Biomedical subjects

S Frinak

Publications and source records attributed to S Frinak.

24 records · Page 2Linked to original sources

PubMedDate not supplied

Brain tissue pH after global brain ischemia and barbiturate loading in rats.

Studies were done on rats to determine whether thiopental loading after complete, transient, global brain ischemia causes more rapid postischemic normalization of brain tissue pH. Fifteen halothane-anesthetized rats were subjected to 16 min of complete global brain ischemia by a combination of systemic arterial hypotension (40 torr) and a high pressure (1500 torr) neck cuff. Brain tissue pH was continuously monitored for up to 2 hour postischemia with microelectrodes (tip diameters of one to two micrometers) inserted about 500 micrometers into the parietal cortex. During ischemia, brain pH fell rapidly within the first 5 min from 7.0 to 6.2 and changed little thereafter. With restoration of arterial pressure and deflation of the neck cuff, pH did not immediately begin to rise back towards normal. Instead, after a few minutes, it transiently fell to even lower values before beginning to increase indicating increased tissue lactic acidosis when the brain is resaturated with glucose upon reperfusion. Beginning at 5 min postischemia, 7 of the 15 rats were infused with thiopental (90 mg/kg, IV over 60 min). At 30 min postischemia, brain tissue pH was similar in both groups and by 60 min, back to preischemic values. We conclude that thiopental loading postischemia does not improve normalization of brain pH. The transient decrease in brain pH with reperfusion is discussed.

Animals↗

PubMedDate not supplied

Intracellular acidosis during and after cerebral ischemia: in vivo nuclear magnetic resonance study of hyperglycemia in cats.

In vivo 31P nuclear magnetic resonance spectroscopy was used to monitor the time course of intracellular pH in cat cerebral cortex subjected to global cerebral ischemia under control and hyperglycemic pretreatment conditions. Transient (16 minutes) global cerebral ischemia was induced in 14 cats using an inflatable cervical cuff combined with systemic arterial hypotension. Six cats were pretreated with infusion of 1.5 g/kg glucose prior to ischemia. Relative concentrations of high-energy phosphate metabolites and intracellular pH were continuously monitored before, during, and for 2 hours after cerebral reperfusion. During ischemia, intracellular pH fell to the same level and followed a similar time course in both groups. However, during initial reperfusion in the hyperglycemic group, there was a severe further decline (p less than 0.003) in intracellular pH. We suggest that the increased neurologic deficit and mortality found in hyperglycemic animals subjected to cerebral ischemia may be attributed to this transient severe tissue acidosis.

Acidosis↗

PubMedDate not supplied

Pyridine nucleotide redox state and blood flow of the cerebral cortex following middle cerebral artery occlusion in the cat.

Acute changes in the redox state of NADH in the cerebral cortex of cats were investigated following occlusion of the middle cerebral cortex (MCA) and were correlated with alterations of regional cerebral blood flow in the ischemic cortex determined autoradiographically. Arterial occlusion was accomplished via the transorbital approach. Cortical fluorescence and reflected light signals were recorded from the central MCA territory by means of a beam-splitting fluorometer, and a fluorescence signal corrected for alterations in intravascular hemoglobin was derived. Following arterial occlusion, there was a rapid increase in cortical NADH fluorescence, peaking within 30 to 70 seconds at 20% to 40% of full scale. This was followed by a slow linear decline in fluorescence over the next several minutes. The behavior of cortical NADH fluorescence was unaffected by replacement of the ambient air over the cortical surface with nitrogen. Mean regional blood flow values in the most ischemic gyri two to 15 minutes following arterial occlusion were 21% to 23% of the corresponding values in the opposite, nonischemic hemisphere. In individual animals, peak NADH fluorescence values following arterial occlusion correlated with the extent of blood flow reduction in the affected ischemic gyri (P less than 0.05).

Animals↗

PubMedDate not supplied

The effect of cooled dialysate on thermal energy balance in hemodialysis patients.

The authors have monitored extracorporeal thermal energy balance using continuous in-line arterial and venous temperature and blood flow measurements. Use of dialysate at 37 degrees C resulted in a mean heat energy gain of 83 +/- 61 cal/min, whereas dialysate at 34 degrees C produced a loss of 463 +/- 121 cal/min. Monitoring extracorporeal thermal energy balance during cooled-dialysate hemodialysis will facilitate the use of feedback loops for dialysate temperature control in order to maximize hemodynamic stability while reducing discomfort. This methodology also may be helpful in assessing the metabolic effects of protein intake, high flux dialysis, membrane biocompatibility, and adequacy of dialysis in relation to thermal energy balance.

Adult↗

PubMedDate not supplied

Detecting vascular access dysfunction.

Access flow (QACC) is a major determinant of patency. Access recirculation (AR > 2%), normalized venous intra-access pressure (vPIA/MAP), and QACC are used to detect access dysfunction. We compared these three measures of access function (ultrasound dilution to measure AR and QACC). A total of 779 measurements were performed on 58 arteriovenous fistulas (AVFs) and 114 polytetrafluoroethylene (PTFE) grafts (1-8/access) over 13 months, and the access parameters at the beginning of each period were related to access events within that period. Pump blood flow averaged > 420 ml/min. AR occurred uncommonly (3.8%), and in half the cases, resulted from technical error by staff. In accesses that thrombosed or underwent intervention for stenosis, AR was present in only 3 of 11 AVFs and 8 of 57 PTFE accesses. When AR was present in grafts, QACC averaged 270 +/- 23, and access thrombosis followed unless intervention occurred. In grafts, vPIA/MAP averaged 0.34 +/- 0.01 in those remaining patent, 0.52 +/- 0.08 in those that had undergone intervention, and 0.54 +/- 0.04 in those that had thrombosed. QACC averaged 1,121 +/- 26, 605 +/- 45, and 550 +/- 65 ml/min, respectively, in the three groups. By contrast, QACC differed significantly in patent AVFs (1,053 +/- 35) compared with failing AVFs (363 +/- 48), but vPIA/MAP did not. AR is thus a late manifestation of access failure. QACC is the best diagnostic test of access dysfunction in AVFs. Interpretation of vPIA/MAP in grafts is enhanced by periodic QACC measurements.

Arteriovenous Shunt, Surgical↗

PubMedDate not supplied

Detection of access strictures and outlet stenoses in vascular accesses. Which test is best?

The location of stenoses within an access may influence the diagnostic value of access monitoring tests. Whereas decreasing access flow (QACC) should occur with both venous outlet stenoses and strictures within the body of the access, normalized intra-access venous pressure (vPIA/MAP) depends on location of the venous needle relative to the lesion. The authors determined the value of vPIA/MAP and direct measurement of percent access recirculation (AR) and QACC in detecting venous outlet stenoses and strictures. Abnormal access studies were evaluated by Doppler ultrasound and fistulography. Well functioning grafts and arteriovenous fistulas (AVFs) have no AR; QACC averages 1,101 +/- 26 and 1,073 +/- 35 mL/min, and vPIA/MAP ratios are 0.34 and 0.16, respectively. Venous outlet stenoses (n = 36) or strictures (n = 32) were detected before thrombosis or intervention in 172 vascular accesses at risk. QACC in accesses with stricture was significantly lower than in those with venous outlet stenosis (361 +/- 11 vs 526 +/- 43 ml/min), as was less than prescribed blood flow (423 +/- 7 ml/min). AR was not detected in any access with stricture and in only 4 of 36 accesses with outlet stenosis. vPIA/MAP was elevated with venous outlet stenosis but not with strictures. The findings of QACC being less than blood pump flow without AR by dilution methods differentiated strictures from venous outlet stenoses.

Arteriovenous Shunt, Surgical↗