myocardial blood flow or oxygen delivery during isoflurane-induced hypotension in dogs.

Experiments were performed on seven fentanyl-pentobarbital-anesthetized, open-chest dogs to determine whether stimulation of coronary alpha 1-adrenergic receptors by phenylephrine causes coronary vasoconstriction and impaired myocardial oxygen delivery when phenylephrine is infused to correct isoflurane-induced hypotension. Myocardial blood flow was measured with radioactive microspheres, and myocardial oxygen and lactate extraction were determined. The Fick equation was used to calculate myocardial oxygen consumption. Measurements were obtained (a) under control conditions, (b) after a 30-min inhalation of isoflurane sufficient to decrease mean aortic pressure by 30%, and (c) while maintaining administration of isoflurane, 5-10 min after restoration of mean aortic pressure by intravenous infusion of phenylephrine. Isoflurane-induced hypotension was accompanied by a baroreceptor-mediated increase in heart rate and by a decrease in myocardial oxygen consumption; however, myocardial blood flow was maintained, resulting in decreased oxygen extraction and increased coronary sinus PO2, thus implying a direct coronary vasodilating effect for isoflurane. Lactate extraction was unaffected. Phenylephrine infusion during inhalation of isoflurane returned mean aortic pressure and heart rate to their respective control values, and it did not change myocardial oxygen consumption, myocardial blood flow, myocardial oxygen extraction, coronary sinus PO2, or lactate extraction from values obtained during isoflurane alone. These latter findings are consistent with undiminished coronary vasodilation by isoflurane in the presence of phenylephrine. In conclusion, infused phenylephrine to restore aortic pressure during isoflurane administration had no vasoconstrictor effect in the coronary circulation and did not impair myocardial oxygen delivery. Apparently, the direct coronary vasodilating action of isoflurane completely nullified phenylephrine-induced vasoconstriction via local alpha 1-adrenergic receptors.

Animals↗
PubMed1991

Hemodynamic responses to pancuronium and vecuronium during high-dose fentanyl anesthesia for coronary artery bypass grafting.

The hemodynamic and electrocardiographic (ECG) effects of pancuronium and vecuronium were compared during high-dose fentanyl anesthesia for coronary artery bypass grafting (CABG) surgery. Forty-eight morphine-scopolamine premedicated patients scheduled for elective CABG were anesthetized with fentanyl (100 micrograms/kg) in divided doses, and either of two muscle relaxants, pancuronium (n = 26; 0.10 mg/kg) or vecuronium (n = 22; 0.09 mg/kg). Hemodynamic data, blood gas samples, and ECG tracings were obtained at the following intervals: (1) control; (2) prior to intubation; (3) 1 minute after intubation; (4) prior to sternotomy; and (5) 1 minute after sternotomy. In the pancuronium group, heart rate (HR), cardiac index (CI), and rate-pressure product (RPP) were increased after induction of anesthesia and following intubation. Eleven patients (42.3%) displayed ischemic ST segment changes. Four patients in this group developed tachycardia and hypertension to an extent requiring pharmacological intervention. Vecuronium-treated patients displayed no increases in HR, MAP, and RPP, and a decrease in CI. Only one patient (5.6%) developed evidence of ischemic ECG changes. Four patients in the vecuronium group, all receiving preoperative beta-blocker therapy, became hypotensive and bradycardic after the induction of anesthesia. The present investigation confirms the increased incidence of myocardial ischemia during high-dose fentanyl-pancuronium anesthesia. Although vecuronium was associated with fewer myocardial ischemic changes, the occurrence of bradycardia and hypotension in some patients receiving preoperative beta-adrenergic blocking drugs remains a concern.

Anesthesia, Intravenous↗
PubMed1991

Intracoronary isoflurane causes marked vasodilation in canine hearts.

Previous studies of coronary vasomotor effects of isoflurane were complicated by changes in systemic hemodynamic conditions and in global cardiac work demands. Accordingly, in the current study, the left anterior descending coronary artery (LAD) of 11 open-chest dogs anesthetized with fentanyl and pentobarbital was cannulated and perfused with isoflurane-free arterial blood or with arterial blood equilibrated in an extracorporeal oxygenator with isoflurane (0.5, 1.0, 2.0% in 95.5% oxygen-4.5% carbon dioxide). Steady-state changes in coronary blood flow (CBF) in LAD were measured electromagnetically, and their transmural distribution (endocardium: epicardium ratio) was evaluated with 15-microns radioactive microspheres. Venous blood was obtained from the anterior interventricular vein and analyzed for oxygen tension (PO2) and oxygen content. Myocardial oxygen consumption (MVO2) was calculated using the Fick equation. Cardiac responses during isoflurane were compared to those during maximal vasodilation with intracoronary adenosine. Perfusion pressure was maintained at 100 mmHg. CBF increased 271, 279, and 503% with 0.5, 1.0, and 2.0% isoflurane, respectively, with no change in the endocardium:epicardium ratio. With 2.0% isoflurane, the increase in CBF was 80% of the maximal, adenosine-induced response. The increases in CBF caused by isoflurane were accompanied by greater than proportional increases in venous PO2 and decreases in the arteriovenous oxygen difference, reflecting the reduction (approximately 40% in MVO2. In conclusion, isoflurane has a direct, concentration-dependent relaxing effect on coronary vascular smooth muscle in the canine heart in situ. The ability of isoflurane to increase CBF nearly maximally while also significantly reducing local myocardial oxygen requirements attests to the potency of isoflurane's direct vasodilator action.

Adenosine↗
PubMed1991

Thoracic aortic trauma: role of dynamic CT.

Two protocols were developed to study the efficacy of both chest radiography and dynamic computed tomography (CT) of the thorax in screening for traumatic aortic injury. Both protocols demonstrated a definite role for dynamic CT in excluding aortic injury in patients with normal initial chest radiographs. The authors studied 164 patients, and preliminary results indicated a high reliability for this method. Their algorithm, with 6-month follow-up, yielded both 100% sensitivity and a 100% negative predictive value. Unnecessary aortography, with its associated morbidity and cost, was decreased by 73%.

Adolescent↗
PubMed1991

Myocardial and systemic hemodynamics during isovolemic hemodilution alone and combined with nitroprusside-induced controlled hypotension.

Myocardial and systemic effects of isovolemic hemodilution alone and combined with controlled hypotension induced with sodium nitroprusside (SNP) were studied in halothane-anesthetized, open-chest dogs. Regional blood flow was measured with radioactive microspheres and used to compute regional oxygen (O2) supply. Values for regional blood flow in myocardium were used to compute myocardial O2 (MVO2) and lactate uptake (MVLAC) using the Fick equation. Hemodilution to hematocrit 50% of baseline increased aortic blood flow and decreased systemic vascular resistance, although other systemic hemodynamic values were not changed. Twofold increases in myocardial blood flow were accompanied by no change in MVO2, MVLAC, or coronary sinus PO2. Hemodilution increased regional blood flow sufficiently in the pancreas, liver, duodenum, skeletal muscle, skin, and brain to preserve O2 supply whereas unchanged blood flow in the spleen and kidney reduced O2 supply. Under hemodilution, 15 min of intravenous SNP sufficient to reduce mean arterial pressure by 50% caused parallel reductions in aortic blood flow, dP/dt max, and left ventricular end-diastolic pressure; systemic vascular resistance was unaffected. Myocardial blood flow and MVO2 decreased proportionally, whereas MVLAC and coronary sinus PO2 did not change. Regional blood flow and O2 supply decreased in the kidney, spleen, liver, and skin. Extending SNP infusion to 60 min increased myocardial blood flow and MVO2, but other hemodynamic values were unchanged. Comparing previous results with adenosine-induced hypotension inferred that coronary vasodilator reserve was greatly reduced at this time. In conclusion, although myocardial O2 supply versus demand balance was well maintained during SNP-induced hypotension under hemodiluted conditions, diminished coronary vasodilator reserve suggests increased vulnerability to ischemia if stresses of augmented cardiac work demand or impaired arterial oxygenation were superimposed. The decrease in O2 supply in the kidney during combined hemodilution and SNP-induced hypotension also warrants concern. These latter findings suggest the need for extensive clinical monitoring when SNP is used for controlled hypotension under hemodiluted conditions.

Analysis of Variance↗
PubMed1991

Hemodynamic responses to endotracheal extubation after coronary artery bypass grafting.

After coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myocardial ischemia and infarction and ventricular dysrhythmias. The hemodynamic responses to endotracheal extubation and the efficacy of intravenous lidocaine pretreatment were studied after CABG surgery and overnight mechanical ventilation. Twenty-five patients were divided into two groups: group 1 (n = 13) patients who had tracheal extubation after pretreatment with a placebo; group 2 patients who received lidocaine (1 mg/kg IV) before tracheal extubation. Hemodynamic data, electrocardiographic tracings, and arterial blood gases were obtained before tracheal extubation, during suctioning, and 1, 5, and 20 min after tracheal extubation. Group 1 patients displayed significant increases in heart rate, arterial blood pressure, rate-pressure product, right atrial pressure, and cardiac index during suctioning and within 1 min of tracheal extubation, returning to preextubation level by 5 min. There were no significant changes in pulmonary and systemic resistance indices. Hemodynamic changes in group 2 patients were similar to those in group 1. Both in the absence and presence of lidocaine, tracheal extubation caused hemodynamic responses that were small in magnitude and brief in duration. These responses were not associated with electrocardiographic or enzymatic evidence of myocardial ischemia or infarction, or with ventricular dysrhythmias. Compared with the well-documented hemodynamic responses to tracheal intubation, we found that extubation of the trachea after CABG surgery was associated with less pronounced responses. This may be related to avoidance of laryngoscopy and possibly accommodation to the endo-tracheal tube. These modest hemodynamic responses of extubation of the trachea after CABG surgery were not modified by intravenous lidocaine.

Coronary Artery Bypass↗
PubMed1991

Myocardial oxygen supply/demand relations during phenylephrine infusions in dogs.

Experiments were performed on 14 fentanyl-pentobarbital-anesthetized dogs to assess changes in myocardial oxygen supply/demand relations during intravenous infusions of phenylephrine (2.8 micrograms.kg-1.min-1). Myocardial blood flow was measured with radioactive microspheres. Myocardial oxygen and lactate extraction were determined. Myocardial oxygen consumption was calculated with the Fick equation. In series 1, measurements were obtained during phenylephrine-induced pressor responses. In series 2, measurements were obtained with aortic pressure maintained constant with an extracorporeal reservoir during phenylephrine infusion, so that coronary vasomotor responses could be assessed in the absence of increases in ventricular afterload and perfusion pressure. In series 1, the phenylephrine-induced increase in mean aortic pressure (+42%) was accompanied by proportional (60%) increases in myocardial blood flow and myocardial oxygen consumption and with no change in the endocardium-to-epicardium flow ratio, oxygen extraction, coronary sinus oxygen tension and oxygen saturation, or myocardial lactate extraction. In series 2, phenylephrine infusion caused a transmurally uniform 15% decrease in myocardial blood flow combined with a 10% decrease in myocardial oxygen consumption. The coronary arteriovenous oxygen difference increased modestly (+5%), resulting in small decreases in coronary sinus oxygen tension and oxygen saturation, whereas lactate extraction was unaffected. The present findings suggest that phenylephrine has a direct vasoconstrictor effect in the coronary circulation that is weak and completely overridden by metabolic autoregulatory mechanisms in response to pressure-induced augmentations in cardiac workload. The authors conclude that the myocardium is not at risk when phenylephrine is used to treat hypotension in patients with adequate cardiac function and coronary vasodilator reserve.

Anesthesia, Intravenous↗
PubMed1991

Hemodynamic effects of nicotine in canine skeletal muscle.

Studies were conducted in 36 artificially ventilated, anesthetized dogs to clarify hemodynamic effects of nicotine in resting gracilis muscle. In Series 1, effects of intravenous nicotine (36 micrograms/kg/min) were evaluated in (i) intact muscles (Condition 1), (ii) denervated muscles (Condition 2), (iii) denervated muscles following local alpha-adrenergic blockade (Condition 3), (iv) denervated muscles following combined local alpha- and beta-adrenergic blockade (Condition 4), and (v) intact muscles with aortic pressure maintained constant (Condition 5). In Series 2, nicotine was infused directly into the gracilis artery at a rate of 3.6 micrograms/kg/min. Muscle blood flow was obtained with an electromagnetic flowmeter and used to calculate vascular resistance and oxygen consumption (Fick equation). Plasma catecholamine levels were determined with a radioenzymatic method. Intravenous nicotine doubled mean aortic pressure under Conditions 1-4. In intact and denervated muscles (Conditions 1 and 2) proportional increases in vascular resistance, reflective of vasoconstriction, held blood flow constant. Muscle oxygen consumption was unchanged. alpha-Adrenergic blockade with phenoxybenzamine following denervation (Condition 3) converted muscle vasoconstriction to vasodilation during nicotine infusion. Additional beta-adrenergic blockade (Condition 4) restored muscle vasoconstriction. Nicotine-induced muscle vasoconstriction was maintained under controlled pressure (Condition 5). Intravenous nicotine significantly increased plasma catecholamine levels. Intra-arterial infusions of nicotine (Series 2) caused no hemodynamic changes in muscle. In conclusion, intravenous nicotine caused vasoconstriction in muscle, which was not due to reduced metabolic demand, pressure-flow autoregulation, or a direct [corrected] effect on vascular smooth muscle, but to stimulation of alpha-adrenergic receptors. Following denervation, this vasoconstriction was maintained by elevated plasma catecholamines. alpha-Adrenergic blockade unmasked nicotine-induced vasodilation mediated by beta-adrenergic receptors, whereas combined alpha- and beta-adrenergic blockade unmasked nicotine-induced vasoconstriction by a nonadrenergic mechanism.

Adrenergic alpha-Antagonists↗
PubMed1990

Contrast media adversely affect oxyhemoglobin dissociation.

Effects of ionic (Hypaque-76) and nonionic (Isovue-370 and Omnipaque-350) contrast media on oxyhemoglobin dissociation of normal human red blood cells were evaluated. In series 1, 4-mL venous blood samples were obtained from 15 normal human volunteers. One blood sample served as control, and 1 mL of either of the three contrast media was added in vitro to the other 4-mL blood samples. P50 values were estimated from the linear portion of the oxyhemoglobin dissociation curve obtained by tonometry. Determinations of P50 were performed at either pH 7.4 or 7.2. At pH 7.4, P50 in the absence of contrast media was 26.3 +/- 0.4 mm Hg (mean +/- SEM). The contrast media caused comparable decreases in P50 from this value (Hypaque-76, 20.0 +/- 0.5 mm Hg; Omnipaque-350, 21.6 +/- 0.4 mm Hg; Isovue-370, 20.7 +/- 0.4 mm Hg). Reducing pH to 7.2 in the absence of contrast media increased P50 to 33.3 +/- 1.0 mm Hg, evidence of the Bohr effect. The presence of contrast media either completely abolished (Hypaque-76 and Omnipaque-350) or markedly attenuated (Isovue-370) this effect. In series 2 (five patients), blood samples were withdrawn from the external iliac artery during injection of Isovue-370 (60-78 mL) into the proximal abdominal aorta to evaluate peripheral vascular disease. Measurement of P50 of these samples yielded findings consistent with those of series 1. The present findings demonstrate that both ionic and nonionic contrast media increase the affinity of hemoglobin for oxygen and, therefore, that they may inhibit oxygen delivery to body tissues.

Angiography↗
PubMed1989

Myocardial and systemic responses to arterial hypoxemia during cardiac tamponade.

Experiments were performed on 14 anesthetized, open-chest dogs to assess myocardial and systemic responses to cardiac tamponade alone (TAMP) and combined with arterial hypoxemia (HYP). Regional blood flow (RBF) was measured with radioactive microspheres and used to compute regional O2 supply. Myocardial oxygen and lactate extraction were determined. Myocardial oxygen consumption (MVO2) was calculated with Fick equation. An increase in pericardial pressure, sufficient to reduce mean aortic pressure (MAP) by 20%, caused proportional decreases in myocardial RBF and MVO2 but had no effect on endo-to-epi flow ratio or on myocardial lactate extraction. TAMP alone decreased RBF and O2 supply in kidney, splanchnic organs, skeletal muscle, and skin, but it had no effect in brain. HYP (arterial PO2, 35 +/- 2 mmHg) during TAMP restored MAP and caused transmurally uniform increases in myocardial RBF that were adequate to maintain MVO2 and lactate extraction. RBF increased sufficiently in brain to maintain regional O2 supply, whereas unchanged or inadequate increases in RBF in other tissues accentuated reductions in O2 supply. During combined TAMP and HYP, local vasodilator mechanisms were capable of maintaining adequate oxygen supply in myocardium and brain but not apparently in the nonvital tissues where these mechanisms were antagonized by reflex vasoconstriction.

Animals↗
PubMed1989

Regional hemodynamic responses to nicotine in conscious and anesthetized dogs: comparative effects of pentobarbital and chloralose.

This study was conducted in 12 dogs to evaluate regional hemodynamic responses during intravenous infusion of nicotine (36 micrograms/kg/min) in the conscious state and compare them with those in the same dogs following either pentobarbital (n = 6) or chloralose anesthesia (n = 6). Values for regional blood flow were obtained with 15-microns radioactive microspheres and used to calculate regional vascular conductance. In the conscious state, nicotine increased aortic pressure (+70%) and caused hyperventilation that reduced arterial PCO2 (-44%). These systemic effects were associated with decreases in vascular conductance in the renal cortex (-48%), pancreas (-81%), duodenum (-58%), and cerebral cortex (-55%), whereas no significant change in vascular conductance was evident in spleen, liver, or myocardium. Pentobarbital anesthesia blunted the increases in aortic pressure and respiratory activity and the reductions in vascular conductance in the renal cortex, pancreas, duodenum, and cerebral cortex during nicotine infusion. In contrast, chloralose anesthesia accentuated the increase in aortic pressure and the decrease in vascular conductance in the renal cortex during nicotine infusion, while it converted no change in vascular conductance in the spleen into a decrease and no change in vascular conductance in the myocardium into an increase. Chloralose anesthesia blunted nicotine-induced hyperventilation. These findings demonstrate that general anesthetic agents may have markedly different effects on cardiovascular reflex pathways. They emphasize the importance of considering the particular characteristics of the anesthetic agent used in interpreting results from studies of cardiovascular pharmacology and physiology in anesthetized animals.

Animals↗
PubMed1989

Influence of nifedipine on systemic and regional hemodynamics during adenosine-induced hypotension in dogs.

Previous pharmacologic studies indicating competitive interactions between adenosine and nifedipine at the adenosine vascular receptor suggest that adenosine may be a less effective hypotensive drug after pretreatment with nifedipine. This hypothesis was tested in 18 pentobarbital-anesthetized, open-chest dogs by evaluating the hypotensive effects and regional hemodynamic responses to 60-minute intravenous adenosine infusions before and after bolus injection of nifedipine (20 micrograms/kg, IV). Regional blood flow was measured with 15-microns radioactive microspheres. Before nifedipine, infusion of adenosine at a rate of 126 +/- 30 mumol/min caused a 50% reduction in mean aortic pressure that in the presence of no change in aortic blood flow was attributable to a proportional decrease in systemic vascular resistance. These systemic effects were associated with heterogeneous changes in regional blood flow; blood flow decreased in the renal cortex (-68%), pancreas (-50%), spleen (-77%), and skin (-61%); increased in the left (+112%) and right (+265%) ventricular myocardium; and did not change significantly in the duodenum, liver, skeletal muscle, or brain. Nifedipine did not alter the dose requirement or time course of the adenosine-induced hypotensive response or affect the associated systemic hemodynamic changes. Furthermore, nifedipine caused only minor alterations in the regional blood flow changes during adenosine-induced hypotension. Apparently the high plasma levels of adenosine required for controlled hypotension in the present study were sufficient to overcome the blocking influence of nifedipine at the adenosine vascular receptor. The study demonstrates that the hypotensive action of adenosine remains unimpaired after pretreatment with nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Regional hemodynamics and oxygen supply during isovolemic hemodilution in the absence and presence of high-grade beta-adrenergic blockade.

Studies were performed in 16 pentobarbital-anesthetized dogs to evaluate regional circulatory effects of isovolemic hemodilution in the absence (group 1) and presence (group 2) of high-grade beta-adrenergic blockade with propranolol. Regional blood flow measured with 15 microm radioactive microspheres was used to calculate regional oxygen supply. In group 1, hemodilution with 5% dextran (40,000 molecular weight) reduced arterial hematocrit and oxygen content by approximately one half and had heterogeneous effects on regional blood flows. Blood flow was unchanged in the renal cortex, liver, and spleen, and it increased in the pancreas, duodenum, brain, and myocardium; however, only in the brain and myocardium were increases in blood flow sufficient to maintain oxygen supply at baseline (pre-hemodilution) levels. In group 2, intravenous administration of propranolol (1 mg/kg) itself decreased blood flow in the spleen and myocardium and had no other regional effects. Hemodilution after propranolol caused regional circulatory changes that were essentially similar to those in the absence of propranolol. It is concluded that (1) during isovolemic hemodilution, oxygen supply to the brain and myocardium is maintained at the expense of oxygen supply to less critical organs, and (2) this pattern of regional circulatory response during hemodilution remains intact in the presence of high-grade beta-adrenergic blockade with propranolol.

Adrenergic beta-Antagonists↗
PubMed1988

Coronary hemodynamic responses during local hemodilution in canine hearts.

To evaluate the effect of hemodilution per se on coronary hemodynamics, experiments were performed in 36 anesthetized, open-chest dogs whose left anterior descending coronary artery (LAD) was perfused selectively with either normal arterial blood or arterial blood diluted with lactated Ringer solution. LAD blood flow (CBF) was measured with an electromagnetic flowmeter and its transmural distribution assessed with 15-microns radioactive microspheres. LAD perfusion pressure was set at the normal level (approximately 100 mmHg) or at 50% of that level to simulate coronary insufficiency. Dilator reserve capacity was calculated from ratio of reactive hyperemic peak flow following release of 90-s occlusion to control (preocclusion) flow. Systemic hemodynamic parameters were maintained near control values during coronary hemodilution. With perfusion pressure normal, graded hemodilution caused progressive, transmurally uniform increases in CBF that showed a nonlinear relationship to inflow hematocrit. Increased peak reactive hyperemic flow and decreased dilator reserve ratio indicated that both reduced viscosity and vasodilation contributed to increased CBF during hemodilution. Hypotension alone reduced CBF, with greater effect in the subendocardium. Additional hemodilution returned CBF to normotensive value, but relative subendocardial hypoperfusion persisted. The present study provides fundamental information on effects of hemodilution on coronary hemodynamics without the systemic responses that complicated previous studies utilizing whole body exchange transfusions.

Animals↗
PubMed1988

Regional hemodynamics and oxygen supply during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension.

Studies were performed in ten pentobarbital-anesthetized, open chest dogs to evaluate regional circulatory effects of isovolemic hemodilution alone, and in combination with adenosine-induced controlled hypotension. Regional blood flow measured with 15-microns radioactive microspheres was used to calculate regional oxygen supply. Hemodilution with 5% dextran (40,000 molecular weight) reduced arterial hematocrit and oxygen content by approximately one-half and caused heterogeneous changes in regional blood flows; flow decreased in the spleen, was unchanged in the renal cortex, liver, skeletal muscle and skin, and increased in the duodenum, pancreas, brain and myocardium; however, only in the brain and myocardium were increases in flow sufficient to preserve oxygen supply. Intravenous infusion of adenosine reduced aortic pressure by 50% and reduced flow in most tissues (renal cortex, pancreas, liver, spleen, skin, and brain), with the result that oxygen deficits were produced or accentuated in these organs. The magnitude of flow reductions in the renal cortex (-73%) and cerebral cortex (-37%) were noteworthy. In the myocardium, direct coronary vasodilation by adenosine caused parallel increases in blood flow and oxygen supply to levels exceeding prevailing metabolic requirements. It is concluded that 1) during isovolemic hemodilution alone, oxygen supply to the brain and myocardium is maintained at the expense of oxygen supply to less critical organs and, 2) during combined isovolemic hemodilution and adenosine-induced hypotension, oxygen is oversupplied to the myocardium but undersupplied to the brain and kidney. These latter effects suggest the need for extensive clinical monitoring of patients in whom combined isovolemic hemodilution and adenosine-induced hypotension is utilized.

Adenosine↗
PubMed1988

Myocardial oxygen consumption and segmental shortening during selective coronary hemodilution in dogs.

Experiments were conducted in 33 open chest, anesthetized dogs to evaluate direct effects of hemodilution on myocardial oxygenation and contractile function. The left anterior descending coronary artery (LAD) was perfused selectively from a controlled pressure reservoir with either normal arterial blood or arterial blood diluted with lactated Ringer's solution. Systemic hemodynamic parameters were held stable. In the LAD bed, values were obtained for coronary blood flow (CBF) with an electromagnetic flowmeter, myocardial oxygen consumption (MVO2) using the Fick principle, and percentage segmental shortening (%SS), an index of local myocardial contractility, by sonomicrometry. Studies were conducted with LAD perfusion pressure (PP) set at control (100 mm Hg) and at 50% of that level to simulate coronary insufficiency (CI). CI abolished coronary reactive hyperemia after release of a 90-second occlusion, indicating exhausted vasodilator reserve capacity. With PP at control, reductions in LAD hematocrit to as low as 10% had no effect on MVO2 or %SS, because increases in blood flow were sufficient to offset induced falls in arteriovenous oxygen content difference. However, during CI, a more modest reduction in hematocrit to 17% caused reductions in both MVO2 and %SS, because of inadequate flow responses during hemodilution. The following conclusions can be made: 1) Extreme hemodilution is well tolerated by the normal heart with a stable work requirement and; 2) Relatively modest hemodilution may compromise myocardial oxygenation and contractile function when in the presence of exhausted or severely depleted vasodilator reserve capacity.

Animals↗