Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Heart Injuries”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

[Heart injuries].

The work is based on the results of an analysis of medical care of 453 patients with wounds of the heart and pericardium. It has been shown that the successful treatment of such patients is possible only in cases of complete succession of performing medical procedures at the prehospital and hospital stages based on urgent in time and adequate in volume life-saving interventions, arriving to the wounded of a specialist included in the surgical resuscitation team. It was found that in 32.4% of the wounded who died at the prehospital stage the wound of the heart was not absolutely fatal. So, the volume of medical care at the prehospital stage must be wider and more intensive.

Adult↗

Hypoxic brain and heart injury thresholds in piglets.

Both heart and brain are at risk for damage from asphyxia. However, these 2 organs' relative injury-thresholds have remained poorly defined. The present study using 16 anesthetized newborn piglets attempts to separate brain and heart damaging exposures from those that leave these organs unaffected. The hypoxic exposure (mean PaO2 = 3.6 +/- 0.6 kPa (27 mmHg) lasted for an average duration of 40 minutes and was associated with hypotension less than 4.7 kPa (35 mmHg) MABP. For brain damage assessment, 9 piglets that survived greater than 12 hours following resuscitation permitting histologic evaluation were used. For heart outcome assessment, those piglets that developed a postexposure, secondary hypotension to less than 4.7 kPa (35 mmHg) were compared to those without excluding 3 with uncertain cause of death. BRAIN-RESULTS: Six piglets remained brain intact while 3 exhibited brain edema and diffuse neuronal damage. The damaged animals' exposures differed from those that remained brain intact in sustaining significantly lower lowest MABPs (1.6 +/- 0.1 vs 3.3 +/- 0.4 kPa (12 vs 25 mmHg] and longer durations of MABP below 3.3 kPa (25 mmHg): 6 vs 1 min. and below 2.7 kPa (20 mmHg): 4 vs 0 min. HEART-RESULTS: Six of 13 animals developed marked delayed post-exposure hypotension requiring 5 to be killed prior to complete cardiovascular collapse. The only significant difference observed during exposure differentiating the two outcome groups (blood pressure maintenance vs cardiogenic shock) was the latter's more marked systemic acidosis (lowest mean arterial blood pH: 6.61 +/- 0.10 vs 6.91 +/- 0.10). These results suggest the brain is at risk for damage during hypoxia only when accompanied by an extreme lowering of blood pressure and the heart when accompanied by a severe acidosis. Further, the heart and brain need not both be damaged by the same hypoxic exposure. Contrary to common belief, the brain is not readily damaged from hypoxia alone absent marked circulatory changes.

Animals↗

Cardioprotective effects of [5-(2-methyl-5-fluorophenyl)furan-2-ylcarbonyl]guanidine (KR-32568) in an anesthetized rat model of ischemia and reperfusion heart injury.

The effects of a novel sodium/hydrogen exchanger-1 (NHE-1) inhibitor, KR-32568, were studied in an anesthetized rat model of 30 min ischemia/2.5 h reperfusion heart injury. KR-32568 dose-dependently inhibited NHE-1-mediated rabbit platelet swelling induced by intracellular acidification. In our anesthetized rat model, KR-32568 reduced infarct size from 67 (control) to 43 and 24% at 0.1 and 1.0 mg/kg (i.v. bolus, given 10 min before ischemia), respectively. KR-32568 at the same doses also significantly reduced the total number of ventricular premature beats during ischemia/reperfusion from 530 (control) to 266 and 115 beats, ventricular tachycardia (VT) incidence from 51 (control) to 21 and 8, VT duration from 238 s (control) to 63 and 33 s, ventricular fibrillation (VF) incidence from 17 (control) to 8 and 0, and VF duration from 85 s to 18 and 1 s. These results indicate that KR-32568 may exert potent cardioprotective effects in rats via inhibition of sodium/hydrogen exchanger-1.

Anesthesia↗