PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 7954102

Temporal changes in left ventricular function after massive sympathetic nervous system activation.

S A Lang·M B Maron·F J Bosso·C F Pilati
View original source ↗Export metadata ↓

Abstract

Intense activation of the sympathetic nervous system (SNS) decreases the contractile state of the rabbit left ventricle (LV). In this study, we determined the time course of LV dysfunction after massive central activation of the SNS in dogs. Veratrine (40-80 micrograms/kg) was injected intracisternally to activate the SNS in six chloralose-anesthetized dogs, and LV end-diastolic pressure (LVEDP), cardiac output, heart rate, and aortic pressure (Pa) were measured at 30-min intervals for 3 h. Pa increased from 147 +/- 8 (SE) to 272 +/- 7 mmHg (1 mmHg = 133.3 Pa) within 15 min, then declined to 148 +/- 16 mmHg by 1 h LV function curves (stroke work versus LVEDP or stroke work verus LV transmural pressure) showed a marked decrease in slope and a shift to the right within minutes after activating the SNS, which persisted for the duration of the experiment. These data indicate that LV contractility was diminished in these animals. No changes in LV function were observed in three dogs serving as time-matched controls. In three additional dogs, LV pressure was raised to a degree similar to that observed after SNS activation by constricting the ascending aorta for 1 h. These animals exhibited only modest shifts in the LV function curve during and after aortic constriction. Mean plasma catecholamine concentration increased by one to two orders of magnitude in animals after SNS activation, but only minor changes were observed in the other two groups. We conclude that myocardial contractility declines markedly soon after massive SNS activation and is not solely a function of the initial hypertensive period.

Explore related subjects

AcidosisAnesthesiaAnimalsBlood PressureCardiac OutputCatecholaminesDogsFemaleHeart RateHeart VentriclesHypertensionMaleMicroscopy, ElectronSympathetic Nervous SystemVentricular Function, LeftVeratrineJournal ArticleResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S A Lang, M B Maron, F J Bosso, C F Pilati. 1994. Temporal changes in left ventricular function after massive sympathetic nervous system activation.. https://doi.org/10.1139/y94-098

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1997

Neuronal injury in experimental status epilepticus in the rat: role of acidosis.

Systemic and cerebral acidosis accompanies generalized tonic-clonic seizures and status epilepticus. Acidosis during status may be modified by neuromuscular paralysis, intubation and ventilation, or administration of a base, but the effect of acidosis on neuronal injury from status is uncertain. We studied the effect of acidosis, induced by hypercarbic ventilation, on heat-shock protein (HSP72) induction in rat brain as a measure of neuronal injury in experimental status epilepticus. Acidosis was found to attenuate neuronal injury, independent of its anticonvulsant effect.

Acidosis↗
PubMed1997

A rapid and simple screening method for detection of orotic aciduria by capillary zone electrophoresis.

A rapid and selective capillary zone electrophoretic method for screening of patients with orotic aciduria is described. The method is based on direct measurement of orotic acid in untreated urine. Total analysis time is 5 min with the limit of quantification of 10 mumol/l. Selectivity of the method is given by the use of a low pH of background electrolyte at which practically no interferences from native urine appeared, as well as by using a fast scanning detector which enables the identification of orotic acid via its characteristic UV spectra. This method can be used for quantitative assessment of orotic acid present in urine at physiological conditions after an ion exchange chromatography-clean up and preconcentration procedure. Urine samples containing orotic acid at pathological concentrations (typically more than 1 mol/mol creatinine) could be successfully analysed. The method described was applied to urine specimens collected from both healthy volunteers and patients with orotic acidurias of various origin.

Acidosis↗
PubMed1997

Metabolic acidosis stimulates H+ secretion in the rabbit outer medullary collecting duct (inner stripe) of the kidney.

The outer medullary collecting duct (OMCD) absorbs HCO3- at high rates, but it is not clear if it responds to metabolic acidosis to increase H+ secretion. We measured net HCO3- transport in isolated perfused OMCDs taken from deep in the inner stripes of kidneys from control and acidotic (NH4Cl-fed for 3 d) rabbits. We used specific inhibitors to characterize the mechanisms of HCO3- transport: 10 microM Sch 28080 or luminal K+ removal to inhibit P-type H+,K+-ATPase activity, and 5-10 nM bafilomycin A1 or 1-10 nM concanamycin A to inhibit H+-ATPase activity. The results were comparable using either of each pair of inhibitors, and allowed us to show in control rabbits that 65% of net HCO3- absorption depended on H+-ATPase (H flux), and 35% depended on H+,K+-ATPase (H,K flux). Tubules from acidotic rabbits showed higher rates of HCO3- absorption (16.8+/-0.3 vs. 12.8+/-0.2 pmol/min per mm, P < 0.01). There was no difference in the H,K flux (5.9+/-0.2 vs. 5.8+/-0.2 pmol/min per mm), whereas there was a 61% higher H flux in segments from acidotic rabbits (11.3+/-0.2 vs. 7.0+/-0.2 pmol/min per mm, P < 0.01). Transport was then measured in other OMCDs before and after incubation for 1 h at pH 6.8, followed by 2 h at pH 7.4 (in vitro metabolic acidosis). Acid incubation in vitro stimulated HCO3- absorption (12.3+/-0.3 to 16.2+/-0.3 pmol/min per mm, P < 0.01), while incubation at pH 7.4 for 3 h did not change basal rate (11.8+/-0.4 to 11.7+/-0.4 pmol/min per mm). After acid incubation the H,K flux did not change, (4.7+/-0.4 to 4.6+/-0.4 pmol/min per mm), however, there was a 60% increase in H flux (6.6+/-0.3 to 10.8+/-0.3 pmol/min per mm, P < 0.01). In OMCDs from acidotic animals, and in OMCDs incubated in acid in vitro, there was a higher basal rate and a further increase in HCO3- absorption (16.7+/-0.4 to 21.3+/-0.3 pmol/min per mm, P < 0.01) because of increased H flux (11.5+/-0.3 to 15.7+/-0.2 pmol/min per mm, P < 0.01) without any change in H,K flux (5.4+/-0.3 to 5.6+/-0.3 pmol/min per mm). These data indicate that HCO3- absorption (H+ secretion) in OMCD is stimulated by metabolic acidosis in vivo and in vitro by an increase in H+-ATPase-sensitive HCO3- absorption. The mechanism of adaptation may involve increased synthesis and exocytosis to the apical membrane of proton pumps. This adaptation helps maintain homeostasis during metabolic acidosis.

Acidosis↗