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Biomedical subjects

B Santak

Publications and source records attributed to B Santak.

14 recordsLinked to original sources
PubMed1996

[Nitric oxide--a basic mediator of vasodilation and septic shock].

Nitric oxide is synthesized from the amino acid I-arginine by a family of enzymes, the nitric oxide synthases. The synthesis of nitric oxide by vascular endothelium is responsible for the vasodilatator tone that is essential for the regulation of blood pressure. NO also contributes to the control of platelet aggregation and the regulation of cardiac contractility. These actions are all mediated by the activation of soluble guanylate cyclase and the consequent increase in the concentration of cGMP in target cells. Several studies suggests that some diseases are related to defects in the generation or action of nitric oxide. Some of the features of septic shock, including hypotension, vascular hyporeactivity, myocardial depression and tissue damage appears to result from excess production of NO. Controlled clinical trials to assess the effects of nitric oxide synthase inhibitors on mortality and morbidity in septic shock seem justified and are already planned.

Animals↗
PubMed1995

The effects of prostacyclin on gastric intramucosal pH in patients with septic shock.

OBJECTIVE: To investigate whether infusing prostacyclin (PGI2) in patients with septic shock improves splanchnic oxygenation as assessed by gastric intramucosal pH (pHi). DESIGN: Interventional clinical study. SETTING: Surgical ICU in a university hospital. PATIENTS: 16 consecutive patients with septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine to maintain arterial blood pressure. INTERVENTIONS: All patients received PGI2 (10 ng/kg x min) after no further increase in oxygen delivery could be obtained by volume expansion, red cell transfusion and dobutamine infusion. The results were compared with those before and after conventional resuscitation. The patients received continuous PGI2 infusion for 33-32 days. MEASUREMENTS AND RESULTS: O2 uptake was measured directly in the respiratory gases, pHi was determined by tonometry. Baseline O2 delivery, O2 uptake and pHi were 466 +/- 122 ml/min.m2, 158 +/- 38 ml/min.m2, and 7.29 +/- 0.09, respectively. While O2 uptake remained unchanged, infusing PGI2 increased O2 delivery (from 610 +/- 140 to 682 +/- 155 ml/min.m2, p < 0.01) and pHi (from 7.32 +/- 0.09 to 7.38 +/- 0.08, p < 0.001) beyond the values obtained by conventional resuscitation. While 9 of 11 patients with final pHi > 7.35 survived, all patients with final pHi < 7.35 died (p < 0.01). CONCLUSIONS: Infusing PGI2 in patients with septic shock increases pHi probably by enhancing blood flow to the splanchnic bed and thereby improves splanchnic oxygenation even when conventional resuscitation goals have been achieved.

Adult↗
PubMed1995

Prostacyclin aerosol in an infant with pulmonary hypertension.

Prostacyclin aerosol (100 ng/kg.min) caused selective pulmonary vasodilation without causing systemic hypotension in an infant with idiopathic pulmonary hypertension. Cardiac index increased suggesting improved right ventricular function. CONCLUSION Aerosolized prostacyclin causes selective pulmonary vasodilation and may thereby improve systemic haemodynamics in infants with primary pulmonary hypertension. Because of the lack of known toxicity and the uncomplicated mode of administration it may be a useful alternative to inhaled nitric oxide.

Aerosols↗
PubMed1993

A case of breath holding and ascent-induced circulatory hypotension.

We report a case of transient circulatory depression due to inadvertent apnea of a subject during decompression from a stimulated dive. The dive consisted of exposure to air at 5 bar and subsequent decompression stops. Arterial blood pressure and a lead II ECG were recorded continuously. During decompression from 1.6 to 1.3 bar, the subject inadvertently held his breath. Arterial pressure fell rapidly from 120/80 to 60/53 mmHg within 20 s. Recognizing that the subject held his breath, one of the supervisors ordered him to resume breathing, and arterial blood pressure was restored rapidly. This circulatory depression was probably due to reduced stroke volume such as described for the syncope of ascent: with the subject retaining his breath, the expanding lung volume increased intrathoracic pressure resulting in impaired venous return.

Atmosphere Exposure Chambers↗
PubMed1992

Fat emulsions containing medium chain triglycerides in patients with sepsis syndrome: effects on pulmonary hemodynamics and gas exchange.

Fat emulsions containing medium chain triglycerides (MCT) have recently been introduced into clinical practice as a component of total parenteral nutrition. Since several authors reported increased pulmonary artery pressure and impaired gas exchange during intravenous (i.v.) fat use, in particular in septic patients, we studied the pulmonary hemodynamic and gas exchange effects of i.v. fat containing MCT and long chain triglycerides (LCT) in patients with sepsis syndrome. As the effects of fat emulsions have been attributed to increased formation of prostanoids, the production of thromboxane A2 and prostacyclin was investigated by the determination of urinary thromboxane B2 and 6-keto-prostaglandin F2 alpha, respectively. The i.v. fat use did not induce any alterations in pulmonary hemodynamics and gas exchange, the distribution of ventilation and perfusion nor urinary prostaglandin content. We conclude that fat emulsions containing MCT induce little alterations in pulmonary hemodynamics and gas exchange. This result is probably due to reduced prostaglandin formation because fat emulsions containing MCT provide less prostaglandin precursors than pure LCT emulsions.

Adult↗
PubMed1991

Influence of SIMV plus inspiratory pressure support on VA/Q distributions during postoperative weaning.

Since the introduction of synchronized intermittent mandatory ventilation (SIMV) several advantages have been attributed to this ventilatory mode, one of them being a more homogeneous distribution of ventilation and perfusion than during controlled mechanical ventilation (CMV). Up to now no data are available to confirm whether this is true when SIMV is used in combination with inspiratory pressure support (IPS). Therefore, we compared the influence of CMV and SIMV + IPS on the distributions of ventilation and perfusion in 9 patients undergoing weaning from postoperative mechanical ventilation. Continuous distributions of ventilation and perfusion were assessed using the multiple inert gas elimination technique (MIGET). SIMV + IPS did not induce any change in the hemodynamic or oxygenation parameters, in particular CI and PaO2 remained constant. Physiological dead space (VD/VT) increased, but PaCO2 remained unchanged due to increased minute ventilation (from 9.5 +/- 0.9 l.min-1 to 11.3 #/- 1.2 l.min-1). The perfusion distributions remained unaltered; there was no change in QS/QT nor in the perfusion of the low VA/Q lung regions. This result was underscored by the unchanged dispersion of the perfusion distribution (log SDQ). The increased VD/VT was caused by increased inert gas dead space (from 22.0 +/- 9.6 to 26.8 +/- 8.7%) which was accompanied by increased ventilation of lung regions with high VA/Q ratios (10 less than VA/Q less than 100) in 3 patients. These results show that in our group of patients partial removal of CMV together with pressure support assistance of spontaneous ventilation did not induce a clinically significant loss of the efficiency of the breathing pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS.

Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng.kg-1.min-1) for 45 min. We examined whether reducing the right ventricular (RV) outflow pressures by PGI2 infusion would increase the right ventricular ejection fraction (RVEF) measured by thermodilution. PGI2 reduced the pulmonary artery pressure (PAP) from 35.6 to 29.1 mmHg (p less than 0.01). The cardiac index (CI) increased from 4.2 to 5.81.min-1.m-2 (p less than 0.01) partly due to an increased stroke volume. The decreased PAP together with the increased CI resulted in a fall of the calculated pulmonary vascular resistance index (PVRI, from 5.1 to 2.5 mmHg.min.m2.1-1, p less than 0.01). In the patients with subnormal baseline RVEF the increased stroke volume was associated with an increased RVEF (from 47.6% to 51.8%, p less than 0.05) suggesting improved RV function. This result was underscored by a significant relationship between the changes in PVRI and RVEF (r = 0.789, delta % RVEF = 2.11.delta PVRI-1.45). Despite an increased venous admixture from 27.8% to 36.9% (p less than 0.05) the arterial PO2 remained constant resulting in an increased oxygen delivery from 657 to 894 ml.min-1.m-2 (p less than 0.01). We conclude that short term infusions of PGI2 increased CI concomitant to improved RV function parameters when baseline RVEF was depressed. Since improved oxygen availability should be a major goal in the management of patients with ARDS PGI2 may be useful to lower pulmonary artery pressure in ARDS.

Adult↗
PubMed1990

Prostacyclin for the treatment of pulmonary hypertension in the adult respiratory distress syndrome: effects on pulmonary capillary pressure and ventilation-perfusion distributions.

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.

Adult↗
PubMed1990

Nitrogen partial pressures in man after decompression from simulated scuba dives.

In five subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure at rest to air at 6 bar for 30 min. corresponding to a depth of 50 m. Afterwards the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6 and 1.3 bar with a total decompression time of 73 min. Immediately after decompression and every 40 min. until the 240th min. arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min. after decompression indicating still incomplete nitrogen wash-out at least two hours after decompression had been accomplished. Bubble formation is discussed as a cause for prolonged nitrogen elimination. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest.

Arteries↗
PubMed1990

Nitrogen partial pressures in man after decompression from simulated scuba dives at rest and during exercise.

In 5 subjects arterial and central venous nitrogen partial pressures (PN2) were measured after decompression from a chamber dive following a decompression schedule for scuba diving. The simulated dives consisted of exposure to air at 6 bar for 30 min corresponding to a depth of 50 m. Afterward the subjects were decompressed with decompression stops at 2.5, 2.2, 1.9, 1.6, and 1.3 bar with a total decompression time of 67 min. In 3 of the subjects the measurements were repeated after they had exercised (workload 75 W) during bottom time. Immediately after decompression and every 40 min until Minute 240 arterial and central venous blood samples were analyzed for PN2 using a manometric Van Slyke apparatus. Venous PN2 remained elevated until 160 min after decompression, indicating still incomplete nitrogen washout for at least 2 h after decompression had been accomplished. We did not find any difference in PN2 values after decompression from dives at rest and after exercise. Applying a computer program based on a wide range of theoretical tissue half-times nitrogen elimination proved to be consistent with Haldanian theories when using our decompression profile. Our data confirm that nitrogen elimination is prolonged after decompression from simulated dives at rest and after exercise.

Adult↗
PubMed1989

Prostaglandin E1 and nitroglycerin reduce pulmonary capillary pressure but worsen ventilation-perfusion distributions in patients with adult respiratory distress syndrome.

Pulmonary artery hypertension associated with adult respiratory distress syndrome (ARDS) may increase microvascular filtration pressure by increasing pulmonary capillary pressure (PCP). To evaluate the potential to reverse this consequence of pulmonary artery hypertension, the effects of short-term vasodilator treatment were compared with prostaglandin E1 (PGE1) or nitroglycerin (NTG) on pulmonary hemodynamics and gas exchange. The two vasodilators were infused in ten patients with mild or moderate ARDS at a dosage rate achieving a 20% reduction of the mean arterial pressure. PCP was estimated by graphic analysis of the pulmonary artery occlusion curve, and continuous ventilation-perfusion (VA/Q) distributions were assessed using the multiple inert gas technique. At the given dosages both drugs induced equivalent reductions of the mean pulmonary artery pressure (PAP) from 28.2 +/- 3.6 to 23.7 +/- 3.2 with PGE1 and to 23.4 +/- 3.2 mmHg with NTG. The right atrial and pulmonary artery wedge pressure (PAWP) were also decreased to the same extent associated with the expected decrease in PCP from 17.4 +/- 2.6 to 15.1 +/- 3.3 with PGE1 and to 15.6 +/- 2.7 mmHg with NTG. The estimated PCP values were closely correlated with the values calculated according to Gaar's equation (r = 0.822. n = 23, P less than 0.001) with a regression close to the identity line. The contribution of pulmonary venous resistances to the resistance of the whole pulmonary vascular bed computed as the ratio (PCP- PAWP)/(PAP-PAWP) was 0.28 and remained unchanged during vasodilator infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗