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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular responses to isoflurane (forane)-nitrous oxide-oxygen anaesthesia were studied in seven older premedicated patients. Anaesthesia was induced with the new non-barbiturate induction agen etomidate. All patients were intubated and mechanically ventilated to maintain normal PaCO2. Clinical concentrations of isoflurane (0.75 and 1.5 vol.-% inspiratory) decreased mean arterial pressure 22%-42%. Only small reductions in cardiac output and stroke volume were seen. Heart rate, central venous and pulmonary artery pressure remained nearly unaffected. The major cause of the arterial hypotension was a fall in total peripheral resistance by 36% as anaesthesia deepened. Left ventricular maximum dp/dt and load data indicated that isoflurane also possesses negative inotropic properties. Tension-time-index and total body oxygen consumption decreased by 47% and 20% respectively. AVDO2 values remained within the normal range. We take this to mean that the oxygen supply was adequate to meet the metabolic demands of the body as a whole. This was corroborated by the finding that base excess did not change significantly. Conclusions considering the use of isoflurane in patients with diminished cardiovascular reserve are drawn.
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PMID:[Cardiovascular effects of the new inhalation anaesthetic isoflurane in man (author's transl)]. 119 Apr 13

A 20 year old male motorist with multiple injuries, including bilateral lung laceration, developed cardiac tamponade 12 hours after injury. X-ray showed characteristic findings of pneumopericardium with air all around the cardiac silhouette, which was diminished in size. A chest tube was inserted intrapericardially through a subxiphoid incision. Blood pressure increased immediately, and central venous pressure became normal. Cardiac left ventricular stroke work increased by 86% to normal value. The drain was removed after three days. Another patient was a 15 year old male cyclist who had been overrun by a trailer. Left-sided emergency thoracotomy was performed during laparotomy for liver and vena cava injury, in the course of which procedures there was a sudden decrease in blood pressure with marked elevation of the central venous pressure. The pericardium was incised. Air hissed out, leading to normalisation of arterial and venous pressures. Both patients recovered. Pneumopericardium without symptoms may be treated by observation. Tension pneumopericardium is rare and is best treated by open drainage.
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PMID:[Traumatic pneumopericardium with cardiac tamponade]. 152 29

Tension lag time on electric stimulation (TLTe), i.e., latency from the stimulus to the rise of tension, and contraction time (CT) of the rectus femoris muscle on twitch contraction were measured on the affected and non-affected sides of eight patients with spastic hemiparesis due to stroke. Both TLTe and CT were significantly longer on the affected side than on the non-affected side, suggesting changes in contractile properties of the spastic muscle.
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PMID:Prolonged tension lag time of knee extensor muscle on twitch contraction in patients with spastic hemiparesis. 319 4

We have performed thin-section electron microscopy on muscle fibers fixed in different mechanically monitored states, in order to identify structural changes in myosin crossbridges associated with force production and maintenance. Tension and stiffness of fibers from glycerinated Lethocerus flight muscle were monitored during a sequence of conditions using AMPPNP and then AMPPNP plus increasing concentrations of ethylene glycol, which brought fibers through a graded sequence from rigor relaxation. Two intermediate crossbridge forms distinct from the rigor or relaxed forms were observed. The first was produced by AMPPNP at 20 degrees C, which reduced isometric tension 60 to 70% below rigor level without reducing rigor stiffness. Electron microscopy of these fibers showed that, in spite of the drop in tension, no obvious change from the 45 degrees crossbridge angle characteristic of rigor occurred. However, the thick filament ends of the crossbridges were altered from their rigor positions, so that they now marked a 14.5 nm repeat, and formed four separate origins at each crossbridge level. The bridges were also less slewed and bent than rigor bridges, as seen in transverse sections. The second crossbridge form was seen in glycol-AMPPNP at 4 degrees C, just below the glycol concentration that produced mechanical relaxation. These fibers retained 90% of rigor stiffness at 40 Hz oscillation, but would not bear sustained tension. Stiffness was also high in the presence of calcium at room temperature under similar conditions. Electron microscopy showed crossbridges projecting from the thick filaments at an angle that centered around 90 degrees, rather than the 45 degree angle familiar from rigor. This coupling of relaxed appearance with persistent stiffness suggests that the 90 degree form may represent a weakly attached crossbridge state like that proposed to precede force development in current models of the crossbridge power stroke.
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PMID:Two attached non-rigor crossbridge forms in insect flight muscle. 322 90

1. A technique was developed to generate 2-8 degrees C step temperature perturbations (T-jumps) in single muscle fibres to study the thermodynamics of muscle contraction. A solid-state pulsed holmium laser emitting at 2.065 microns heated the fibre and surrounding solution in approximately 150 mus. The signal from a 100 microns thermocouple fed back to a heating wire maintained the elevated temperature after the laser pulse. 2. Tension of glycerol-extracted muscle fibres from rabbit psoas muscle did not change significantly following T-jumps when the fibre was relaxed. 3. In rigor, tension decreased abruptly on heating indicating normal (not rubber-like) thermoelasticity. The thermoelastic coefficient (negative ratio of relative length change to relative temperature change) of the fibre was estimated to be -0.021 at sarcomere lengths of 2.5-2.8 microns. Rigor tension was constant after the temperature step and returned to the original value on recooling. 4. In maximal Ca2+ activation, tension transients initiated by T-jumps had several phases. An immediate tension decrease suggests that thermoelasticity during contraction is similar to that in rigor. Active tension then recovered to the value before the T-jump with an apparent rate constant of approximately 400 s-1 (at 10-20 degrees C). This rate constant did not have an appreciable dependence on the final temperature. Finally, tension increased exponentially to a new higher level with a rate constant of approximately 20 s-1 at 20 degrees C. This rate constant increased with temperature with a Q10 of 1.4. 5. At submaximal Ca2+ activation the tension rise was followed by a decay to below the value before the T-jump. This decline was expected from the temperature dependence of steady pCa-tension curves. The final tension decline occurred on the 1-5 s time scale. 6. The value and amplitude dependence of the rate constant for the quick recovery following T-jumps were similar to those of the quick recovery following length steps during active contractions. The enthalpy change associated with the quick tension recovery following temperature-step perturbations was estimated to be positive suggesting that the recovery process is an endothermic reaction. Slower reaction steps on the 10-30 ms timescale, as well as reactions corresponding to the quick recovery, may contribute to the cross-bridge power stroke.
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PMID:Transient tension changes initiated by laser temperature jumps in rabbit psoas muscle fibres. 344 91

The time course of tension development produced by fast isometric contraction of the quadriceps femoris muscle for knee extension was examined on eight normal subjects and 14 patients with spastic hemiparesis due to stroke. Tension lag time (TLT), the latency from the onset of EMG activities to the rise of tension, and contraction time (FTmax), the period from the rise of tension to its maximum, were longer in the patients than in the normal subjects. The prolongation of FTmax correlated with the decreased rate of tension development. The results indicated that the temporal characteristics of tension development altered in the spastic paresis, reflecting functional changes in the muscle and motor neurons.
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PMID:The altered time course of tension development during the initiation of fast movement in hemiplegic patients. 357 13

A study was made of the effects of different inotropic factors on mechanical tension in the left ventricular wall and in the apex of the heart and of the participation of these regions in the formation of hemodynamic characteristics. Adrenaline caused similar effects whereas CaCl2 exerted different inotropic effects on the left ventricular wall and the apex of the heart. Changes in mechanical tension of the wall correlated with variations in the pressure inside the left ventricle. Tension in the apex of the heart produced alterations in the stroke volume.
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PMID:[Mechanical tension in different parts of the left ventricle of the heart exposed to inotropic factors]. 402 60

Vasopressin (0.01-0.3 IU/ml) contracted isolated segments of rat basilar arteries from stroke-prone SHR (SP-SHR) and normotensive Wistar-Kyoto rats (WKY) unequally. Basilar arteries from SP-SHR were more responsive to vasopressin than were those from WKY when adrenergic nerve endings were present in both preparations. After destruction of adrenergic nerve endings by in vitro 6-hydroxydopamine treatment, the ED50 for vasopressin in both WKY and SP-SHR arteries decreased by a factor of three, indicating that the contractions caused by vasopressin were similarly modulated by prejunctional neurotransmitter release. However, only arteries from WKY showed prominent rhythmic relaxation-contraction cycles superimposed upon the vasopressin-induced tone. The tension cycles were 20-100 dyn in amplitude and occurred at 1-3 cycles/min. These tension oscillations of WKY were pronounced and obvious, sometimes amounting to as much tension as the underlying tonic contraction. Tension cycles could reflect a physiological contraction-relaxation phasing mechanism that fails to occur in basilar arteries of SP-SHR. The rhythmic activity was enhanced by K+-free solution and abolished by 30 mM K+ solution, suggesting that pacemaker changes in K+ conductance may underlie the WKY tension oscillations. It is suggested that the absence of rhythmic contractions in SP-SHR basilar arteries may be explained by greater activity of the electrogenic Na+-pump, which would tend to prevent the rhythmic oscillations in tension. These observations suggest that vasopressin has a differential action on basilar arteries of SP-SHR and WKY.
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PMID:Difference in vasopressin-induced contraction of basilar arteries from stroke-prone spontaneously-hypertensive rats (SP-SHR) and control Wistar-Kyoto rats (WKY). 644 11

We have evaluated left ventricular function in anaesthetized (morphine, pentobarbital), artificially ventilated, normotensive beagle dogs immediately (0 to 30 min) after i.v. bolus injection of clonidine (1, 3, 5, 7, 10 and 15 micrograms/kg of b.w.) using computer assisted catheterization technique. Clonidine decreased heart rate and prolonged pre-ejection, ejection and diastolic periods significantly. Cardiac output, mean systolic ejection rate, left ventricular (LV) dP/dtmax and Vmax decreased (p less than 0.05 to 0.01). LV peak pressure and aortic pressures decreased but the decrease was preceded by an initial rise at doses 5 to 10 micrograms/kg. At dose 15 micrograms/kg the rise persisted through the whole period. LV filling and end-diastolic pressures increased while end-diastolic and stroke volumes decreased. These changes indicate negative chronotropic and inotropic effects and increment in preload with the latter being a situation met in the case of proper LV filling. Tension time index and mean outflow resistance, however, indicate reduction in LV oxygen consumption at doses less than 10 micrograms/kg. It is suggested that enhancement of parasympathetic tone would account for these changes.
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PMID:Left ventricular responses to intravenous administration of clonidine in anaesthetized dogs. 659 61

To assess the hemodynamic effects of Clonidine in hypertensive patients (pts) with an acute myocardial infarction (AMI), we administered the drug to 12 such patients either in a single bolus (75--150 micrograms in 5 min - 8 pts) or by continuous infusion (0.4--5 micrograms/min - 4 pts). Hemodynamic measurements were obtained by means of a Swan-Ganz thermodilution catheter, before and 60 min after the administration of the drug. Clonidine did not significantly affected Heart Rate (from 80.5 +/- 3.9 to 78.4 +/- 5.9 beats/min), Mean Pulmonary Arterial Pressure (from 18.6 +/- 1.7 to 15.1 +/- 1 mmHg), Mean Pulmonary Wedge Pressure (from 12.5 +/- 1.1 to 10.6 +/- 0.7 mmHg), central Venous Pressure (from 4 +/- 0.8 to 3 +/- 0.9 mmHg), Cardiac Index (from 2.6 +/- 0.07 to 2.6 +/- 0.7 L/min/m2), Stroke Volume (from 65.2 +/- 2.8 to 68.5 +/- 5.5 ml/b). Conversely Mean Arterial Pressure fell significantly from 127 +/- 3.1 to 96.2 +/- 7.2 mmHg (P less than 0.001). Left Ventricular Systolic Work Index was reduced from 62.3 +/- 3.3 to 50.4 +/- 4.4 gm/beats/m2 (P less than 0.025), Total Systemic Resistances from 1888 +/- 50 to 1412 +/- 117 dyne sec cm-5 (P less than 0.005) and Tension Time Index from 3536 +/- 495 to 2389 +/- 385 x 10(3) mmHg x sec/min (p less than 0.05). Clonidine is a safe and useful drug to obtain a fall of high blood pressure often complicating AMI, without depressing left ventricular performance, as suggested by no significant changes of CI, WP and LVSWI. The reduction of TTI suggests a beneficial effect on the balance between myocardial oxygen delivery and demand. Clonidine is a hypotensive drug which can be safely used in patients with AMI, without depressing the left ventricular performance.
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PMID:[Hemodynamic effects of intravenous clonidine in patients with acute myocardial infarction]. 676 71


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