PubMed Health⌕ Search

Biomedical subjects

J Martner

Publications and source records attributed to J Martner.

At least 37 records · Page 2Linked to original sources
PubMed1985

Cardiovascular studies during controlled baroreflex activation in the dog: II. Effects of metoprolol and enflurane.

An experimental model was designed to study circulatory drug effects with or without barostatic reflex influences. In dogs anaesthetized with chloralose, both carotid sinuses were perfused from a femoral by-pass either with systemic arterial pressure or with a pump in order to control the sinus pressure. Cardiac and aortic baroreceptors were denervated. I.v. metoprolol (240 micrograms X kg-1 + 102 micrograms X kg-1 X h-1) with constant carotid sinus pressure and thereby constant baroreceptor activation reduced cardiac output, heart rate, cardiac contractility and left ventricular stroke work index. Systemic vascular resistance increased. This response was independent of the degree of baroreflex activation. During the combined administration of enflurane (1.6% end-tidal concentration) and metoprolol, cardiac performance (cardiac output, stroke volume, heart rate, cardiac contractility and left ventricular stroke work index) was depressed independent of the degree of baroreflex activation. Barostatic reflexes, however, counteracted an observed decrease in systemic vascular resistance. This reflex vascular response was, during metoprolol-enflurane administration, associated with an increased left ventricular end-diastolic pressure.

Animals↗
PubMed1985

Vasodilator responses to enflurane in the small intestine.

Local effects of enflurane on intestinal vascular resistance were studied in vivo in cats. A jejunal segment was prepared and perfused at constant flow with blood from the femoral arteries. The intestine was either: (1) left with intact sympathetic innervation, (2) denervated and exposed to electrical post-ganglionic vasoconstrictor nerve stimulation, or (3) excluded from neurogenic remote control by post-ganglionic denervation. Enflurane dissolved in lipid and intra-arterially administered to the jejunal segment in doses comparable to those clinically encountered, decreased intestinal vascular resistance in relation to the intra-arterial concentration of the drug. The vasodilator response was, at the highest enflurane doses studied (blood concentration: 400 and 800 mg X 1(-1], most pronounced in the intestine with intact sympathetic innervation. Otherwise, no differences were observed in vasodilator responses between the three different investigated modes of neurogenic influence on the intestine. In vitro enflurane (-in-lipid) did not affect the vasoconstrictor response to electrical field stimulation in the rat mesenteric arterioles. Enflurane, however, dose-dependently reduced spontaneous contractile activity in the rat portal veins.

Animals↗
PubMed1985

Intestinal vascular effects of inhaled and locally administered enflurane in the cat.

The effects of enflurane on intestinal vascular resistance and blood flow in the intestine were studied in cats during basal chloralose anaesthesia. A jejunal segment was prepared and perfused with blood from both femoral arteries, allowing control of intestinal inflow pressure. Mesenteric venous blood flow was measured with an optical drop recorder. During constant intestinal arterial pressure (75 mmHg; 10 kPa), intestinal vascular resistance was calculated during enflurane inhalation at MAC 0.5 and 1.0 before and after postganglionic denervation of the jejunal segment. Inhalation of enflurane reduced intestinal vascular resistance in a dose-dependent fashion. The decrease in vascular resistance was attenuated but not abolished by post-ganglionic denervation, indicating both peripheral and central nervous sites of action for enflurane. Furthermore, with the intestinal segment perfused at systemic arterial pressure, the effects of locally intraarterially infused enflurane dissolved in a fat emulsion was studied. A vasodilator response was elicited in the intestine when exposed to local arterial enflurane concentrations in the same range as encountered during surgical anaesthesia in man, supporting the hypothesis of a peripheral site of action.

Anesthesia, Inhalation↗
PubMed1985

Effects of isoflurane on vascular tone and circulatory autoregulation in the feline small intestine.

The vascular response in autoperfused small intestine was studied in ten cats during basal chloralose anaesthesia and controlled ventilation with either air, nitrous oxide/oxygen (70/30) or 0.7% end-tidal concentration of isoflurane + nitrous oxide/oxygen (70/30). Intestinal blood flow was measured by the optical drop recording technique, and intestinal perfusion pressure was kept constant at either 100, 75 or 50 mmHg (13.30, 9.98 or 6.65 kPa). At perfusion pressures of 100 and 75 mmHg (13.30 and 9.98 kPa), intestinal blood flow was significantly increased and intestinal vascular resistance decreased during isoflurane- + nitrous oxide/oxygen anaesthesia, compared with nitrous oxide/oxygen or air. According to the equation of closed loop gain (Gf), autoregulation was active in the pressure range 100-75 mmHg (13.30-9.98 kPa). In the pressure range 75-50 mmHg (9.98-6.65 kPa), the autoregulatory capacity was attenuated during air or nitrous oxide/oxygen and absent during isoflurane + nitrous oxide/oxygen. The vasodilator responses and the autoregulatory pattern were not changed by post-ganglionic intestinal denervation. The intestinal vasodilator effect of isoflurane was further investigated in the denervated intestine, perfused at systemic arterial pressure by local intra-arterial administration of isoflurane dissolved in a fat emulsion. A dose-dependent vasodilator response was hereby observed.

Anesthesia, General↗
PubMed1985

Does dopamine suppress stress-induced intestinal and renal vasoconstriction?

Dopamine interference with intestinal and renal sympathetic reflex vasoconstrictor responses was studied in cats anaesthetized with diazepam, fentanyl and nitrous oxide. Vasoconstriction was induced by electric stimulation of the hypothalamic defence-alarm area and by stimulation of somatic and visceral afferents. In addition, intestinal vasoconstriction was elicited by direct stimulation of postganglionic sympathetic efferent nerves. In the intestine, dopamine administration (7.5 microgram X kg-1 X min-1) was not associated with an attenuation of the investigated sympathetic vasoconstrictor responses, although dopamine per se decreased intestinal vascular resistance by 36 +/- 4%. Due to this dopamine-induced background vasodilation, the intestinal blood flow level during stimulation procedures and concomitant dopamine infusion was higher than during similar stimulations prior to dopamine (for defence-alarm area stimulation 45 +/- 16%, for afferent nerve stimulation 79 +/- 22% and for efferent postganglionic nerve stimulation 66 +/- 16%). In the kidney, dopamine per se had only minor effects on vascular resistance and on changes in vascular tone elicited by the stimulation procedures. The renal blood flow level in response to the stimulation procedures was not significantly affected by dopamine. In conclusion, dopamine may contribute to a sustained intestinal blood flow level when administered during supervening stress-related sympathetic activation.

Anesthetics↗
PubMed1985

Effects of hyperventilation and hypoventilation on stress-induced intestinal vasoconstriction.

The combined effects of defined changes in ventilation and stress-induced vasoconstriction were studied in the intestinal vascular bed in cats (n = 20) anaesthetized with fentanyl, nitrous oxide and diazepam. Intestinal reflex vasoconstriction was induced by stimulation either of the hypothalamic defence-alarm area or of somatic and visceral pain afferents. The volume-controlled ventilation was changed by altering the tidal volume, and stimulations were performed during either control conditions (Paco2 4.5-5.0 kPa), hyperventilation (Paco2 3.0-3.5 kPa) or hypoventilation (Paco2 6.5-7.5 kPa). The increase in intestinal vascular resistance (IVR) elicited by defence-alarm area stimulation was potentiated during hyperventilation (306 +/- 83% vs 198 +/- 62%; P less than 0.01) and attenuated during hypoventilation (176 +/- 62% vs 240 +/- 44%; P less than 0.05). The increase in IVR elicited by pain fibre stimulation was potentiated during hyperventilation (73 +/- 21% vs 54 +/- 19%; P less than 0.01), but not significantly changed during hypoventilation (47 +/- 19% vs 68 +/- 34% during control ventilation). Our data indicate that the ventilatory pattern can be decisive for the vasoconstrictor response during experimental stress. We suggest that remote neurogenic mechanisms account for the increased responsiveness during hyperventilation. The decreased responsiveness during hypoventilation, on the other hand, seems to correlate with the local vasodilator effects of carbon dioxide.

Animals↗
PubMed1984

Intravenous infusion of halothane dissolved in fat. Haemodynamic effects in dogs.

Eight harrier dogs received an i.v. infusion of halothane dissolved 1:9 in a fat emulsion for i.v. nutrition (Intralipid, Vitrum). The rate of infusion was adjusted to maintain end-tidal halothane concentrations of 0.7% and 1.4%. At 1.4%, mean arterial pressure decreased to 76 +/- 8 mmHg (10.1 +/- 1.0 kPa) (mean +/- s.e.mean) from a pre-infusion value of 122 +/- 6 mmHg (16.2 +/- 0.8 kPa) (P less than 0.01). The concomitant decrease in cardiac output was 39% and left ventricular maximum dp/dt decreased by 50% (P less than 0.01). Changes in systemic vascular resistance and pulmonary arterial pressure were small. The haemodynamic responses during halothane inhalation, to corresponding end-tidal concentrations, were similar. Arterial and mixed venous halothane concentration increased in proportion to end-tidal concentration. There were no changes in arterial PO2 during the halothane-in-fat infusion. Triglyceride concentrations in plasma increased 12-fold. Haemodynamic recovery after the infusion was fast. We conclude that the halothane-in-fat infusion caused a dose-dependent depression of myocardial contractility and arterial pressure, similar to that seen during inhalation, and that end-tidal concentration could be used for control of the infusion rate.

Anesthesia, Intravenous↗
PubMed1984

Evidence for cardiac volume-receptor regulation of feline jejunal blood flow and fluid transport.

The aim of the study was to investigate the role of cardiac mechanoreceptors in the reflex regulation of intestinal blood flow and fluid transport. Feline cardiac mechanoreceptor activity was modified with two noninvasive techniques: positive-pressure ventilation (PPV) and inspiratory resistance breathing (IRB). A jejunal segment with intact vascular and nervous supply was isolated and exposed to cholera toxin as a model for intestinal secretion. The results revealed that PPV induced a pronounced intestinal vasoconstriction and a marked inhibition of choleraic secretion. IRB had the opposite effects. The responses were well correlated with changes in central blood volume and either markedly reduced or abolished by vagotomy, intestinal alpha-adrenoreceptor blockade, or postganglionic mesenteric denervation. The results indicate that cardiac mechanoreceptors with vagal afferents may mediate the observed reflex responses, and hence this receptor station may be of importance in the normal reflex control of intestinal hemodynamics and fluid transport.

Animals↗
PubMed1983

Intestinal vascular responses to dopamine during fentanyl-nitrous oxide anaesthesia, supplemented with dixyrazin.

Intestinal haemodynamics in response to continuous i.v. administration of dopamine were investigated in cats anaesthetized with fentanyl-nitrous oxide either with or without supplement of dixyrazin. A dose-dependent vasodilatation was observed in the dopamine dose range 2.5-35 micrograms . kg-1 . min-1 and the subsequent maximal intestinal blood flow increase was 121%. No net intestinal vasoconstriction was evident even at the largest dopamine doses, although the vascular response reached a plateau at 17.5 micrograms . kg-1 . min-1. Control experiments during chloralose anaesthesia gave similar results. Changes in mean arterial pressure and heart rate were small. Renal blood flow was virtually unchanged at dopamine doses below 10 micrograms . kg-1 . min-1, while renal vasoconstriction was evident following dopamine doses above that level. The addition of i.v. dixyrazin (0.15-0.30 mg . kg-1) to the fentanyl-nitrous oxide anaesthesia substantially potentiated the intestinal vasodilator response to i.v. dopamine and the maximal blood flow increase was 183% at 10-15 micrograms . kg-1 . min-1. In vitro experiments using mesenteric resistance vessels from the rat demonstrated a dose-dependent relaxation to dopamine. At very large doses this response was counteracted, but not reversed into vasoconstriction by dopamine-induced alpha-adrenergic stimulation.

Animals↗
PubMed1983

Modification by baroreceptor feedback of circulatory responses to noxious stimuli during anaesthesia in cats.

In eight cats anaesthetized with chloralose, the carotid sinus on one side was either exposed to systemic arterial pressure or perfused with a pump in order to control sinus pressure. Baroreceptor influences from the contralateral carotid sinus and from the aortic arch were interrupted by denervation. Arrangements were made for intermittent electric stimulation of pain fibres in somatic and visceral nerves with stimulation parameters chosen to elicit reproducible increases in arterial blood pressure and in skeletal muscle vascular resistance. The elicited increases in arterial pressure and muscle vascular resistance were both about 40% smaller when the carotid sinus was exposed to systemic arterial pressure in comparison with the experimental condition of a constant carotid sinus pressure. I.v. metoprolol (0.1-0.3 mg kg-1) reduced base-line arterial pressure, but did not attenuate the arterial blood pressure increase in response to pain stimulation. The baroreceptor modulation of the haemodynamic response to the pain stimulation was not affected by metoprolol.

Anesthesia, General↗
PubMed1983

Influence of dixyrazine on intestinal and renal vasoconstrictor responses during fentanyl-nitrous oxide anaesthesia.

In cats (n = 24) anaesthetized with fentanyl-nitrous oxide and diazepam, stimulation of the hypothalamic defence-alarm area (DA) or afferent activation of somatic pain fibres (SA), elicited a pronounced increase in intestinal (DA 297%, SA 107%) and renal (DA 214%, SA 90%) vascular resistance as well as a decrease in diuresis. These stress-related responses were markedly counteracted by dixyrazine (0.15-0.5 mg X kg-1 b.w.i.v.), especially in the kidney where the subsequent increase in vascular resistance to DA and SA stimulations amounted to only 25% and 13%, respectively, while diuresis increased. Corresponding data for stimulation-induced increases in intestinal vascular resistance after dixyrazine were DA 156% and SA 28%. Dixyrazine is suggested to act both through interaction with peripheral alpha-adrenergic mechanisms in control of vascular tone and through central nervous cardiovascular reflex depression. In man (n = 7), during a similar form of anaesthesia, portal vein blood flow (1137 +/- 177 ml) was measured by the continuous thermodilution method. Preportal tissue vascular resistance during surgery decreased significantly (11.3 vs 8.7 kPa X min X ml-1 X 10(-3] after i.v. dixyrazine (0.15 mg X kg-1 b.w.). A concomitant increase in oxygen uptake in preportal tissues occurred (19.9 ml min-1 vs 24.5 ml X min-1).

Aged↗
PubMed1982

Anaesthesia and cardiovascular regulation.

Cardiovascular homeostasis is dependent on the efficient performance of the effector organs, i.e. the vascular smooth muscle and the heart. Besides inherent activity and local control mechanisms, these effector organs are regulated by circulatory control centres within the central nervous system, which in turn receives information from receptors inside and outside the cardiovascular system. All these components of the circulatory systems, i.e. receptors, afferent and efferent pathways, control centres and effector organs, are possible sites for interactions by anaesthetics. Since different anaesthetics have different potencies and special predilections, there are a large variety of interaction patterns, as is discussed in the paper. Another way of evaluating circulatory effects of drugs used in anaesthesia is to analyse how these drugs may modify circulatory reflexes associated with surgery and trauma. For example, pain, hypoxia and/or hypovolaemia may evoke circulatory adjustments which correspond to and are functionally related to, from experimental physiology, well-known reflex patterns such as the somatosympathetic reflex, the chemoreceptor reflex and the baroreceptor reflex. These reflex adjustments are liable to modification by anaesthetics, as exemplified in the paper. Due to the complexity of circulatory control and the varying effects of different anaesthetic agents, it is difficult to draw general conclusions. It can, however, be stated that most general anaesthetics depress cardiovascular reflexes in proportion to the depth of anaesthesia, and that suprabulbar centres are more easily depressed than bulbar ones. Opiates seem to have a specific inhibitory effect on circulatory adjustments induced by noxious stimuli. Transmission in efferent and afferent pathways is liable to modification by local anaesthetics, ganglionic blockers or alpha- and beta-receptor antagonists.

Anesthesia↗
PubMed1982

Influence of amygdala lesions on cardiovascular responses to alerting stimuli, on behaviour and on blood pressure development in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR), and often also humans genetically predisposed to hypertension, exhibit cardiovascular hyperreactivity to alerting stimuli, which derives from limbic-hypothalamic levels and seems important for inducing primary hypertension. It is further known that the limbic amygdala complex normally reinforces emotionally induced defence reactions. The amygdala were therefore bilaterally destroyed in 6 week old SHR, and compared with sham-operated SHR concerning development of hypertension, cardiovascular reactivity to environmental stimuli and explorative behaviour. When related to controls, the arterial pressure elevation was significantly attenuated in the amygdalalesioned SHR, though their pressure was nevertheless raised 40% at 6 months of age. Concerning cardiovascular responsiveness to mild environmental stimuli the groups did not differ; neither concerning explorative behaviour nor in general motor activity. However, the amygdala-lesioned SHR responded decidely less than controls to stressful, fear-inducing stimuli. The amygdala complex may therefore play an important role in aggravating SHR hypertension by reinforcing defence reactions to stressful influences, when such stimuli are at hand. However, according to the present study the amygdala nuclei are not the origin of the centrally determined cardiovascular hyperreactivity, which in SHR seems decisive for inducing hypertension.

Amygdala↗
PubMed1981

Hemodynamic consequences of defence area stimulation and afferent somatic nerve stimulation during fentanyl-nitrous oxide anesthesia. Modifying effects of droperidol.

Stimulation of the hypothalamic defence area and activation of somatic afferents in combination with carotid baroreceptor unloading was performed in cats anesthetized with fentanyl-nitrous oxide in order to investigate the circulatory consequences in terms of regional blood flow changes. These stimulation procedures, suggested to mimic activation of central neurogenic cardiovascular control mechanisms caused by anesthesia and surgical stress, were found to induce pronounced reductions in intestinal and renal blood flow as well as in diuresis. However, administration of droperidol markedly diminished the renal vasoconstriction as well as the reduction in diuresis in the dose range 0.025--0.10 mg/kg b.w. Doses of 0.15--0.25 mg/kg b.w. virtually abolished any stimulation-induced increase in renal vascular resistance, whether elicited through activation of the defence area or somatic afferents. This dose also partly blocked the neurogenic increment of intestinal vascular resistance.

Animals↗
PubMed1977

Apnoea and bradycardia from submersion in "chronically" decerebrated cats.

In "chronically" but not in acutely decerebrated cats, submersion of the head caused apnoea and marked bradycardia, associated with a maintained or slightly raised arterial pressure. Since these reflex adjustments, though very reproducible, occurred with a varying latency and could be induced also by nasal injection of water, they appeared to be, at lest in part, elicited from the upper respiratory passages. Thus, a terrestrial mammal, reputed to shun any form of immersion, can exhibit adjustments during head submersion, similar to those in habitually diving species. This response pattern is basically organized at the lower brainstem level.

Animals↗
PubMed1975

Influences on colonic and small intestinal motility by the cerebellar fastigial nucleus.

The fastigial influence on intestinal motility was investigated in acute experiments on chloralosed cats. Motility was recorded both from the small and large intestine. Electrical stimulation of the rostral fastigial pole produced, in combination with a blood pressure rise, increased motor activity in ileum and colon while jejunum could respond with either increased on decreased motility. The intestinal responses were neither secondary to changes in intestinal blood flow, nor to baroreceptor reflexes induced by the increased blood pressure. The excitatory responses were not due to increased parasympathetic activity since sectioning of such pathways failed to abolish the responses. Instead, interruption of adrenergic sympathetic discharge, accomplished either by guanethidine or by sectioning of relevant nerves, aid eliminate the responses, indicating that the fastigial effects were mediated by suppression of prevailing adrenergic tone. Noxious stimuli to the abdomen, including laparotomy, inhibit intestinal motility by a reflex increase in adrenergic discharge. It is suggested that fastigial influence on intestinal motility is mainly due to suppression of this reflex.

Animals↗