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Biomedical subjects

M C Rogers

Publications and source records attributed to M C Rogers.

At least 37 records · Page 2Linked to original sources
PubMed1989

Cerebral blood flow and evoked potentials during Cushing response in sheep.

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

Animals↗
PubMed1989

Noninvasive determination of hemoglobin saturation in dogs by derivative near-infrared spectroscopy.

An in vivo method utilizing derivative near-infrared spectroscopy was developed to noninvasively determine cerebral venous hemoglobin O2 saturation (SVO2). The method was tested on eight pentobarbital-anesthetized dogs ventilated with differing inspired O2 mixtures to force changes in SVO2 over a wide range. Spectral data obtained by transilluminating the tissues surrounding the superior sagittal sinus (SS) were transformed into first derivative units for correlation with SVO2 data measured from the SS. Linear regression analysis was applied to data obtained from five dogs and used to build a three-wavelength algorithm for predicting brain SVO2. In three dogs, SVO2 was varied to test this equation ability to predict SVO2. The standard deviation of differences between measured SVO2 and SVO2 predicted from 31 separate spectra was 3.2%. These predicted values, when regressed against the sampled SVO2, yielded an r value of 0.97. The results demonstrate that during hypoxic hypoxia (HH) it is possible to noninvasively quantify SVO2 with the use of infrared spectroscopy.

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

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

Effect of PEEP and jugular venous compression on canine cerebral blood flow and oxygen consumption in the head elevated position.

Cerebral blood flow (CBF) (radiolabelled microspheres) and oxygen consumption (CMRO2) were studied in nine dogs during 30 min of either neck vein compression or application of positive end-expiratory pressure (PEEP) ventilation. With the animal in the prone position, elevation of the head from horizontal to 30 cm above the heart markedly decreased cisterna magna (PCSF) and dorsal sagittal sinus pressure (PCV). With the head elevated, compression of neck veins using neck tourniquet (pressure 40 mmHg) increased PCSF and PCV from 3.6 +/- 2.2 to 6.8 +/- 4.8 and -2.5 +/- 2.7 to 2.3 +/- 2.3 mmHg (mean +/- SE, P less than 0.05), respectively, while total or regional CBF and CMRO2 remained unchanged. Application of PEEP (15 cm H2O) increased right atrial pressure (-4.7 +/- 1.7 to -0.1 +/- 3.4 mmHg, P less than 0.05), but did not affect PCSF or PCV (3.4 +/- 3.3 to 3.3 +/- 3.7 and -3.5 +/- 2.6 to -4.1 +/- 2.4 mmHg, respectively, P greater than 0.05). Total or regional CBF and CMRO2 were also unaffected. These data demonstrate that, although neither maneuver affects CBF or CMRO2, neck vein compression elevates PCV above atmospheric pressure, but PEEP does not. In patients at risk for cerebral venous embolism, intermittent neck vein compression should be used as a prophylactic measure to prevent air embolism.

Animals↗
PubMed1987

Effects of halothane on myocardial high-energy phosphate metabolism and intracellular pH utilizing 31P NMR spectroscopy.

Utilizing 31phosphorus nuclear magnetic resonance (NMR) spectroscopy, the authors tested the two hypotheses that the negative inotropic action of halothane is the result of: 1) myocardial intracellular acidosis, and 2) a decrease in myocardial high-energy phosphates. In isolated, paced, Langendorff-perfused rabbit hearts, halothane (1.5 vol %) dissolved in the coronary perfusate produced a 48 +/- 2% decrease (P less than 0.01) in left ventricular developed pressure. In contrast, halothane administration had no significant effect on myocardial intracellular pH (7.18 +/- 0.04 at control vs 7.21 +/- 0.02 during halothane). Halothane exposure decreased (P less than 0.01) the forward rate constant of the creatine kinase reaction by 32 +/- 6%, as measured using saturation transfer NMR, suggesting a decline in the rate of high-energy phosphate metabolism. This was further indicated by a concomitant decrease (P less than 0.05) in myocardial oxygen consumption (20 +/- 5%). During the halothane-induced reduction in left ventricular developed pressure, only small decreases in the myocardial steady state concentrations of phosphocreatine (7 +/- 1%; P less than 0.01) and beta ATP (12 +/- 4%; P less than 0.05), and an increase in Pi (18 +/- 6%; P less than 0.05) were observed. However, similar changes in steady-state high-energy phosphate metabolites were also measured in time-control hearts not exposed to halothane. These results indicate that the negative inotropic action of halothane is not mediated by myocardial intracellular acidosis. Moreover, these findings do not support the concept that the negative inotropic action of halothane is the result of a reduction in myocardial high-energy phosphates.

Adenosine Triphosphate↗
PubMed1987

Evaluation of sepsis in a critically ill surgical population.

We report a new clinical rating system which assesses septic patients' ongoing disease course and its severity. Our system incorporates the Therapeutic Intervention Scoring System (TISS) and Acute Physiology and Chronic Health Evaluation to measure discrete organ system abnormalities, plus a multiple system organ failure scale to quantify the number of abnormal organ systems. The resulting score, which reflects the severity of multiple organ dysfunction and grades responsiveness to therapy, was validated against the actual disease course. Retrospective and prospective profiles of individual surgical ICU patients demonstrated that this tracking method was a more effective indicator of severity of sepsis and more sensitive to the day-to-day changes in clinical status than either the TISS or APACHE II components alone. We also demonstrate that a graphic illustration of daily system scores yields clinically useful information relevant to the patients' septic course.

Bacterial Infections↗
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↗
PubMed1987

O2 radicals mediate reperfusion lung injury in ischemic O2-ventilated canine pulmonary lobe.

This study was undertaken to determine whether lung injury after a period of ischemia reperfusion is caused by O2 ventilation during ischemia and whether this injury is mediated by reactive O2 metabolites. Isolated canine left lower pulmonary lobes were subjected to room temperature ischemia for 6 h while being ventilated with either 100% O2, room air, or 100% N2. After the ischemic period, all lobes were perfused with autologous blood and ventilated with 100% O2 for an additional 4 h. In lobes ventilated with 100% O2 during the ischemic period, massive weight gain (228%) occurred 4 h after reperfusion. A marked increase in pulmonary shunt was noted. Lobes ventilated with room air behaved similarly. In contrast, lobes ventilated with 100% N2 gained significantly less weight (54%) and did not manifest any increase in pulmonary shunt. When lobes ventilated with 100% O2 or room air were pretreated with superoxide dismutase (SOD), the injury was significantly reduced. Pressure-volume deflation study of lobes, after ischemia only, demonstrated that ventilation with 100% O2 and with 100% N2 both equally decreased pulmonary compliance. We conclude that lung ischemia-reperfusion injury is related to O2 ventilation during ischemia and that injury can be prevented by administration of SOD or ventilation with 100% N2. This suggests that the injury is related to O2 metabolites produced during O2 ventilation in the absence of the circulation.

Animals↗
PubMed1986

Increased myocardial infarct size by thiopental after coronary occlusion in the dog.

The effect of a single dose (10 mg/kg) of intravenous thiopental (TP), during acute myocardial infarction, on infarct size was studied in conscious dogs randomized 10 minutes after left circumflex coronary artery occlusion to either the TP group (n = 10) or a control group given 0.9% saline solution (n = 10). During the first hour following therapy, myocardial blood flow (microspheres), arterial pressure, left atrial pressure, and arterial blood gases were similar in the two groups, but the heart rate (140 +/- 3 vs 110 +/- 3 bpm; p less than 0.001) and rate-pressure product (15,090 vs 12,210 bpm X mm Hg; p less than 0.025) were greater in the TP group. Infarct size (planimetry) and occluded bed size (postmortem coronary arteriography) measured 2 days later revealed that: the slope of the relation between infarct and occluded bed mass, as a percentage of the left ventricle (% LV) was greater with TP than with saline solution (1.10 vs 0.61; p less than 0.001); excluding hearts (four TP and three saline solution) with small occluded beds (less than 22% LV), infarcts were also larger with TP (n = 6) than with saline solution (n = 7), both as a percentage of the left ventricle (26.4 vs 12.2%; p less than 0.02) or occluded bed (61.5 vs 28.9%; p less than 0.005); and transmural and endocardial extents of the infarcts on topographic maps were greater with TP than with saline solution. In 12 other conscious dogs, increasing the heart rate between 10 and 70 minutes after left circumflex coronary artery occlusion to the average rate of the TP group (140 bpm) by atrial pacing resulted in infarcts larger than those in control dogs but similar to those in the TP group. Thus, TP therapy after left circumflex occlusion increased infarct size in dogs. This effect appeared to be due mainly to the increased heart rate, probably via increased myocardial oxygen demands.

Animals↗
PubMed1986

Lack of validity of diagnosis-related group payment systems in an intensive care population.

Case mix based on diagnosis-related groups (DRGs) was studied over 3 years for duration of stay and mean charges for a pediatric intensive care unit (PICU) and a general ward (WARD) population. Case mix variation for 2403 PICU and 14,552 WARD patients was analyzed, and a subset of 856 PICU and 2222 WARD patients examined for variations in duration of stay and mean charges in nine DRGs. Whereas case mix by DRG was consistent over time for both groups, the PICU case mix differed consistently from WARD case mix (P less than 0.001). After adjustment for inflation and for differences in case mix, average stay for the PICU was 10.7 days, versus 6.1 for the WARD (P less than 0.025), with a mean charge of $7172 per PICU and $2946 per WARD patient (P less than 0.01). Furthermore, the case mix-adjusted differences in duration of stay and mean charge between the PICU and WARD populations increased over time. Pediatricians will need to address DRG-based reimbursement systems that place intensive care units, and their institutions, at a significant financial disadvantage.

Adolescent↗