Biomedical subjects

R C Koehler

Publications and source records attributed to R C Koehler.

At least 127 records · Page 7Linked to original sources

PubMed1989

Postischemic recovery rate of cerebral ATP, phosphocreatine, pH, and evoked potentials.

We tested the hypotheses that after complete cerebral ischemia, first, rate of recovery of ATP, phosphocreatine (PCr), and intracellular pH (pHi) varies with ischemic duration and second, rate of metabolic recovery is a more sensitive predictor of consequent electrophysiological deficit than steady-state metabolic recovery. With the use of transient intracranial hypertension in anesthetized dogs, ischemic duration was set for either 3, 12, or 30 min, which depressed somatosensory-evoked potential (SEP) recovery amplitude by 30, 59, and 88%, respectively. In contrast, ATP, PCr, and pHi, measured by 31P magnetic resonance spectroscopy, fully recovered. When ischemic duration was increased from 3 to 12 min, mean recovery time of ATP (6 min) remained rapid but that of pHi (12-28 min) was prolonged. After 30 min of ischemia, pHi recovery was not slowed further (25 min) but that of ATP was now markedly prolonged (36 min). PCr recovery time increased progressively with ischemic duration (5, 11, and 21 min, respectively) and correlated best with SEP recovery (r = 0.74). We conclude that the brain's ability to rapidly normalize pH is a sensitive predictor of electrophysiological recovery after short ischemia but that ATP regeneration becomes important with prolonged ischemia. PCr recovery rate was the best overall predictor, probably because it depends on both pHi and the ratio of ATP to ADP by the creatine kinase reaction.

Adenosine Triphosphate↗

PubMed1989

Relationship of diaphragmatic contractility to diaphragmatic blood flow in newborn lambs.

We determined the relationship of diaphragmatic contraction rate to diaphragmatic blood flow (Qdi), metabolism, and contractility in nine open-chested mechanically ventilated newborn lambs. The diaphragm was paced for 15 min at slow (20/min) and fast (100/min) contraction rates each followed by a 30-min rest period. There was a mild reduction in transdiaphragmatic pressure (Pdi) during the slow contraction period accompanied by a shift to the right of the curve relating stimulation frequency (10-100 Hz) to Pdi. Pdi returned to control at the start of the fast contraction period, but then fell by 30% within 2 min with continued fast contraction rates. The frequency-Pdi curve was significantly shifted to the right. Qdi, O2 transport, and O2 consumption increased during slow contraction and to an even greater extent during fast contraction. Fractional O2 extraction reached an apparent maximum during slow contraction. Lactate efflux from the right phrenic vein during slow contraction remained unchanged from control. During fast contraction lactate efflux rose proportionately more than did O2 consumption. We conclude that the energy demands at fast rates of diaphragmatic contraction in newborn lambs cannot be met by aerobic metabolism alone despite increasing O2 transport to the diaphragm.

Animals↗

PubMed1989

Hypercapnia and response of cerebral blood flow to hypoxia in newborn lambs.

Individual effects of hypoxic hypoxia and hypercapnia on the cerebral circulation are well described, but data on their combined effects are conflicting. We measured the effect of hypoxic hypoxia on cerebral blood flow (CBF) and cerebral O2 consumption during normocapnia (arterial PCO2 = 33 +/- 2 Torr) and during hypercapnia (60 +/- 2 Torr) in seven pentobarbital-anesthetized lambs. Analysis of variance showed that neither the magnitude of the hypoxic CBF response nor cerebral O2 consumption was significantly related to the level of arterial PCO2. To determine whether hypoxic cerebral vasodilation during hypercapnia was restricted by reflex sympathetic stimulation we studied an additional six hypercapnic anesthetized lambs before and after bilateral removal of the superior cervical ganglion. Sympathectomy had no effect on base-line CBF during hypercapnia or on the CBF response to hypoxic hypoxia. We conclude that the effects of hypoxic hypoxia on CBF and cerebral O2 consumption are not significantly altered by moderate hypercapnia in the anesthetized lamb. Furthermore, we found no evidence that hypercapnia results in a reflex increase in sympathetic tone that interferes with the ability of cerebral vessels to dilate during hypoxic hypoxia.

Animals↗

PubMed1989

Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine.

Pure alpha-adrenergic agonists, such as phenylephrine, and mixed alpha- and beta-adrenergic agonists, such as epinephrine, raise perfusion pressure for heart and brain during cardiopulmonary resuscitation (CPR). However, with the high doses used during CPR, these drugs may directly affect vascular smooth muscle and metabolism in brain and heart. We determined whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 micrograms/kg/min) or epinephrine (4 micrograms/kg/min) leads to equal organ blood flow, cerebral O2 uptake, and cerebral electrophysiologic function. During 20 minutes of CPR initiated immediately upon ventricular fibrillation in anesthetized dogs, left ventricular blood flow was similar with epinephrine (45 +/- 9 ml/min/100 g) or phenylephrine (47 +/- 8 ml/min/100 g) infusion. The ratio of subendocardial to subepicardial blood flow fell equivalently during CPR with either epinephrine (1.23 +/- 0.06 to 0.70 +/- 0.05) or phenylephrine (1.32 +/- 0.07 to 0.77 +/- 0.05) administration. At similar levels of cerebral perfusion pressure (44 +/- 3 mm Hg), similar levels of cerebral blood flow were measured in both groups (27 +/- 3 ml/min/100 g). Cerebral O2 uptake was maintained at prearrest levels in both groups. Somatosensory-evoked potential amplitude was modestly reduced during CPR, but it promptly recovered after defibrillation. During CPR and at 2 hours after resuscitation, there were no differences between drug groups in the level of regional cerebral or coronary blood flow, cerebral O2 uptake, or evoked potentials. Therefore, with minimal delay in the onset of CPR and with equipotent pressor doses of phenylephrine and epinephrine, we found no evidence that one agent provides superior coronary or cerebral blood flow or that epinephrine by virtue of its beta-adrenergic properties adversely stimulates cerebral metabolism at a critical time that would impair brain electrophysiologic function. Moreover, epinephrine did not preferentially impair subendocardial blood flow as might be expected if it enhanced the strength of fibrillatory contractions.

Animals↗

PubMed1989

Cerebral and peripheral circulatory responses to intracranial hypertension in fetal sheep.

Fetal head compression during normal labor can increase intracranial pressure (ICP). We studied the cerebral and peripheral blood flow responses to ICP elevation in utero in chronically catheterized fetal sheep using the radiolabeled microsphere technique. ICP was elevated, stepwise, in increments of 6 +/- 1 mm Hg by infusion of artificial cerebrospinal fluid into a lateral ventricle. When ICP was raised to within 28 mm Hg of baseline mean arterial blood pressure (i.e., ICP above 22 mm Hg), arterial pressure began to increase. Above this ICP level, up to 41 mm Hg, mean cerebral perfusion pressure was maintained by equivalent increases in arterial pressure. Cerebral blood flow and O2 uptake at the highest ICP levels were not different from baseline values. Changes in peripheral organ blood flow were graded according to the level of ICP. At the highest level (ICP = 41 mm Hg), renal, gastrointestinal, and skin blood flow decreased by 68%, 69%, and 65%, respectively. Myocardial and adrenal blood flow doubled, whereas heart rate and cardiac output were unchanged. Placental blood flow increased in proportion to arterial pressure. Arterial plasma epinephrine, norepinephrine and arginine vasopressin increased by nearly two orders of magnitude. Therefore, as ICP approaches baseline mean arterial pressure, fetal lambs are capable of sustaining cerebral perfusion by initiating profound visceral vasoconstriction without curtailing placental blood flow. Since cerebral O2 uptake was maintained, there is no evidence that stimulation of the peripheral response requires pronounced cerebral ischemia. This highly developed Cushing response may be important for ensuring cerebral viability when the fetal head is compressed during parturition.

Animals↗

PubMed1989

Blood flow during cardiopulmonary resuscitation with simultaneous compression and ventilation in infant pigs.

We determined whether the simultaneous chest compression and ventilation (SCV) technique of cardiopulmonary resuscitation (CPR) enhances cerebral (CBF) and myocardial (MBF) blood flows and cerebral O2 uptake in an infant swine model of CPR as it does in most adult animal CPR models. We also tested whether SCV-CPR sustains CBF and MBF for prolonged periods of CPR when these flows ordinarily deteriorate. CPR was performed in two groups (n = 8) of pentobarbital anesthetized piglets (3.5-5.5 kg) with continuous epinephrine infusion (10 micrograms/kg/min). Conventional CPR was performed at 100 compressions/min, 60% duty cycle, 1:5 breath to compression ratio and 25-30 mm Hg peak airway pressure. SCV-CPR was performed at 60 compressions/min, 60% duty cycle and 60 mm Hg peak airway pressure applied during each chest compression. Peak right atrial and aortic pressures in excess of 80 mm Hg were generated during CPR in both groups. At 5 min of conventional and SCV-CPR, MBF was 38 +/- 7 and 46 +/- 7 mL.min-1.100 g-1 (+/- SE), respectively, and CBF was 15 +/- 3 and 13 +/- 2 mL.min1. 100 g-1, respectively. However, as CPR was prolonged to 50 min, the sternum progressively lost its recoil and the chest became more deformed. Lung inflation at high airway pressure with SCV-CPR did not prevent this chest deformation. Aortic pressure gradually declined, whereas right atrial and intracranial pressure remained constant in both groups. Consequently, MBF and CBF fell less than 10 mL.min-1.100 g-1 and cerebral O2 uptake was markedly impaired during prolonged conventional and SCV-CPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Base-line O2 extraction influences cerebral blood flow response to hematocrit.

We have shown that the fall in cerebral blood flow (CBF) as hematocrit (Hct) rises is due to the independent effects of increasing red blood cell (RBC) concentration and arterial O2 content (CaO2). In the present study, we tested the hypothesis that the magnitude of the effect of RBC concentration depends on the base-line cerebral fractional oxygen extraction (E). E is the ratio of O2 demand (cerebral O2 consumption, CMRO2) to supply (cerebral O2 transport: OT = CBF x CaO2) and is assumed to be inversely related to tissue O2 availability. Pentobarbital-anesthetized 1- to 7-day-old sheep were first exchange transfused with plasma to lower Hct to 20%. Base-line E was set to either high or low levels by induction of hypocarbia [arterial CO2 partial pressure (PaCO2) = 15.3 +/- 0.7 mmHg, means +/- SE; n = 7] or hypercarbia (PaCO2 = 62.7 +/- 1.1 mmHg; n = 5), respectively. A second isovolemic exchange transfusion with pure methemoglobin-containing adult sheep red cells then raised Hct (to 38.5 +/- 0.5%) with no significant increase in CaO2. PaCO2 was maintained and other variables (oxyhemoglobin affinity, pH, mean arterial blood pressure) with potential effect on CBF did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗

PubMed1988

Effect of jugular venous pressure on cerebral autoregulation in dogs.

We determined the importance of a myogenic sensor of cerebral autoregulation by assessing the effect of vascular transmural pressure on cerebral blood flow (CBF) as cerebral perfusion pressure (CPP) was decreased. Decreasing CPP by decreased arterial pressure (Pa) or increased intracranial pressure (Pcsf) decreases transmural pressure, whereas increased jugular venous pressure (Pjv) increases transmural pressure. Regional CBF was measured in barbiturate-anesthetized dogs using radiolabeled microspheres. In group 1 (n = 5), CPP was decreased by decreasing Pa; in group 2 (n = 5), CPP was decreased by increasing Pcsf (Pa = 80 mmHg); and in group 3 (n = 5) CPP was decreased by increasing Pjv (Pa = 80 mmHg). CPP was reduced from 80 to 30 mmHg in 10-mm increments in each group. In groups 1 and 2 regional CBF was maintained as CPP was decreased to 40 mmHg; however, at CPP of 30 mmHg, blood flow to cerebrum, caudate, and periventricular white matter decreased, whereas flow to cerebellum and medulla remained unchanged. In group 3 regional CBF was unchanged as CPP decreased from 80 to 50 mmHg but decreased in all regions as CPP decreased further. In all three groups, cerebrovascular resistance continuously declined as CPP was decreased. In all groups, cerebral O2 uptake was unaltered. Autoregulation fails at a higher CPP with increased Pjv than with decreased Pa or increased Pcsf, particularly in brain stem. We conclude that metabolic autoregulation predominates over the myogenic mechanism until CPP is low.

Animals↗

PubMed1987

Effects of fentanyl on peripheral and cerebral hemodynamics in neonatal lambs.

The effects of fentanyl or cardiovascular function, regional distribution of cardiac output, and the dose required for producing anesthesia were studied in ten previously catheterized, newborn lambs. In addition, the effects of fentanyl on cerebral blood flow and oxygen utilization were examined. Fentanyl in cumulative doses as high as 4.4 mg/kg (average plasma levels of 646 +/- 95 ng/ml, maximum plasma level of 862 ng/ml) did not reliably produce anesthesia as assessed by tail and foot clamping, although it did cause profound respiratory depression. With normocapnia maintained by mechanical ventilation, fentanyl did not alter cerebral oxygen delivery or consumption, and the two remained coupled. Fentanyl did not affect cardiac output, heart rate, or mean arterial blood pressure at the highest dose level, nor did it reduce blood flow to specific organ beds, other than the kidney. Thus, the hemodynamic stability seen with fentanyl in the lamb does not occur at the expense of reduced blood flow to organs, such as the gastrointestinal tract or brain, that are particularly vulnerable in the neonate.

Animals↗

PubMed1987

Cerebral blood flow autoregulation during intracranial hypertension in hypoxic lambs.

We tested the hypothesis that hypoxic hypoxia interferes with cerebral blood flow (CBF) autoregulation when intracranial pressure (ICP) is elevated in pentobarbital-anesthetized lambs (3 to 9 days old). Cerebral perfusion pressure (CPP) was lowered stepwise from 73 to 23 mmHg in eight normoxic lambs and from 65 to 31 mmHg in eight other hypoxic lambs by ventricular infusion of artificial cerebrospinal fluid. In normoxic lambs, CBF measured by microspheres was not significantly changed over this range of CPP. In animals made hypoxic [arterial O2 tension (PaO2) of 28 Torr; 47% arterial O2 saturation], base-line CBF was twice that of normoxic lambs. CBF was unchanged as CPP was reduced to 31 mmHg. Lower levels of CPP were not attained because a pressor response occurred with further elevations of ICP. No regional decrements in blood flow to cortical arterial watershed areas or to more caudal regions, such as cerebellum, brain stem, or thalamus, were detected with elevated ICP. Cerebral O2 uptake was similar in both groups and did not decrease when CPP was reduced. These results demonstrate that normoxic lambs have a considerable capacity for effective autoregulation of CBF when ICP is elevated. Moreover, cerebral vasodilation in response to a level of hypoxia approximating that normally seen prenatally does not abolish CBF autoregulation when ICP is elevated during the first postnatal week.

Animals↗

PubMed1987

Effect of hematocrit on cerebral blood flow with induced polycythemia.

Cerebral blood flow (CBF) is lowered during polycythemia. Whether this fall is due to an increase in red blood cell concentration (Hct) or to an increase in arterial O2 content (Cao2) is controversial. We examined the independent effects of Hct and Cao2 on CBF as Hct was raised from 30 to 55% in anesthetized 1- to 7-day-old sheep. CBF was measured by the radiolabeled microsphere technique before and after isovolemic exchange transfusion with either oxyhemoglobin-containing erythrocytes (in 5 control animals) or with methemoglobin-containing erythrocytes (in 9 experimental animals). Following exchange transfusion in the control animals, Hct rose (30 +/- 1 vs. 55 +/- 1%, mean +/- SE), Cao2 increased (15.1 +/- 0.8 vs. 26.7 +/- 0.9 vol%), and CBF fell (66 +/- 9 vs. 35 +/- 5 ml X min-1 X 100 g-1). Because the fall in CBF was proportionate to the rise in Cao2, cerebral O2 transport (CBF X Cao2) was unchanged. Following exchange transfusion in the experimental animals, Hct rose (32 +/- 1 vs. 55 +/- 1%) but Cao2 did not change. Nevertheless, CBF still fell (73 +/- 4 vs. 48 +/- 2 ml X min-1 X 100 g-1) and, as a result, cerebral O2 transport also fell. The latter cannot be attributed to a fall in cerebral O2 uptake, as cerebral O2 uptake was unaffected during each of these conditions. Comparison of the two groups of animals showed that approximately 60% of the fall in CBF may be attributed to the increase in red cell concentration alone. It is probable that this effect is due largely to changes in blood viscosity.

Animals↗

PubMed1987

Age-related changes in chest geometry during cardiopulmonary resuscitation.

We studied alterations of chest geometry during conventional cardiopulmonary resuscitation in anesthetized immature swine. Pulsatile force was applied to the sternum in increments to determine the effects of increasing compression on chest geometry and intrathoracic vascular pressures. In 2-wk- and 1-mo-old piglets, permanent changes in chest shape developed due to incomplete recoil of the chest along the anteroposterior axis, and large intrathoracic vascular pressures were generated. In 3-mo-old animals, permanent chest deformity did not develop, and large intrathoracic vascular pressures were not produced. We propose a theoretical model of the chest as an elliptic cylinder. Pulsatile displacement along the minor axis of an ellipse produces a greater decrease in cross-sectional area than displacement of a circular cross section. As thoracic cross section became less circular due to deformity, greater changes in thoracic volume, and hence pressure, were produced. With extreme deformity at high force, pulsatile displacement became limited, diminishing pressure generation. We conclude that changes in chest geometry are important in producing intrathoracic intravascular pressure during conventional cardiopulmonary resuscitation in piglets.

Adolescent↗

PubMed1986

Adrenal medullary and cortical blood flow during hemorrhage.

We used a radiolabeled microsphere technique to measure adrenal medullary and cortical blood flow during hemorrhagic hypotension. Twenty pentobarbital-anesthetized, ventilated, adult mongrel dogs were bled into a pressurized bottle system to reduce and maintain mean arterial blood pressure at 100, 80, 60, or 40 mmHg (n = 5/group). Blood flow was measured prior to and 2, 5, 10, 15, and 25 min posthemorrhage. Adrenal medullary blood flow increased markedly (100-400%) at all levels of hemorrhage. In contrast, decreases in cortical blood flow were observed (approximately 50%) with hemorrhage to 80, 60, and 40 mmHg. Cortical blood flow returned to control levels at 25 min, except in the 40-mmHg group. Whole adrenal gland blood flow showed early, transient decreases, consistent with the fact that the adrenal cortex comprises the bulk of the gland, but it did not precisely reflect either cortical or medullary blood flow changes. Since this method for measuring adrenal medullary and cortical blood flow was developed for the current experiment, extensive evaluation of the technique was performed (n = 31 animals). These studies included demonstration that injection of 4 X 10(6) microspheres results in sufficient numbers of microspheres in the adrenal medulla and cortex to permit estimation of blood flow (greater than or equal to 400 spheres/sample), that 15-micron spheres are almost completely entrapped in the adrenal gland (greater than 98%), that multiple injections of microspheres (n = 5) do not alter blood flow, and that streaming of microspheres does not appear to occur to any significant extent in this vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗

PubMed1986

Role of O2-hemoglobin affinity in the regulation of cerebral blood flow in fetal sheep.

Cerebral blood flow (CBF) and cerebral O2 transport (CBF X arterial O2 content) in the fetal sheep are nearly twice that in the adult, despite similar rates of cerebral O2 utilization. We tested the hypothesis that the difference depends on the increased oxyhemoglobin affinity in the fetus, using P50 (PO2 at which hemoglobin is 50% saturated) as the index of oxyhemoglobin affinity. We studied 18 unanesthetized fetal sheep in utero. In six animals the P50 was raised from 16.6 +/- 1.2 (SD) mmHg to 31.7 +/- 4.7 mmHg by exchange transfusing the fetus with adult sheep red blood cells. We measured CBF (with radioactive microspheres) and the PO2, PCO2, pH, and O2 content in carotid artery and sagittal sinus blood twice at the original P50 and twice after exchange transfusion. Arterial O2 content fell significantly at the higher P50. Since the fall in O2 content was not accompanied by a corresponding rise in CBF, O2 transport fell by 45%. Cerebral O2 consumption (CMRO2) did not change and cannot be implicated in the fall of O2 transport. E (the ratio CMRO2/O2 transport) rose by 77%. Sham exchange transfusions in six fetuses showed that the exchange transfusion procedure itself was not responsible for this alteration. To determine whether the fall in O2 transport and the rise in E was reproducible over a range of arterial O2 contents, a third group of six fetuses was studied. Fetal arterial O2 content varied from 4 to 12 vol%, first at P50 = 17 +/- 1.8 mmHg and again after exchange transfusion at P50 = 29.6 +/- 3.9 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Effect of hematocrit on cerebral blood flow.

Cerebral blood flow (CBF) falls as hematocrit (Hct) rises. Investigators have differed on the relative importance of the increases in arterial O2 content (CaO2) and red blood cell concentration in mediating the fall. Our experimental protocol attempted to determine the independent effects of these two variables. In 13 unanesthetized lambs (less than 7 days old) we measured arterial and sagittal sinus blood gases, and O2 contents, and CBF (microsphere technique) at oxyhemoglobin Hcts of approximately 20 and 40% and after an isovolemic exchange transfusion with a mixture of normal and pure methemoglobin (MHb) containing red cells. Following MHb exchange, Hct rose (19.7 +/- 0.3 vs. 38.2 +/- 0.4%, mean +/- SEM) with little change in CaO2 (9.3 +/- 0.2 vs. 10.0 +/- 0.3 vol%). Arterial PCO2, pH, mean arterial blood pressure, and cerebral O2 consumption (CMRO2) did not change. However, CBF fell (153 +/- 11 vs. 110 +/- 7 ml . 100 g-1 . min-1). CBF declined further when CaO2 rose (17.3 +/- 0.5 vol%) at the higher oxyhemoglobin Hct (36.9 +/- 0.8%). We calculated that the increase in red cell concentration accounted for 56% of the decrease in CBF that ordinarily occurs as Hct rises from 20 to 40%. The effect of red cell concentration on CBF varied among individual animals. It correlated closely (r = -0.77) with the initial cerebral fractional O2 extraction [E = CMRO2/(CBF X CaO2)]. Animals with the most luxuriant O2 supply (CBF X CaO2) relative to demand (CMRO2) had the greatest decrements in CBF as red blood cell concentration rose.

Animals↗

PubMed1986

Influence of reduced oxyhemoglobin affinity on cerebrovascular response to hypoxic hypoxia.

Increasing P50 (PO2 at 50% oxyhemoglobin saturation) reduces cerebral blood flow (CBF) during arterial normoxia. We tested the hypothesis that increasing P50 also diminishes the CBF response to isocapnic hypoxic hypoxia and that it reduces the response in proportion to the reduced normoxic CBF. P50 was increased in nine unanesthetized newborn lambs from 26.3 +/- 1.7 (+/-SE) to 36.6 +/- 2.0 Torr by isovolemic exchange transfusion with low-affinity, adult sheep blood. Microsphere-determined CBF was decreased 22% during arterial normoxia. The slope of the response curve to reduced arterial O2 content (CaO2) was proportionately attenuated by 26% with no change in O2 uptake. Consequently, O2 transport (CBF X CaO2) was reduced by a constant amount at each CaO2 level. The percentage decrease in CBF at the higher P50 was thus independent of CaO2, and the percentage increase in CBF as CaO2 fell was independent of P50: the effects of P50 and CaO2 were independent. Common to alterations in both P50 and CaO2 are alterations in capillary and tissue PO2. In this study the variable closest to capillary PO2 was sagittal sinus PO2. We found that when venous PO2 was altered by changing CaO2, the change in CBF was equivalent to that following the same alteration in venous PO2 after a change in P50. The percentage increase in venous PO2 after exchange transfusion was approximately one-half that of the increase in P50. About one-half of the potential increase in cerebral venous PO2 was therefore eliminated by a compensatory reduction in cerebral O2 transport over a wide range of CaO2.

Animals↗

PubMed1986

Effect of epinephrine on cerebral and myocardial perfusion in an infant animal preparation of cardiopulmonary resuscitation.

We assessed the efficacy of conventional cardiopulmonary resuscitation (CPR) in 2-week-old piglets. We determined intrathoracic vascular pressures, cerebral (CBF) and myocardial blood flows (MBF), and cerebral oxygen uptake during conventional CPR in this infant animal preparation and contrasted these results with those of previous work on adult animals. We further examined the effects of the infusion of epinephrine on these pressures and flows and on cerebral oxygen uptake, which has not been previously evaluated in adult preparations. Conventional CPR was performed on pentobarbital-anesthetized piglets with a 20% sternal displacement with the use of a pneumatic piston compressor. Chest recoil was incomplete, leading to an 18% to 27% reduction in anteroposterior diameter during the relaxation phase. Aortic and right atrial pressures in excess of 80 mm Hg were generated. These pressures are greater than those generally obtained in adult animals with similar percent pulsatile displacements. CBF and MBF were also initially greater than those reported in adult animals undergoing conventional CPR. However, when CPR was prolonged beyond 20 min, aortic pressure fell and CBF and MBF declined to the near-zero levels seen in adult preparations. At 5 min of CPR, CBF and MBF were 24 +/- 7 and 27 +/- 7 ml . min-1 x 100 g-1 (50% and 17% of the values during cardiac arrest), respectively. With the continuous infusion of epinephrine (4 micrograms/kg/min) in another group of animals, MBF was significantly greater at 20 min of CPR and CBF and cerebral O2 uptake were greater at 35 min of CPR as a result of higher perfusion pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Beneficial effect of epinephrine infusion on cerebral and myocardial blood flows during CPR.

It is hypothesized that epinephrine improves the ability to resuscitate the heart through a mechanism thought to be related to the increase in aortic pressure. Our results with epinephrine infusion during CPR are consistent with this hypothesis. Epinephrine selectively increased vascular resistance in noncerebral, noncoronary vascular beds, as indicated by a decrease in microsphere-determined blood flow in these areas. This increased vascular resistance raised aortic pressure during the chest compression phase and the relaxation phase of CPR. Because intracranial and right atrial pressures were only slightly higher with epinephrine, cerebral and myocardial perfusion pressures and blood flows were significantly improved. This beneficial effect (compared to no administration of a vasopressor) was more pronounced as CPR progressed beyond ten minutes. Enhanced cerebral and myocardial perfusion occurred with epinephrine when either the conventional or simultaneous compression and ventilation (SCV) mode of CPR was employed in dogs. Similar selective perfusion was sustained for 50 minutes of SCV-CPR with epinephrine, even when the onset of CPR was delayed five minutes. Regional brain blood flow differed in the delayed-CPR group in that cerebellum, brain stem, and thalamic regions initially had higher blood flows. In an infant animal model of CPR using conventional CPR in piglets, epinephrine also was found to increase cerebral and myocardial blood flows. These results show that administration of epinephrine benefits different age groups of different species with different modes of CPR; that benefits occur even with delayed onset of CPR which is associated with additional anoxia and acidosis; and that epinephrine administration is particularly effective in sustaining cerebral and coronary perfusion during prolonged CPR.

Aging↗