Effect Of Acute Reduction Research Articles

Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension

The effects of acute reduction in arterial blood pressure in severe anaphylactic shock (AS) on cerebral blood flow are of paramount importance to be investigated. We studied cerebral circulation and oxygenation in a model of severe AS and compared it with a pharmacologically induced arterial hypotension of similar magnitude. Anaphylactic shock was induced by 1 mg intravenous ovalbumin (OVA) in sensitized rats. Rats were randomized to three groups: (i) no resuscitation (OVA; n = 10) (ii) intravenous volume expansion (10 mL in 10 min after OVA injection) (OVA + VE; n = 10); (iii) control hypotension (100 μg of nicardipine followed by continuous infusion of 1 mg · 100 g · h intravenously; NICAR; n = 10). Mean arterial pressure (MAP), carotid blood flow (CBF), cardiac output, cerebral cortical blood flow (CCBF; estimated by laser Doppler technique), and cerebral tissue oxygen pressure (PtiO2) were recorded over the 15 min following AS induction in all three groups. Results are expressed as mean (SD). One minute after OVA or nicardipine injection, there was a rapid and significant 50% decrease in MAP from basal values. In the OVA group, AS severely altered systemic and cerebral hemodynamics in 5 min: 93% (SD, 4%) decrease in CBF, 66% (SD, 8%) in CCBF, and 44% (SD, 8%) in PtiO2; the decrease in CBF was significantly (P < 0.05) attenuated in the OVA + VE group; however, CCBF and PtiO2 were not statistically different in the OVA versus OVA + VE groups. On the contrary, nicardipine-induced hypotension had only a limited impact on CBF, cardiac output, CCBF, and PtiO2 for a similar MAP decrease. There was a linear relation between CCBF and blood pressure in the OVA (regression slope: 0.87 [SD, 0.06]; median r = 0.81) but not in the NICAR group (regression slope: 0.23 [SD, 0.32]; median r = 0.33). Anaphylactic shock resulted in severe impairment of cerebral blood flow and oxygenation, beyond what could be expected from the level of arterial hypotension.

Renin response to hemorrhage in conscious rats: effect of acute reductions in hematocrit

This study examined the effect of prior exchange transfusion and acute reduction in hematocrit on the subsequent plasma renin concentration (PRC) response to 15 ml/kg hemorrhage in conscious cannulated rats. Long-Evans rats (400-500 g) were assigned to one of eight groups (6-8 rats/group). Rats were exchanged transfused (5 ml total) with whole blood, red blood cells and saline, plasma, or isotonic saline, with the two latter groups showing a decrease in hematocrit of 10-20%. Thirty minutes after exchange transfusion, rats were either subjected to a 0- (control) or 15-ml/kg hemorrhage. Control rats showed no change in mean arterial pressure or PRC regardless of exchange transfusion. The rats exchange transfused with saline had a significant decrease in arterial pH and a more profound hypotension after hemorrhage. PRC ranged from 7 +/- 1 to 11 +/- 1 ng.ml-1.h-1 after exchange transfusion. Subsequent hemorrhage resulted in an increase in PRC that was significantly greater in the saline-transfused group (45 +/- 16 ng.ml-1.h-1) 10 min after hemorrhage. We conclude that exchange transfusion with saline leads to an augmented renin response to hemorrhage in part due to a decrease in arterial pH and more severe hypotension.

Effects of acute reduction in blood pressure on the renal function of rats with diseased kidneys.

We studied the effect of an acute reduction in blood pressure, induced by diltiazem, on the renal hemodynamics of spontaneously hypertensive rats (SHR) with focal glomerular sclerosis, as induced by adriamycin (ADR). Renal plasma flow (RPF) and glomerular filtration rate (GRF) were determined before (first period) and during (second period) intravenous infusion of diltiazem in SHR 4-6 weeks after ADR treatment (group 1), 14-20 weeks after treatment (group 2), and in controls without treatment (group 3). Rats in group 1 had a normal renal function (RPF and GFR) in the first period, which was not significantly different from control rats (group 3). Rats in group 2 showed a reduced renal function, reflected by the lower levels of RPF and GFR, compared with groups 1 and 3. Mean blood pressure decreased equally in the 3 groups by about 50 mm Hg after the infusion of diltiazem. During the second period, 13.4 or 12.4% increase in RPF and a 29.0 or 23.2% elevation of GFR were evident in groups 1 or 3, respectively. In contrast, a 32.0% reduction of RPF was observed in group 2, accompanied by a 25.7% decline of GFR. A reduction in renal function (percent change of RPF or GFR) significantly correlated with the severity of renal dysfunction (RPF or GFR in the first period) in group 2. Thus, the renal function of rats with diseased kidneys is sensitive to an acute reduction in blood pressure by diltiazem, and the sensitivity depends on the degree of renal deterioration.

Effect of Acute Reduction in Cardiac Output on the Denervated Kidney

ArticleEffect of Acute Reduction in Cardiac Output on the Denervated KidneyRobert M. Berne, and Matthew N. LevyRobert M. BerneFrom the Department of Physiology, Western Reserve University School of Medicine Cleveland, Ohio, and Matthew N. LevyFrom the Department of Physiology, Western Reserve University School of Medicine Cleveland, OhioPublished Online:30 Nov 1952https://doi.org/10.1152/ajplegacy.1952.171.3.558MoreSectionsPDF (806 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByCirculatory Effects of Modern Inhalation Anesthetic AgentsNiere und HerzinsuffizienzPhysiology of the kidneySalt and water excretion in heart failureProgress in Cardiovascular Diseases, Vol. 3, No. 6Renal function and renal impairment in congestive heart failureProgress in Cardiovascular Diseases, Vol. 3, No. 5Role of the Kidney in the Pathogenesis of Congestive Heart FailureCirculation, Vol. 20, No. 2The alkali metal ions in the organismAnesthesiologyNew England Journal of Medicine, Vol. 250, No. 23 More from this issue > Volume 171Issue 3November 1952Pages 558-563 Copyright & PermissionsCopyright © 1952 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1952.171.3.558PubMed13016802History Received 6 August 1952 Published online 30 November 1952 Published in print 30 November 1952 Metrics

Effect of acute reduction of arterial pressure using hexamethonium on the manifestations of congestive heart failure in man

Effect of acute reduction of arterial pressure using hexamethonium on the manifestations of congestive heart failure in man

The effect of acute reduction of the glomerular filtration rate on sodium excretion in man.

The effect of acute reduction of the glomerular filtration rate on sodium excretion in man.

Effects of acute reduction of cardiac output upon the mechanisms of sodium excretion in the dog.

Effects of acute reduction of cardiac output upon the mechanisms of sodium excretion in the dog.