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Biomedical subjects

P Borgdorff

Publications and source records attributed to P Borgdorff.

27 records · Page 2Linked to original sources
PubMed1984

Closed-loop baroreflex control of total peripheral resistance in the cat: identification of gains by aid of a model.

The baroreflex regulation of total peripheral resistance was quantified in closed-loop conditions. To vary arterial pressure cardiac output was reduced by graded inferior caval vein occlusion or by arterial bleeding. In eight lightly anaesthetised cats the static relation between mean arteriovenous pressure gradient and mean flow could be described by a curve that was convex to the pressure axis and had zero intercept. The ratio of the change in resistance to a given change in arterial pressure was taken as resistance gain (GR). The value of this gain was estimated with the aid of a model which predicts pressure from flow when the right parameter value for gain is filled in. It consists of a non-linear negative-feedback control system with control pressure as reference point and with a constant gain. The estimation was carried out with the aid of an automatic identification procedure. GR varied from 0.002 to 0.010 min . ml-1 in different animals under light anaesthesia. With deeper anaesthesia gain decreased by 35 to 50% and became zero with very deep anaesthesia or barodenervation. Assuming that the reflex is a linear system about control pressure and flow we linearised our model and computed the static overall open-loop gain (GO). Within this narrow range GO varied from 0.64 to 2.30 for different cats under light anaesthesia and decreased by the same percentage as GR with deeper anaesthesia.

Animals↗
PubMed1983

Peripheral resistance after cardiac output reduction in the barodenervated cat.

Studies on the nervous or humoral control of total peripheral resistance are often complicated by concomitant changes in cardiac output. We studied the influence of cardiac output on peripheral resistance in the absence of modulating reflexes. In barodenervated and vagotomized cats, cardiac output was varied by graded inferior caval vein occlusion or by arterial bleeding. Total peripheral resistance was obtained with an analogue device which continuously divided the pressure difference between aorta and caval vein by cardiac output (electromagnetic flowmeter). Cardiac output reduction caused a decrease of peripheral resistance, followed within 2 minutes by a slow increase. Resistance stabilized at preocclusion levels within 5.8 (range 4-9) minutes. The relative changes in resistance and cardiac output were linearly related, when cardiac output was reduced by less than 40%. With larger reductions, the relation became nonlinear, and with a drop of more than 65%, no further change was noticed. These changes in resistance could not be explained by variations in blood viscosity as measured by Hct. They were nonnervous in nature: when all reflexes were abolished by ganglionic blockade, a similar pattern was found. Humoral mechanisms like the vasopressin or the renin-angiotensin system, known to be activated by hypotension, probably played no role, since arterial osmolality remained stable and captopril did not influence the resistance response. The involvement of metabolic autoregulation could not be excluded, but was unlikely because O2 consumption and serum lactate did not change.

Animals↗
PubMed1982

Inhibition of efferent sympathetic nerve activity by centrally administered paraoxon in the cat.

We recently found that central administration of the cholinesterase inhibitor paraoxon lowered blood pressure substantially. It was postulated that the decrease in pressure was mediated by a reduction of sympathetic outflow. In the present study, efferent splanchnic nerve activity in anaesthetized and paralysed cats was recorded, and quantified by measuring the variance of signal amplitude. After administration of 8 micrograms paraoxon into the vertebral arteries, blood pressure and splanchnic nerve activity decreased simultaneously. A mean fall of 46 +/- 6% and 45 +/- 13% (mean +/- S.E.M.) respectively was reached within 12 min and was maintained during the period studied (30 min). When the effect of paraoxon was antagonized by dexetimide, both blood pressure and splanchnic nerve activity returned to control values. Since previous work has shown that the depressor action could not be prevented by efferent vagal blockade it seems likely that the fall in blood pressure after paraoxon was mainly caused by a decreased sympathetic outflow. In addition, we varied the amplifier band width in recording splanchnic nerve activity. The measurement of frequencies between 10 and 225 Hz appeared to be sufficient for studying the change in activity after paraoxon.

Animals↗
PubMed1980

The effect of common carotid artery occlusion on blood pressure in the barodenervated cat.

A 12% blood pressure elevation was found during common carotid occlusion in the barodenervated, thoracotomised cat under Nembutal anaesthesia. This rise in blood pressure appeared to be the net result of an 18% increase of total peripheral resistance and a concomitant 5% decrease of mean aortic flow. When the occlusions were repeated after ganglionic blockade similar values were found, indicating that the increase in resistance had not resulted from reflex vasoconstriction. To test if this increase of total peripheral resistance was caused by a mechanical exclusion, Ohm's law for parallel resistances was applied to the systemic tree to calculate the rise in resistance due to obstruction of the carotid flow. The results thus obtained matched the observed increase of peripheal resistance. It is concluded that common carotid artery occlusion can be used to test completeness of barodenervation in the cat, if an increase in blood pressure of about 12% is allowed for.

Animals↗
PubMed1975

Respiratory fluctuations in pupil size.

Regular fluctuations in pupil size of the cat were measured and the properties, nervous pathways, and origin of these oscillations were investigated. The rhythm of pupil movements under control conditions appeared to be either locked to the central respiratory cycle or to the artificial ventilatory cycle. These movements were only seen in lightly anesthetized or tranquilized cats, but not in alert or deeply anesthetized cats (ether, halothane or pentobarbital). The fluctuations proved to be independent of sympathetic innervation but related to variations in parasympathetic outflow. At least two sources for pupil oscillations appeared to be involved: central respiratory activity and respiratory blood pressure fluctuations that modulated pupil width via sinoaortic baroreceptors. Lung movements per se, as a third possible factor, did not modulate pupil width, whereas electrical stimulation of the afferent lung vagi did; therefore the role of this mechanical factor is not clear. A review of the pertinent literature shows that in the organism there are many phenomena exhibiting respiratory oscillations. It seems likely that these oscillations have the same origin as the respiratory pupil fluctuations.

Anesthesia, General↗
PubMedDate not supplied

Pump perfusion causes vasodilation by activation of platelets.

Use of a pump in extracorporeal circuits depresses autoregulation and vascular tone. To study whether platelets are involved, we perfused rat hindlegs by means of an extracorporeal shunt between carotid and femoral artery. Autoperfusion could instantaneously be replaced by pump perfusion. To avoid interference by effects caused by blood-material contact, the circuit was coated with albumin. Spontaneous flow did not elicit platelet aggregation as recorded continuously with a photometric device inserted into the tubing, nor did it affect femoral vascular resistance. However, pump perfusion immediately evoked strong platelet aggregation that stabilized at a lower level after 2-3 minutes. Femoral resistance rose slightly during the first 2 minutes, but thereafter fell to 63% of control and stayed at approximately 70% for the next 2 hours. Pump induced platelet aggregation and fall in vascular resistance could be prevented with aurintricarboxylic acid, which specifically inhibits shear induced platelet aggregation. We conclude that pump perfusion with blood in coated systems elicits shear-induced platelet aggregation that, in turn, leads to vasodilation in the perfused vascular bed. These effects can be prevented by blocking the binding of von Willebrand factor to the platelet glycoprotein Ib receptors.

Animals↗
PubMedDate not supplied

Small changes in heart rate following alpha-1 adrenoceptor stimulation in the anaesthetized dog.

In a previous work (1) we observed a weak alpha-1 adrenoceptor mediated chronotropic effect in anaesthetized dogs: the intracoronary injection of 100 micrograms of amidephrine, an alpha-1 agonist, increased heart rate by 2.5 +/- 0.8 bpm (mean +/- SEM). Since these experiments had been performed in the presence of alpha-2 blockade with yohimbine, one could argue that alpha-1 adrenoceptors had been partially blocked as well. To test for this possibility 5 additional experiments were performed with the same protocol, just omitting yohimbine administration. The chronotropic effect of amidephrine was larger (6.2 +/- 1.9 bpm after i.c. injection of 100 micrograms), but the difference was not significant. This confirms our earlier finding that alpha-1 adrenoceptors are not involved in heart rate control of the anaesthetized dog.

Animals↗