Biomedical subjects

R Sandin

Publications and source records attributed to R Sandin.

44 records · Page 3Linked to original sources

PubMed1991

Effects of diltiazem on postischaemic renal cortical microcirculation in the pig.

Diltiazem--a calcium entry blocker--was tested in a porcine model under continuous chlormethiazole-pancuronium anaesthesia as protection against renal failure following 60 min of renal ischaemia. Fourteen pigs were randomly allocated to one experimental (diltiazem and ischaemia) and one control group (only ischaemia) (n = 7 in each). Diltiazem was administered as a continuous intravenous infusion started before the ischaemic insult. In two additional animals diltiazem was given but ischemia was not induced. The postischaemic renal cortical microcirculation was simultaneously investigated in four different regions in the left kidney during the first 4 h of reperfusion. Laser Doppler flowmetry (LDF) was performed in two different regions and measurement of tissue oxygenation was done in two other regions. In the two animals treated with diltiazem without ischaemia, only minor variations in central haemodynamic and renal microcirculatory parameters were evident. In the control group (ischaemia), superficial renal cortical blood flow (Qsrc) decreased from 49 +/- 11 (s.d.) arbitrary units at baseline to 24 +/- 4 arb. units 4 h after start of reperfusion (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗

PubMed1991

Postischaemic renal cortical microcirculation and tissue oxygenation in the pig.

Porcine and human renal physiology are similar in important aspects. Renal cortical microcirculation and its relation to inulin clearance (CIn) was therefore studied before and after renal ischaemia in 28 pigs under continuous intravenous chlormethiazole-pancuronium anaesthesia. The anaesthesia used provided essential stability in central haemodynamics. The animals were studied for 90 min of reperfusion following 0, 30 or 60 min of renal ischaemia. Twelve of the animals (four were subjected to each duration of ischemia) were also studied 18 h after start of reperfusion. Regional blood flow in the superficial renal cortex was measured by laser Doppler flowmetry (LDF), and tissue oxygenation (PtO2) by surface microelectrode technique. These techniques allow continuous or repeated measurements. During the first 90 min of reperfusion, superficial renal cortical blood flow measured by LDF (Qsrc) underwent considerable temporal variation which followed a certain pattern. Thus, when the renal arterial blood flow was restored after ischaemia, we observed an instant peak in Qsrc followed by a decreasing flow until a minimum value (Qmin) was reached between 3 and 9 min after start of reperfusion (tQmin). Thereafter, Qsrc increased until a maximal value (Qmax) was reached between 11 and 64 min after start of reperfusion (tQmax). The parameters tQmin and tQmax were related to inulin clearance 18 h after start of reperfusion (P less than 0.05 and P less than 0.01, respectively). Thus, it might be possible soon after start of reperfusion--to evaluate the severity of ischaemic damage. This could be useful in the evaluation of different prophylactic strategies, since the full extent of the ischaemic damage, as assessed by clearance determinations, cannot be established until hours later.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗

PubMed1991

Postischaemic regional microvascular variations in the porcine renal cortex.

Regional microcirculatory differences in the superficial renal cortex were studied before and during 4 h following 60 min of renal ischaemia in seven pigs under continuous intravenous chlormethiazole-pancuronium anaesthesia. Superficial renal cortical blood flow (Qsrc) was measured by laser Doppler flowmetry (LDF) in two different regions. In two other different regions tissue oxygenation (PtO2) was measured by surface electrodes. Thus, microcirculatory measurements were simultaneously carried out in each animal in four different regions of the left kidney. After 60 min of renal ischaemia, pronounced renal cortical microcirculatory disturbances were found. The regional microcirculatory differences were notable, especially after ischaemia. On average, Qsrc was 49 +/- 11 (s.d.) arbitrary units at baseline and decreased to 24 +/- 4 arb. units 4 h after start of reperfusion (P less than 0.05). Before ischaemia the average difference between Qsrc simultaneously measured in two different parts of the renal cortex was 26 +/- 15% of the mean of both measurements, and it was 30 +/- 22% 4 h after start of reperfusion (n.s.). Mean PtO2 (m-PtO2) was on average 4.5 +/- 1.3 kPa at baseline and 2.4 +/- 1.5 kPa 4 h after start of reperfusion (P less than 0.05). The average difference between m-PtO2 simultaneously measured in two different parts of the renal cortex at baseline was 24 +/- 13% of the mean of both measurements and 57 +/- 49% 4 h after start of reperfusion (n.s.). In each of the two measured regions of the renal cortex m-PtO2 was calculated from 160 small tissue volumes distributed within a surface area of about 1 mm2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Disturbances in renal cortical perfusion with reference to the microsphere technique.

The microsphere technique for studying renal blood flow is based on injection of a small volume containing radioactively labelled microspheres into the left atrium, left ventricle or possibly the root of the aorta. In the present methodological study, superficial renal cortical blood flow and tissue oxygenation were measured in anaesthetized pigs by laser Doppler flowmetry and by oxygen surface electrode technique. Rapid and profound transient decreases in superficial renal cortical blood flow and tissue oxygenation were found after injection of small volumes of plasma and saline into the left atrium. This response was present also when solutions without microspheres were injected. The reaction was not abolished by careful adjustment of the injectate temperature. When the rapid onset of flow reduction is related to the estimated time of delivery of the bolus with microspheres, the validity of regional blood flow measurements using the microsphere technique within the superficial renal cortex must be seriously questioned.

Animals↗

PubMed1988

Haematological, physiological and survival data in a porcine model of adult respiratory distress syndrome induced by endotoxaemia. Effects of treatment with N-acetylcysteine.

The effects of N-acetylcysteine (NAC)--which is supposed to act as a free radical scavenger--were evaluated on lung function, haemodynamics and oxygen transport in a porcine model of pulmonary and cardiovascular failure induced by endotoxaemia. Three pigs, serving as controls, received NAC without endotoxin (E) for 6 h, and no notable physiological changes were found. Five pigs received a continuous infusion of E alone for 6 h and displayed a 90% decrease in leukocyte count and a 66% decrease in platelet count. Physiologically a four-fold increase in venous admixture (Qva/Qt), a nearly 2-3 fold increase in mean pulmonary arterial pressure (MPAP) and a progressive decline in cardiac output (Qt) of 60% were documented. Extravascular lung water (EVLW) increased 66%, mean arterial pressure (MAP) decreased 46% and oxygen delivery decreased 52%, leading to a metabolic acidosis. Three animals died during the observation period. Contrastingly, eight pigs, pretreated with NAC 150 mg.kg-1 which was continued at 20 mg.kg-1.h-1, showed a significantly attenuated response to E. Thus, leukocyte and platelet counts decreased 70% and 48%, respectively. Physiologically Qva/Qt increased 2.5-3 fold, MPAP increased 1.3-2 fold, and Qt decreased 32%. EVLW increased 27%, MAP decreased 27% and oxygen delivery decreased only 33% which kept the pH in the normal range. All animals survived the observation period, a significant difference from the E alone group. Thus, NAC significantly attenuated all monitored haematological and pathophysiological changes in the endotoxin model of ARDS in pigs. In addition to a reported free radical scavenger effect of NAC, our results support the assumption that NAC may counteract leukocyte and platelet aggregation in the lung thereby contributing to the beneficial outcome.

Acetylcysteine↗

PubMed1987

The influence of epidural analgesia on the splanchnic exchange of amino acids during upper abdominal surgery.

Splanchnic turnover of plasma amino acids was studied in 10 patients given thoracic epidural analgesia combined with general anaesthesia for elective cholecystectomy. Ten other patients given only general anaesthesia for cholecystectomy served as a control group. All patients received an infusion of glucose during the investigation. The total concentration of amino acids in arterial plasma did not change in the patients given epidural analgesia but decreased by approximately 15% in the non-epidural group. In both groups splanchnic uptake of amino acids increased during surgery and was found to be more than doubled in the early postoperative period. The addition of epidural analgesia to general anaesthesia did not modify the splanchnic uptake of amino acids during surgery and in the immediate (2 h) postoperative period.

Abdomen↗

PubMed1987

Volume substitution and treatment with prostaglandin E1 in a porcine model of endotoxaemia-induced pulmonary and cardiovascular failure.

The effects of prostaglandin E1 (PGE1) and volume substitution (5% albumin) on pulmonary haemodynamics and oxygen transport were evaluated in a porcine model of pulmonary and cardiovascular failure. Albumin was infused i.v. to maintain baseline mean left atrial pressure throughout the experiments. Ten pigs received endotoxin + albumin and showed ten-fold increase in venous admixture, 90% increased extravascular lung water and 25% fall in cardiac output. Oxygen delivery and base excess decreased significantly and four pigs died. In ten other endotoxin-albumin-treated pigs PGE1 infusion (0.25 micrograms X kg-1 X min-1) was begun after established pulmonary and cardiovascular dysfunction, for closer mimicking of clinical use. The raised pulmonary vascular resistance thereafter normalized and extravascular lung water increased by only 15%, but the increase in venous admixture was not influenced. Cardiac output was maintained at baseline. PGE1 prevented further derangement of oxygen delivery and base excess. All the animals survived. The clinical implications may be that volume infusion, even optimally titrated, is not optimum treatment in endotoxemic pulmonary and cardiovascular failure. PGE1 added to optimum volume treatment may be a useful adjuvant in endotoxaemia.

Albumins↗

PubMed1986

Treatment with prostaglandin E1 in a porcine model of early adult respiratory distress syndrome.

The effects of treatment with PGE1 were evaluated in a porcine model of early adult respiratory distress syndrome induced by endotoxaemia. Spontaneously breathing pigs under ketamine anaesthesia were infused i.v. with E. coli endotoxin (10 micrograms X kg-1 X h-1) for 6 h. Thirteen pigs were given endotoxin, and 11 pigs were treated with a continuous infusion of PGE1, 0.25 microgram X kg-1 X min-1 for 4 h, beginning 2 h after start of endotoxin and established lung injury. Four pigs served as controls and receiving only PGE1 (0.25 microgram X kg-1 X min-1) during the whole observation period of 6 h. PGE1 treatment did not influence the decline in platelet and polymorphonuclear cell counts, whereas it markedly decreased the pulmonary hypertension induced by endotoxaemia. The increased extravascular lung water returned towards baseline after institution of PGE1. The increased venous admixture was not significantly influenced by PGE1. Treatment with PGE1 induced an exacerbated hypotensive state in the endotoxaemic animals primarily due to vasodilation. The decline in cardiac output and oxygen delivery noted in endotoxaemic pigs were not influenced by PGE1 and survival was not improved. Although one should be extremely careful in extrapolating these data to the clinical situation the results from the present study suggest the need for optimum volume replacement when starting PGE1 infusion in endotoxin-induced ARDS.

Alprostadil↗